Knowledge and perceptions of medical abortion among potential users

Great advances in surgical techniques, perfusion technology and cardiac anesthesia have made heart surgery safer. However, the mayor advance over the past 15 years has been in the field of myocardial protection. Much remains to be done in this field and there is not complete agreement about the different methods of myocardial protection. At the Institute of Cardiac Surgery of Parma a research is developing to concern three different cardioprotective strategies, of which preliminary results are showing. Three groups of patients with the same clinical, surgical, anesthesiological features, who underwent cardiac surgery have been selected. In patients of group A intermittent cold hyperkalemic crystalloid cardioplegia has been used, in those of group B intermittent cold blood cardioplegia and in those of group C intermittent cold blood cardiolegia associated a warm glucose blood cardioplegic reperfusion before aortic unclamping. In all patients enzyme levels (CPK; CPK-MB; LHD; SGOT; SGPT) were measured 12, 24, 72, 120 hours postoperatively; data were collected, also, on spontaneous return to sinus rhythm, perioperative myocardial infarction and the need or not for inotropic agents. All data at first and then those of patients who underwent only coronary rivascularization (75% of patients) were statistically analyzed (one-way Fischer's test). It appears that the use of antegrade cold intermittent blood cardioplegia with reperfusion is more optimal for myocardial protection, how show lower levels of CPK-MB especially in the first postoperative period. In group C remains greater spontaneous resumption of normal sinus rhythm compare to group A and this suggests a best preservation of cellula-integrity and function with use of blood cardioplegia.     

Warm reperfusion and myocardial protection

BACKGROUND: The aim of this study was to determine whether warm reperfusion improves myocardial protection with cardiac troponin I as the criteria for evaluating the adequacy of myocardial protection. METHODS: One hundred five patients undergoing first-time elective coronary bypass surgery were randomized to one of three cardioplegic strategies of either (1) cold crystalloid cardioplegia followed by warm reperfusion, (2) cold blood cardioplegia followed by warm reperfusion, or (3) cold blood cardioplegia with no reperfusion. RESULTS: The total amount of cardiac troponin I released tended to be higher in the cold blood cardioplegia with no reperfusion group (3.9+/-5.7 microg) than in the cold blood cardioplegia followed by warm reperfusion group (2.8+/-2.7 microg) or the cold crystalloid cardioplegia followed by warm reperfusion group (2.8+/-2.2 microg), but not significantly so. Cardiac troponin I concentration did not differ for any sample in any of the three groups. CONCLUSIONS: Our study showed that the addition of warm reperfusion to cold blood cardioplegia offers no advantage in a low-risk patient group.     

Ischemic preconditioning prior to myocardial protection with cold blood cardioplegia in coronary surgery

OBJECTIVE: Encouraging results on myocardial preconditioning in experimental models of infarction, stunning or prolonged ischemia raise the question whether preconditioning techniques may enhance conventional cardioplegic protection used for routine coronary surgery. METHODS: A prospective clinical trial was conducted to investigate the effect of additional ischemic normothermic preconditioning prior to cardioplegic arrest applying cold blood cardioplegia in patients scheduled for routine coronary surgery (3 vessel disease, left ventricular ejection fraction > 50%). Two cross clamp periods of 5 min with the hearts beating in sinus rhythm were applied followed by 10 min of reperfusion, each (n = 7, group I). Inducing moderate hypothermia cold blood cardioplegia was delivered antegradely. In control groups, cold intermittent blood cardioplegia (n = 7, group II) was used alone. Coronary sinus effluents were analyzed for release of creatine kinase (CK), CK-MB, lactate, and troponin T at 1, 3, 6, 9, and 12 h. In addition, postoperative catecholamine requirements were monitored. RESULTS: The procedure was tolerated well, and no perioperative myocardial infarction in any of the groups studied occurred. Concentrations of lactate tended to be higher in group I, but this difference was not significant. In addition, no significant differences for concentrations of CK, CK-MB, and troponin T were found. Following ischemic preconditioning an increased dosage of dopamine was required within the first 12 h postoperatively (group I: 2.63 +/- 1.44 microg/kg/min, group II: 0.89 +/- 1.06 microg/kg/min). CONCLUSIONS: Combining ischemic preconditioning and cardioplegic protection with cold blood cardioplegia does not appear to ameliorate myocardial protection when compared to cardioplegic protection applying cold blood cardioplegia alone. Inversely, contractile function seemed to be impaired when applying this protocol of ischemic preconditioning.     

Crystalloid versus cold blood cardioplegia and cardiac troponin I release

BACKGROUND: Cardiac troponin I (CTnI) has been shown to be a marker of myocardial injury. The aim of this study was to compare antegrade crystalloid cardioplegia with antegrade cold blood cardioplegia with warm reperfusion using CTnI release as the criteria for evaluating the adequacy of myocardial protection. METHODS AND RESULTS: Seventy patients were randomly assigned to receive crystalloid or blood cardioplegia. CTnI concentrations were measured in serial venous blood samples drawn just before cardiopulmonary bypass and after aortic unclamping at 6, 9, 12, and 24 hours and daily thereafter for 5 days. ANOVA with repeated measures was performed to test the effect of the type of cardioplegia on CTnI release. The total amount of CTnI released was higher in the crystalloid cardioplegia group than in the blood cardioplegia group (11.2 +/- 8.9 versus 7.8 +/- 8.6 micrograms, P < .02). CTnI concentration was significantly higher in the crystalloid group than in the blood group in the samples drawn at hours 9 and 12. Three patients in each group had ECG evidence of perioperative myocardial infarction. Eight patients in the crystalloid group and five patients in the blood group had CTnI evidence of perioperative myocardial infarction. CTnI release was significantly lower in patients requiring no electrical defibrillation after aortic unclamping. CONCLUSIONS: Cold blood cardioplegia followed by warm reperfusion is beneficial in an unselected group of patients with a preserved left ventricular function undergoing an elective first coronary artery bypass grafting. CTnI allowed the diagnosis of small perioperative necrotic myocardial areas. The need for electrical defibrillation after aortic unclamping was related to a higher release of CTnI. A further study is necessary to determine whether this technique was beneficial because of cold blood cardioplegia, warm reperfusion, or both.     

Effects of cold and warm blood cardioplegia assessed by myocardial pH and release of metabolic markers

The optimal temperature of blood cardioplegia remains controversial. Interstitial myocardial pH was monitored online with a probe that was inserted in the anterior wall of the left ventricle. Venous pH, lactate production, and creatine kinase and troponin T release were measured in coronary sinus blood obtained in 14 dogs after ischemic arrest periods of 5, 10, 20, and 40 minutes with warm (n = 7; mean myocardial temperature, 35 degrees +/- 2 degrees C) and cold (n = 7; mean myocardial temperature, 12 degrees +/- 1 degree C) blood cardioplegic protection. Blood cardioplegic solution was delivered at a rate of 100 mL/min during the 10 minutes between each ischemic arrest. The interstitial myocardial pH decreased significantly (p < 0.05) from 7.1 +/- 0.3 to 6.53 +/- 0.3 after ischemia in animals perfused with warm blood cardioplegia and from 7.04 +/- 0.3 to 6.64 +/- 0.1 in those receiving cold blood cardioplegic protection; however, the difference between the groups was not significant (p > 0.05). Lactate production and creatine kinase and troponin T release increased significantly after ischemia, but there was no difference in the changes between the warm and cold blood cardioplegia groups. In conclusion, ischemia caused significant changes in all variables measured, and these changes were directly proportional to the duration of ischemia. However, there was no significant difference (p > 0.05) in the myocardial metabolic changes between the warm and cold blood cardioplegia groups in terms of the duration of ischemic arrest studied.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of myocardial protection with DBcAMP in crystalloid cardioplegic solutions

The potential for myocardial protection during cardiac operation was evaluated by adding Dibutyryl cyclic AMP (DBcAMP) to the crystalloid cardioplegic solutions. We have compared the cold crystalloid cardioplegia with DBcAMP (Group D n = 15) and without DBcAMP (Group n = 20) in patients undergoing cardiac operation. In hemodynamics, both groups were no difference before and after operation. CPK and CPK-MB was significantly (p < 0.01) high level after cardiopulmonary bypass (CPB) in group C. Myoglobin was also high value after CBP in group C, but not significant. Myocardial oxygen extraction rate and coronary blood PCO2 release were similar change in both groups. Insulin/glucose ratio was high level during and after CBP in group D. Myocardial lactate/pyruvate ratio was very high level after CBP in group C without significant difference. We consider that the cardioplegic solution with DBcAMP is effectual for the myocardial metabolism and preservation of myocardial damage during cardiac arrest.     

The effect of ionic strength on liposome-buffer and 1-octanol-buffer distribution coefficients

BACKGROUND: To evaluate the safety and effectiveness of tepid perfusion and isothermic blood cardioplegia in coronary surgery. METHODS: We studied 200 patients undergoing myocardial revascularization: 100 procedures were performed with moderate systemic hypothermia (28 degrees C) and cold crystalloid cardioplegia (4 degrees C); the other 100 patients received tepid systemic perfusion (TP) (34 degrees C) and intermittent blood cardioplegia at the same temperature according to the minicardioplegia technique (Group 2). The two groups were comparable with regards to age, extent of disease, preoperative left ventricular function and extra-corporeal circulation (ECC) time. RESULTS: In the tepid group we observed a higher incidence of spontaneous resumption of cardiac rhythm at cross-clamp removal compared to the hypothermic group (93% vs 34%; p<0.001). No difference was found in cardiac index at specified intervals, myocardial enzymes, inotrope requirements, arrhythmias, need for vasopressors and postoperative blood loss. Fluid balance at the end of ECC was significantly lower in the tepid group (343+/-635 ml vs 883+/-925 ml; p<0.001). Hospital mortality and morbidity were the same in the two groups. CONCLUSIONS: Our data suggest that TP and isothermic blood cardioplegia represent a simple, safe and effective method of systemic and myocardial protection which may be an alternative to traditional hypothermia.     

Antimicrobial activity in the skin of the channel catfish Ictalurus punctatus: characterization of broad-spectrum histone-like antimicrobial proteins

BACKGROUND: A major reduction in the energy demand of the myocardium results from the electromechanical arrest, and cooling contributes to a lesser degree to this reduction. It is from this assumption that strategies of myocardial protection, utilizing warm blood cardioplegic induction, followed by cold cardioplegia with terminal warm reperfusion before removal of the aortic cross clamp, became established as optimal myocardial protection. Continuous normothermic perfusion 'closed the loop' by avoiding myocardial ischemia and linking warm induction and terminal reperfusion. A series of laboratory and clinical data confirmed the benefits of warm heart surgery on myocardial function and metabolism. The disadvantages of continuous warm blood cardioplegia including disturbance of the operative field, led surgeons to administer warm hyperkalaemic blood intermittently as a new cardioplegic strategy. METHODS: This review examines the laboratory and clinical data with reference to the intermittent warm blood cardioplegia, to establish its experimental basis and place in clinical practice. CONCLUSIONS: Experimental observation and clinical application have established intermittent warm blood cardioplegia as a practical, effective and cheap myocardial protection technique, particularly with reference to coronary artery surgery.     

Intermittent antegrade tepid versus cold blood cardioplegia in elective myocardial revascularization

BACKGROUND: The ideal temperature for blood cardioplegia administration remains controversial. METHODS: Fifty-two patients who required elective myocardial revascularization were prospectively randomized to receive intermittent antegrade tepid (29 degrees C; group T, 25 patients) or cold (4 degrees C; group C, 27 patients) blood cardioplegia. RESULTS: The two cohorts were similar with respect to all preoperative and intraoperative variables. The mean septal temperature was higher in group T (T, 29.6 degrees +/- 1.1 degrees C versus 17.5 degrees +/- 3.0 degrees C; p < 0.0001). After reperfusion, group T exhibited significantly greater lactate and acid release despite similar levels of oxygen extraction (p < 0.05). The creatine kinase-MB isoenzyme release was significantly lower in group T (764 +/- 89 versus 1,120 +/- 141 U x h/L; p < 0.04). Hearts protected with tepid cardioplegia demonstrated significantly increased ejection fraction with volume loading, improvement in left ventricular function at 12 hours, and decreased need for postoperative inotropic support (p < 0.05). The frequency of ventricular defibrillation after cross-clamp removal was lower in this cohort (p < 0.05). There were no hospital deaths, and both groups had similar postoperative courses. CONCLUSIONS: Intermittent antegrade tepid blood cardioplegia is a safe and efficacious method of myocardial protection and demonstrates advantages when compared with cold blood cardioplegia in elective myocardial revascularization.     

Resistance of the failing dystrophic hamster heart to the cardioprotective effects of diltiazem and clentiazem: evidence of coronary vascular dysfunctions

Although hypothermia and cardioplegic cardiac arrest provide effective protection during cardiac surgery, ischemia of long duration, poor preoperative myocardial function, and ventricular hypertrophy may lead to heterogeneous delivery of cardioplegic solutions, incomplete protection, and impaired postischemic recovery. Calcium antagonists are potent cardioprotective agents, but their efficacy in the presence of cold cardioplegia is still controversial, especially in heart failure, since it is often believed that failing hearts are more sensitive to their negative inotropic and chronotropic actions. However, recent data have demonstrated that the benzothiazepine-like calcium antagonists diltiazem and clentiazem, in selected dose ranges, elicit significant cardioprotection independently of intrinsic cardiodepression, thus lending support to their use in cardioprotective maneuvers involving the failing heart. We therefore evaluated the cardioprotective interaction of diltiazem, clentiazem, and cold cardioplegia in both normal and failing ischemic hearts. Hearts were excised from 200- to 225-day-old cardiomyopathic hamsters (CMHs) of the UM-X7.1 line and age-matched normal healthy controls. Ex vivo perfusion was performed at a constant pressure (140 cmH2O; 1 cmH2O = 98.1 Pa) according to the method of Langendorff. Heart rate, left ventricular developed pressure (LVDP), and coronary flow were monitored throughout the study. Global ischemia was produced for 90 min by shutting down the perfusate flow, followed by reperfusion for 30 min. Normal and failing CMH hearts were either untreated (control) or perfused at the onset of global ischemia with one of the following combinations: cold cardioplegia alone (St. Thomas' Hospital cardioplegic solution, 4 degrees C, infused for 2 min), cold cardioplegia + 10 nM diltiazem, or cold cardioplegia + 10 nM clentiazem. The cardiac and coronary dilator properties of 10 nM diltiazem and 10 nM clentiazem alone were investigated in separate groups of isolated preparations. Failing CMH hearts had lower basal LVDP (42 +/- 2 vs. 77 +/- 2 mmHg (1 mmHg = 133.3 Pa) for normal hearts, p < 0.05), while coronary flow was only slightly reduced (5.6 +/- 0.2 vs. 6.2 +/- 0.2 mL/min for normal hearts). Following 90 min global ischemia, coronary flow was increased in both groups, but the peak hyperemic response declined only in failing CMH hearts (+50 +/- 17 vs. +82 +/- 17% in normal hearts). In normal hearts, LVDP virtually recovered within 5 min of reperfusion but steadily decreased thereafter (-37 +/- 4% at 30 min). In contrast, in failing CMH hearts, LVDP significantly decreased early during reperfusion but improved over time (-19 +/- 7% at 30 min). In normal hearts, the addition of diltiazem or clentiazem to cold cardioplegic solutions resulted in improved postischemic contractile function for the duration of reperfusion (85 +/- 4% vs. only 71 +/- 6% for cardioplegia, p < 0.05). The post-ischemic increase in coronary flow was similar in all groups. In failing CMH hearts, the addition of diltiazem or clentiazem afforded no significant contractile benefit at reperfusion. In nonischemic normal hearts, infusion of diltiazem or clentiazem (10 nM) alone increased coronary flow (+6 +/- 1% for diltiazem and +24 +/- 3% for clentiazem) without significant negative inotropic or chronotropic effects. In nonischemic failing CMH hearts, infusion of diltiazem or clentiazem did not elicit cardiodepression. In contrast their coronary dilator actions reverted to vasoconstriction (diltiazem) or were significantly attenuated (clentiazem). From these experiments we can conclude that, compared with the normal heart, the failing CMH heart adapted differently to global ischemia.     

The effects of using a leukocyte removal filter during cold blood cardioplegia

During myocardial ischemia, neutrophils and platelets exert negative effects on the myocardium. In this study, we used a leukocyte removal filter during cardioplegia, and investigated its effect on myocardial damage during reperfusion by measuring the plasma levels of granulocyte components, platelet components, and cardiac enzymes [creatinine phosphokinase (CK) and creatinine phosphokinase myocardial band (CK-MB)] in 24 patients who underwent cardiopulmonary bypass. The patients were divided into two groups of 12 according to whether or not a filter was placed in the cardioplegic route. Blood samples were drawn directly from the coronary sinus before aortic cross clamping, and at 1, 5, and 15 min after declamping. Group F, which had the filter, showed better cardiac enzyme and lipid peroxidation results than group N, which did not. The results of this study suggest that the application of a filter during cold blood cardioplegia may reduce myocardial damage.     

Clinical trial of retrograde warm blood reperfusion versus standard cold topical irrigation of transplanted hearts

BACKGROUND: A prospective, randomized clinical study involving 34 patients undergoing heart transplantation compared myocardial preservation of donor hearts maintained with continuous reperfusion with retrograde warm blood cardioplegia during surgical implantation versus the standard cold topical irrigation. METHODS: Hearts in both groups were arrested with a standard crystalloid solution and maintained in a cold saline solution during transportation. In the retrograde group, cardioplegia was administered through a catheter in the coronary sinus during surgical implantation. An average of 471 +/- 30 mL of hyperkalemic crystalloid solution diluted 1:4 in warm blood from the oxygenator was infused. In the standard group, the heart was kept cold by topical irrigation of cold saline solution and was reperfused only when the ascending aorta was unclamped. RESULTS: Preoperative characteristics of donors and recipients were similar in the two cohorts. Ischemic time average 139 +/- 12 minutes in the retrograde group compared with 130 +/- 11 minutes in the standard group (p = 0.57). Cardiopulmonary bypass time averaged 89 +/- 4 minutes in the retrograde group and 110 +/- 12 minutes in the standard group (p = 0.12). Defibrillation at reperfusion was performed in 4 patients (4/17, 24%) in the retrograde group and 12 patients (12/18, 67%) in the standard group (p = 0.01). There were no deaths in the retrograde group (0/17), whereas in the standard group, 3 patients (3/17) died of early graft failure (p = 0.11). Four early graft failures occurred in the standard group (p = 0.06). Two patients (2/17, 12%) were weaned from bypass with ventricular assist devices in the standard group. The number of subendocardial necrotic cells in the first two weekly endomyocardial biopsy specimens averaged 2.7 +/- 0.8 cells/mm2 in the retrograde group and 5.9 +/- 2.4 cells/mm2 in the standard group (p = 0.12). CONCLUSIONS: Retrograde warm blood reperfusion appears to improve the initial recovery of transplanted hearts. The technique is easy to use and may be a useful approach to graft protection during surgical implantation.     

Coronary vascular regulation during postcardioplegia reperfusion

BACKGROUND: This study extends previous investigations of global and regional myocardial blood flow during early postcardioplegia reperfusion. The hypothesis tested is that coronary vascular regulation becomes abnormal within 3 minutes after the start of postcardioplegia reperfusion. METHODS: Pigs (n = 40) were supported by cardiopulmonary bypass and 38 degrees C blood cardioplegic solution was infused. A control preischemic microsphere injection (No. 1) was given in asystolic hearts. Groups 1 to 3 had 1 hour of hypothermic cardioplegic arrest. Group 4 (control group) had 1 hour of perfusion without cardioplegia. A blood cardioplegic solution at 38 degrees C and 70 mm Hg pressure was infused to maintain asystole during the initial 7 to 10 minutes of reperfusion in all groups. Left ventricular intracavitary pressures were set at 0, 10, 20, or 0 mm Hg in groups 1, 2, 3, and 4 (n = 10 pigs per group), respectively, during the initial 7 minutes of reperfusion. The ventricle was then decompressed. At 30 seconds, 3 minutes, and 6 minutes after reperfusion, microsphere injections 2, 3, and 4 were given in asystolic hearts. Microsphere injection No. 5 was given 10 minutes after reperfusion in beating vented hearts. RESULTS: (1) Left ventricular distention during the initial 7 minutes of reperfusion after hypothermic cardioplegic arrest attenuates postischemic hyperemia. (2) Left ventricular intracavitary pressure of 20 mm Hg during reperfusion causes a decrease in endocardial blood flow relative to epicardial blood flow at 6 minutes after reperfusion. (3) Global myocardial blood flow during postcardioplegia reperfusion falls significantly below preischemic control values despite the return of electromechanical activity. INFERENCE: Coronary vascular regulation (i.e., coronary resistance and metabolic flow recruitment) becomes abnormal within 3 minutes after the start of reperfusion after hypothermic blood cardioplegic arrest.     

Homeobox genes in hematopoiesis and leukemogenesis

The effect of cold and warm intermittent antegrade blood cardioplegia, on the intracellular concentration of taurine in the ischaemic/reperfused heart of patients undergoing aortic valve surgery, was investigated. Intracellular taurine was measured in ventricular biopsies taken before institution of cardiopulmonary bypass, at the end of 30 min of ischaemic arrest and 20 min after reperfusion. There was no significant change in the intracellular concentration of taurine in ventricular biopsies taken after the period of myocardial ischaemia in the two groups of patients (from 10.1 +/- 1.0 to 9.6 +/- 0.9 mumol/g wet weight for cold and from 9.3 +/- 1.3 to 10.0 +/- 1.3 mumol/g wet weight for warm cardioplegia, respectively). Upon reperfusion however, there was a fall in taurine in both groups but was only significant (P < 0.05) in the group receiving cold blood cardioplegia (6.9 +/- 0.8 mumol/g wet weight after cold blood cardioplegia versus 8.0 +/- 0.8 mumol/g wet weight following warm blood cardioplegia). Like taurine, there were no significant changes in the intracellular concentration of ATP after ischaemia in the two groups of patients (from 3.2 +/- 0.32 to 2.95 +/- 0.43 mumol/g wet weight for cold and from 2.75 +/- 0.17 to 2.62 +/- 0.21 mumol/g wet weight for warm cardioplegia, respectively). However upon reperfusion there was a significant fall in ATP in both groups with the extent of the fall being less in the group receiving warm cardioplegia (1.79 +/- 0.19 mumol/g wet weight for cold and 1.98 +/- 0.27 mumol/g wet weight for warm cardioplegia, respectively). This work shows that reperfusion following ischaemic arrest with warm cardioplegia reduces the fall in tissue taurine seen after arrest with cold cardioplegia. Accumulation of intracellular sodium provoked by hypothermia and a fall in ATP, may be responsible for the fall in taurine by way of activating the sodium/taurine symport to efflux taurine.     

Molecular cloning of cDNA for pro-phenol-oxidase-activating factor I, a serine protease is induced by lipopolysaccharide or 1,3-beta-glucan in coleopteran insect, Holotrichia diomphalia larvae

BACKGROUND: To evaluate the effects of minimally diluted tepid blood cardioplegia, a prospective, randomized study was undertaken. METHODS: Thirty-seven patients undergoing isolated primary coronary artery bypass grafting were randomized to receive standard 4:1 diluted tepid blood cardioplegia (4:1 group, n = 18) or minimally diluted tepid blood cardioplegia (Mini group, n = 19). Cardioplegic solution was delivered in an intermittent antegrade fashion in both groups. Myocardial oxygen and lactate metabolism, release of the MB isoenzyme of creatine kinase and thiobarbituric acid reactive substances, and cardiac function were measured during and after the operation. RESULTS: Myocardial oxygen consumption was significantly greater and lactate release was significantly lower in the Mini group than in the 4:1 group during cardioplegia. Minimally diluted blood cardioplegia resulted in more prompt resumption of lactate extraction, lower levels of release of the myocardial-specific isoenzyme of creatine kinase and thiobarbituric acid reactive substances during reperfusion, and better postoperative left ventricular function compared with the standard 4:1 cardioplegia. CONCLUSIONS: Minimally diluted tepid blood cardioplegia may provide superior myocardial protection than the standard 4:1 dilution technique by optimizing the aerobic environment through an increase in oxygen supply during intermittent cardioplegia.     

Enflurane and isoflurane, but not halothane, protect against myocardial reperfusion injury after cardioplegic arrest with HTK solution in the isolated rat heart

To investigate the effects of halothane, enflurane, and isoflurane on myocardial reperfusion injury after ischemic protection by cardioplegic arrest, isolated perfused rat hearts were arrested by infusion of cold HTK cardioplegic solution containing 0.015 mmol/L Ca2+ and underwent 30 min of ischemia and a subsequent 60 min of reperfusion. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial function and cellular injury, respectively. In the treatment groups (each n = 9), anesthetics were given during the first 30 min of reperfusion in a concentration equivalent to 1.5 minimum alveolar anesthetic concentration of the rat. Nine hearts underwent the protocol without anesthetics (controls). Seven hearts underwent ischemia and reperfusion without cardioplegia and anesthetics. In a second series of experiments, halothane was tested after cardioplegic arrest with a modified HTK solution containing 0.15 mmol/L Ca2+ to investigate the influence of calcium content on protective actions against reperfusion injury by halothane. LV developed pressure recovered to 59%+/-5% of baseline in controls. In the experiments with HTK solution, isoflurane and enflurane further improved functional recovery to 84% of baseline (P < 0.05), whereas halothane-treated hearts showed a functional recovery similar to that of controls. CK release was significantly reduced during early reperfusion by isoflurane and enflurane, but not by halothane. After cardioplegic arrest with the Ca2+-adjusted HTK solution, halothane significantly reduced CK release but did not further improve myocardial function. Isoflurane and enflurane given during the early reperfusion period after ischemic protection by cardioplegia offer additional protection against myocardial reperfusion injury. The protective actions of halothane depended on the calcium content of the cardioplegic solution. IMPLICATIONS: Enflurane and isoflurane administered in concentrations equivalent to 1.5 minimum alveolar anesthetic concentration in rats during early reperfusion offer additional protection against myocardial reperfusion injury even after prior cardioplegic protection. Protective effects of halothane solely against cellular injury were observed only when cardioplegia contained a higher calcium concentration.     

Prospective, randomized trial comparing blood and oxygenated crystalloid cardioplegia in reoperative coronary artery bypass grafting

OBJECTIVES: Reoperative coronary artery bypass grafting presents unique challenges for myocardial preservation. The purpose of this study was to compare oxygenated blood cardioplegia with oxygenated crystalloid cardioplegia during reoperative coronary artery bypass grafting using transesophageal echocardiography to assess regional wall motion of the left ventricle before and after cardiopulmonary bypass. METHODS: Sixty-one patients undergoing reoperative coronary artery bypass grafting were prospectively randomized to receive oxygenated blood cardioplegia or oxygenated crystalloid cardioplegia delivered with a combined antegrade-retrograde technique. Transgastric short axis views of the left ventricle were made with transesophageal echocardiography during the operation before cardiopulmonary bypass and immediately after cardiopulmonary bypass. Regional wall motion was graded by a blinded observer, and before cardiopulmonary bypass scores were compared with after cardiopulmonary bypass scores. RESULTS: No significant differences were found in the change in regional wall motion score from before cardiopulmonary bypass to after cardiopulmonary bypass between the blood and crystalloid cardioplegia groups. CONCLUSIONS: This study found blood and crystalloid cardioplegia to be equally efficacious for myocardial preservation during reoperative coronary artery bypass grafting.     

Differential regulation of vitamin D receptors in clonal populations of a chronic myelogenous leukemia cell line

BACKGROUND: Both crystalloid and blood cardioplegia result in cardiac dysfunction associated with myocardial edema. This edema is partially due to the lack of myocardial contraction during cardioplegia, which stops myocardial lymph flow. As an alternative, acceptable surgical conditions have been created in patients undergoing coronary artery bypass operations with esmolol-induced minimal myocardial contraction. We hypothesized that minimal myocardial contraction during circulatory support using either standard cardiopulmonary bypass (CPB) or a biventricular assist device would prevent myocardial edema by maintaining cardiac lymphatic function and thus prevent cardiac dysfunction. METHODS: We placed 6 dogs on CPB and 6 dogs on a biventricular assist device and serially measured myocardial lymph flow rate and myocardial water content in both groups and preload recruitable stroke work only in the CPB dogs. In all dogs we minimized heart rate with esmolol for 1 hour during total circulatory support. RESULTS: Although myocardial lymph flow remained at baseline level during CPB and increased during biventricular assistance, myocardial water accumulation still occurred during circulatory support. However, as edema resolved rapidly after separation from circulatory support, myocardial water content was only slightly increased after CPB and biventricular assistance, and preload recruitable stroke work was normal. CONCLUSIONS: Our data suggest that minimal myocardial contraction during both CPB and biventricular assistance supports myocardial lymphatic function, resulting in minimal myocardial edema formation associated with normal left ventricular performance after circulatory support. The concept of minimal myocardial contraction may be a useful alternative for myocardial protection, especially in high-risk patients with compromised left ventricular function.     

Percutaneous urethral suspension with bone anchorage (Vesica) in the treatment of stress urinary incontinence. Results after a year of follow-up

We studied the clinical advantages and myocardial protection of normothermal CPB with comparing to hypothermal CPB. 22-cases of adult CABG were classified under two groups, according to the temperature of CPB. (Normothermal group: 37 degrees C, Hypothermal group: 32 degrees C) In both groups, the assistant CPB time after aortic declamp, the use of cardioversion that meaned the spontaneous recovery to sinus rhythm appeared or not, the dose of cathecholamines in- and post-operation, and the amounts of postoperative bleeding (after 6 h and 12 h) were compared as the clinical results and the data of CPK-MB, Myocin LC-II, and Troponin-T were measured as the effects of myocardial protection. The method of myocardial protection was the intermittent antegrade cold blood cardioplegia with terminal warm blood for all cases. As a result, the assistant CPB time after aortic declamp, the use of cardiovasion, and the amounts of postoperative bleeding (both of 6 h and 12 h) were less in normothermal group rather than in hypothermal group. (p < 0.05). However we had no differences about the dose of cathecholamines in post-operation and the data of three items between two groups. So, it suggests that the sufficient effects of myocardial protection could be obtained in normothermal CPB as in hypothermal CPB. Therefore we conclude that normothermal CPB could provide some clinical advantages, such as shortening CPB time, recovery of sinus rhythm, and prevention of postoperative bleeding, compared to hypothermal CPB and sufficient myocardial protection.     

Concerning the effect of the K+ channel blocking agent glibenclamide on ischaemic and reperfusion arrhythmias

Reports on effects of ATP-dependent K+ channel modulating drugs on ischaemia-induced cardiac arrhythmias have been scarce and contradictory. The channel blocking agent glibenclamide (glyburide) has been considered as an antiarrhythmic candidate, because it antagonizes the ischaemic K+ efflux and the shortening of the refractory period. In the present investigation its effects were tested, therefore, in rat hearts with coronary occlusion and reperfusion. In untreated hearts, tachyarrhythmias occurred during the reperfusion, and less pronounced during the coronary occlusion itself. Large amounts of adenosine and its degradation products were released during the coronary reperfusion, particularly from hearts which developed ventricular fibrillation. Glibenclamide (0.1 and 1.0 micromol/l perfusion fluid) neither antagonized the ischaemic nor the reperfusion arrhythmias. Ischaemic arrhythmias were even intensified. Also in control hearts without coronary occlusion, pro-arrhythmic effects of glibenclamide were observed. Furthermore, the coronary flow was considerably decreased by the drug, and the release of adenosine and its metabolites was significantly increased. Sodium nitroprusside antagonized the glibenclamide-induced decrease in the coronary flow, but did not prevent the arrhythmias. The Ca2+ channel blocking agent gallopamil increased the coronary flow, decreased the adenosine release, and antagonized the arrhythmias in hearts with and without glibenclamide. In conclusion, the present findings do not favour the idea of an antiarrhythmic effect of glibenclamide. Rather, some propensity to the occurrence of arrhythmias can be produced by the drug.