Renoprotective effect of enalapril in uninephrectomized spontaneously hypertensive rats with neonatal streptozotocin-induced diabetes

We compared the renoprotective effect between angiotensin-converting enzyme inhibitor, enalapril, and a dihydropyridine-type calcium channel blocker, nicardipine, in a severe form of renal injury in rats. Two-day-old spontaneously hypertensive rats (SHR) were injected with streptozotocin or vehicle as control. UNX was performed at 3 weeks of age, and enalapril or nicardipine was administered in drinking water from 7 weeks of age. Uninephrectomy (UNX) markedly exacerbated hypertension and renal injury in the nondiabetic and diabetic SHR. Enalapril and nicardipine comparably reduced blood pressure in UNX diabetic SHR. However, serum creatinine was significantly elevated in the nicardipine-treated group as compared with the enalapril-treated group at 24 weeks of age (nicardipine-treated group, 67 +/- 4 microM; enalapril-treated group, 49 +/- 3 microM; P < 0.01; untreated group 57 +/- 4 microM). Furthermore, the incidence of glomerular sclerosis was similar between untreated and nicardipine-treated groups, whereas it tended to be reduced in the enalapril-treated group. In a separate experiment of diabetic SHR without UNX, enalapril therapy significantly ameliorated hyperglycemia and albuminuria (P < 0.01). This study showed that a renoprotective effect was seen in enalapril but not in nicardipine in UNX diabetic SHR despite the comparable reduction of blood pressure. This suggests that enalapril may be more effective than nicardipine in delaying the progression of a severe form of diabetic nephropathy.     

Contribution of nitric oxide to the acute antihypertensive effect of blockers of AT1 angiotensin receptors in spontaneously hypertensive rats

The acute vasodepressor effect of AT1 angiotensin receptor blockers losartan and CL329167 was compared in spontaneously hypertensive rats (SHR) pretreated and not pretreated with NG-monomethyl-L-arginine (LNMMA; 15 mg/kg i.v. bolus plus infusion at 10 mg/kg/h), an inhibitor of nitric oxide (NO) synthesis. The antihypertensive effect of losartan (30 mg/kg, i.v.) in SHR pretreated with LNMMA (-13 +/- 4 mmHg) was greatly diminished (P < 0.01) relative to the antihypertensive effect of losartan in SHR not pretreated with LNMMA (-44 +/- 8 mmHg). Similarly, the antihypertensive effect of CL329167 (5 mg/kg, i.v.) in SHR pretreated with LNMMA (-12 +/- 3 mmHg) was surpassed (P < 0.01) by the antihypertensive effect in SHR not pretreated with LNMMA. (-41 +/- 4 mmHg). However, pretreatment of SHR with LNMMA did not minimize the vasodepressor effect of prazosin, isoproterenol or sodium nitroprusside. The impairment in vasodepressor responsiveness to losartan in rats pretreated with LNMMA was not demonstrable in rats concurrently receiving sodium nitroprusside to correct for the loss of endogenous NO, or atrial natriuretic peptide which also increases vascular cGMP. These data suggest that a mechanism mediated by NO and/or cGMP is necessary for the full expression of the acute antihypertensive effect of AT1 angiotensin receptor blockers in SHR.     

Metoclopramide blocks bromocriptine induced antihypertensive effect in hypertensive patients

Two groups of patients with essential hypertension were studied at the Vargas Hospital of Caracas. The first group of 9 patients under placebo treatment for 1 week received a single 2.5 mg oral dose of bromocriptine. Cardiovascular and biochemical parameters including arterial pressure, heart rate, plasma renin activity, and plasma aldosterone levels were evaluated during the 6-hour period before and after the administration of drugs. The second experimental design was as follows: 9 patients received 30 mg metoclopramide daily (divided in 3 doses) for 1 week. At the end of the period a single oral dose of 2.5 mg of bromocriptine was given to each patient. The cardiovascular and biochemical parameters were also determined. Bromocriptine reduced both systolic and diastolic arterial pressure. The peak antihypertensive effect was shown 3 hours after administration of the drug, but the reduction of arterial pressure lasted approximately 6 hours. At the same time bromocriptine reduced plasma aldosterone levels and plasma renin activity. This reduction persisted 6 hours after its administration. Metoclopramide reversed the antihypertensive effect of bromocriptine and its effect on aldosterone secretion and plasma renin activity. We conclude from these findings that bromocriptine acts as an antihypertensive agent by stimulating DA2 dopaminergic receptor, the dopaminergic receptor involved in aldosterone and renin secretion is possibly DA2.     

Do kinins mediate cardioprotective and renoprotective effects of cilazapril in spontaneously hypertensive rats with renal ablation?

1. We assessed the potential of the kallikrein-kinin system in mediating the cardioprotective and renoprotective effects of an angiotensin-converting enzyme inhibitor (ACEI), cilazapril (CIL) in rats with renal ablation. 2. Eight week old spontaneously hypertensive rats (SHR) were subjected to 5/6 nephrectomy. One week after the operation, the rats were divided into 5 groups: (i) vehicle; (ii) CIL 1 mg/kg per day per os (p.o.); (iii) Hoe140 (HOE) 70 mu g/kg per day given intraperitoneally (i.p.); (iv) CIL 1 mg/kg per day p.o. plus HOE 7 mu g/kg per day i.p.; (v) CIL 1 mg/kg per day p.o. plus HOE 70 mu g/kg per day i.p. The treatment lasted for 4 weeks. 3. CIL alone significantly reduced systolic blood pressure, urinary protein excretion, heart weight and serum creatinine level. HOE alone did not induce any significant changes in these parameters. CIL in combination with HOE (7 or 70 mu g/kg per day) did not induce any changes in these parameters, in addition to those associated with the effects of CIL alone. 4. These results indicate that the kallikrein-kinin system might not play a major role in the cardioprotective and renoprotective effects of ACE inhibitors in the rat remnant kidney model of chronic renal failure.     

Alterations in alpha subunit expression of cardiac Na+,K+-ATPase in spontaneously hypertensive rats: effect of antihypertensive therapy

The alpha-2 subunit abundance of Na+,K(+)-ATPase in the rat heart has been reported to be reduced in several induced hypertensive models. To determine whether this reduction also occurs in a genetic model of hypertension, we studied expression of the alpha subunits in left ventricles of spontaneously hypertensive rats (SHR), and normotensive Wistar-Kyoto (WKY) and Sprague-Dawley rats using Western blotting and quantitative dot-blotting analysis with monoclonal antibodies. While the alpha-1 subunit was not affected in any of the strains, a significant reduction of the alpha-2 subunit expression was noted in 19-week-old SHRs, but not in age-matched WKY and Sprague-Dawley rats, supporting the hypothesis that elevated arterial pressure may differentially downregulate the alpha-2 subunit in the rat heart. To further test this hypothesis we designed experiments in which hypertensive rats were treated with the antihypertensive agents hydralazine and nifedipine. Both agents effectively normalized the blood pressure in the SHRs with no significant effect on the blood pressure in the WKY and Sprague-Dawley rats. The alpha-2 subunit in SHRs treated with hydralazine and nifedipine showed a 63.3% (n = 6, P < 0.05, analysis of variance and Fischer's test) and a 27.4% increase, respectively, over the hypertensive SHR controls, although the reversal effect of nifedipine did not quite reach significance. The alpha-1 subunit expression was not affected by any of the drug treatments. No effect of either of the drugs on the alpha-1 or alpha-2 subunit was observed in the WKY or Sprague-Dawley rat groups. These data support our hypothesis that the alpha-2 subunit may be a pressure-sensitive isoform of the cardiac Na+,K(+)-ATPase and that high blood pressure is, directly or indirectly, responsible for the reduction of the alpha-2 subunit protein expression.     

Differential cerebrovascular responsiveness in spontaneously hypertensive rats following antihypertensive treatment with clonidine and verapamil

Numerous studies have been reported examining the effects of antihypertensive treatment on peripheral vascular responsiveness in spontaneously hypertensive rats (SHR). This study was conducted to determine the effects of chronic treatment with 2 antihypertensive agents on cerebrovascular responsiveness in male SHR and Wistar-Kyoto (WKY) rats. SHR and WKY (3-4 weeks old) received either placebo, clonidine (CLON, 10 mg pellet) or verapamil (VER, 5 mg pellet). Vascular reactivity studies on the basilar artery, using standard smooth muscle bath techniques, were conducted following 6 weeks of treatment. Both CLON and VER significantly attenuated the rise in blood pressure in SHR. Basilar artery responsiveness to KCl, serotonin (5-HT), and calcium were significantly increased whereas responses to acetylcholine (ACH), isoproterenol (ISO) and sodium nitroprusside (SNP) were significantly reduced in SHR compared to WKY. CLON had no effect on basilar artery responsiveness to either the contractile or relaxation agents in SHR. However, although responses to KCl, 5-HT and calcium were not affected by VER in SHR, VER significantly increased the responses to ACH, ISO and SNP. Neither CLON nor VER treatment affected basilar artery responsiveness to any of the agents in WKY. These data demonstrate that, even though CLON and VER have similar antihypertensive effects, differential effects of the 2 agents on cerebrovascular responsiveness in the SHR are apparent. This would suggest that the vascular effects of VER and CLON are dependent upon the mechanism of action of the agents and not simply due to prevention of the elevation in blood pressure.     

Role of kinins in basal and furosemide-stimulated renin secretion

OBJECTIVE: To determine risk factors predictive of outcomes to aid in the cost-effective preoperative evaluation and postoperative management of patients who are undergoing tonsillectomy and adenoidectomy for obstructed breathing during sleep. DESIGN: A historical cohort study with a nested case-control analysis that examined risk factors associated with postoperative respiratory complications. SETTING: Children's Medical Center of Dallas, Dallas, Tex, which is a pediatric referral hospital for secondary and tertiary pediatric care with both private and university-appointed physicians. PATIENTS: A convenience sample of 355 patients who were undergoing tonsillectomy and adenoidectomy for obstructed breathing during sleep throughout a 1-year period. INTERVENTION: None. MAIN OUTCOME MEASURE: The occurrence of postoperative complications, including airway obstruction, apneas with oxygen desaturations, airway interventions (e.g., endotracheal intubation), or administration of supplemental oxygen, as they related to associated medical conditions (e.g., cerebral palsy or prematurity) and diagnostic tests (e.g., chest x-ray film and electrocardiogram). RESULTS: Five associated medical conditions (cerebral palsy; seizures; age, < or = 3 years; congenital heart disease; and prematurity) were identified as important predictors of a complicated postoperative course using stepwise logistic regression analysis. Those children with an abnormal chest x-ray film or electrocardiogram were also identified as having an associated medical condition that was predictive of postoperative complications. CONCLUSIONS: Children with 1 or more of the associated risk factors identified should be considered candidates for postoperative inpatient observation. A preoperative chest x-ray film and electrocardiogram were found to be of little predictive value, and they are probably not cost-effective screening tests for postoperative respiratory complications.     

Treatment with enalapril modifies the pain perception pattern in hypertensive patients

The cardiovascular system shares numerous anatomic and functional pathways with the antinociceptive network. The aim of this study was to investigate whether angiotensin-converting enzyme (ACE) inhibitor treatment could affect hypertension-related hypalgesia. Twenty-five untreated hypertensive patients, together with a control group of 14 normotensive subjects, underwent dental pain perception evaluation by means of a pulpar test (graded increase of test current applied to healthy teeth). After the evaluation of the dental pain threshold (occurrence of pulp sensation) and tolerance (time when the subjects asked for the test to be stopped), all the subjects underwent a 24-hour ambulatory blood pressure monitoring. The hypertensive group then was treated with 20 mg/d enalapril, whereas the normotensive subjects remained without any treatment. After a time interval of 6+/-2 months, the dental pain sensitivity was retested in all the subjects, and ambulatory blood pressure was recorded during treatment in the hypertensive patients. At the first assessment, hypertensive patients showed a higher pain threshold than normotensive subjects (P<.001). On retesting of pain sensitivity in hypertensive patients, a significant decrease of both pain threshold and tolerance, leading to their normalization, was observed during treatment (P<.001 and P<.005, respectively), in the presence of reduced 24-hour and office blood pressure values. A slight, though significant, correlation was observed between variations in pain tolerance and baseline blood pressure changes occurring during treatment. During follow-up, the normotensive subjects did not show any significant pain perception or office blood pressure changes. Hypertension-related hypalgesia was confirmed. Mechanisms acting both through lowering of blood pressure and specific pharmacodynamic properties may account for the normalization of pain sensitivity observed in hypertensive patients during treatment with ACE inhibitors.     

Potentiation of natriuretic peptide action by the beta-adrenergic blocker carvedilol in hypertensive rats: a new antihypertensive mechanism

PURPOSE: We report the development of a questionnaire to assess health-related quality-of-life (HRQOL) in people with epilepsy and the process of cross-cultural translations of the questionnaire. METHODS: A sample of 304 adults with epilepsy from 25 seizure clinics in the United States was used to derive an abbreviated questionnaire focusing on epilepsy-related issues from a longer, 89-item instrument (QOLIE-89). A rigorous forward-backward-forward system was used for cross-cultural translation. RESULTS: A 31-item questionnaire (QOLIE-31, version 1.0) resulted, comprising seven subscales covering general and epilepsy-specific domains. Subscale and total scores can be calculated. The subscales were grouped into two factors: Emotional/Psychological Effects (seizure worry, overall QOL, emotional well-being, energy/fatigue subscales) and Medical/Social Effects (medication effects, work-driving-social limits, cognitive function subscales). Cross-cultural translations were made from U.S.-English into Danish, Dutch, German, Canadian French, French, Italian, Spanish, Swedish, and U.K. English Versions 1.1. CONCLUSIONS: Our results support the reliability and validity of the QOLIE-31 (U.S.-English version 1.0) as a measure of HRQOLIE. Cross-cultural translations into nine other languages make it feasible to use the QOLIE-31 (version 1.1) in multinational clinical trials after validation in each population or concurrent with the clinical trial.     

Role of NO on pressure-natriuresis in Wistar-Kyoto and spontaneously hypertensive rats

We investigated the role of the endothelium-derived relaxing factor nitric oxide (NO) on pressure-natriuresis in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) using in vivo perfusion studies. Differences in the neural and hormonal background to the kidney were minimized by renal denervation and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, elevation of renal perfusion pressure (RPP) from 115 to 157 mm Hg increased urinary sodium excretion 4.5 to 14.8 microEq/min/g kidney wt, and the slope of its linear regression was 0.21 microEq/min/g kidney wt/mm Hg. Infusion of an inhibitor of NO synthase, L-NMMA (1 mg/min/kg), lowered this slope (P < 0.05) but L-arginine (3 mg/min/kg) did not change it. By contrast, the impaired pressure-natriuresis response of SHR was ameliorated by L-arginine (slope: 0.08 to 0.16; P < 0.05), while L-NMMA did not blunt it further. GFR and renal plasma flow (RPF) were well autoregulated in both strains, but L-NMMA lowered RPF significantly (SHR: from 4.2 to 2.6 ml/min/g kidney wt; WKY: 4.5 to 2.5 ml/min/g kidney wt). Moreover, when infused simultaneously, all these individual effects of L-NMMA and L-arginine were nullified. These results suggest that NO plays an important role in the pressure-natriuresis mechanism.     

Effects of the antihypertensive drug efonidipine hydrochloride on albuminuria and renal histopathology in young spontaneously hypertensive rats with diabetes

We examined 199 consecutive referrals to the Lipid Clinic at the National hospital in 1995 in order to compare referral- and chart data on familial hyperlipidaemia, familial cardiovascular disease, diagnosis, and lifestyle. 78% of referrals were from general practitioners. Most of the referrals included information on familial hyperlipidaemia and cardiovascular disease and on diet, but did not specify a lipid diagnosis. Less than half of the referrals included information on smoking habits (which was almost always specified in the chart). Up to 80% did not include information on alcohol, body mass index and physical activity, which was also often missing in the chart. We conclude that the referring doctors, and to some extent the clinic physicians, identified patients with a familial risk of cardiovascular disease, but they did not appear to characterise important lifestyle habits related to cardiovascular risk.     

Involvement of renin-angiotensin system in hypertensive effect of cadmium in rats

Role of renin-angiotensin system in hypertension induced by cadmium chloride (CdCl2) in rats has been investigated. Intravenous administration of CdCl (1 mg/kg) produced a biphasic response i.e. a transient fall followed by a marked and consistent rise in blood pressure. The peak hypertensive effect was accompanied by raised PRA levels. Pretreatment with captopril (1 mg/kg, i.v.) losartan (1 mg/kg, i.v.) or captopril + losartan attenuated the pressor response to Cd by 62%, 42% and 100% respectively in separate groups. Central administration of Cd (10 micrograms/rat, i.c.v.) showed a biphasic response similar to that observed after i.v. route. However, it was not accompanied by raised PRA levels. Prior treatment with losartan (10 micrograms/rat, i.c.v.) completely abolished the pressor response to Cd (i.c.v.) whereas it was not affected significantly by captopril (10 micrograms/rat, i.c.v.). On the other hand, centrally administered losartan only partially reduced the pressor response to i.v. Cd. The results are discussed in light of a differential involvement of central vs peripheral renin-angiotensin system in the hypertensive effect of Cd.     

Oscillatory potentials of the electroretinogram in hypertensive patients with different antihypertensive treatment

Three-dimensional structures of laterally aggregated bundles of collagen molecules, segment-long-spacing (SLS) crystallites, were imaged by atomic force microscopy (AFM) in atmosphere. The overall image of the type I collagen SLS in a height-amplified mode was semi-cylindrical, approximately 300 nm in length, with two bands of elevation near both N- and C- ends of the molecule. Its 'cross-sectional' profile (across the molecular axis) was a smooth arch. The 'axial' profile (along the molecular axis) had two prominent peaks approximately 250 nm apart, corresponding to the two bands of elevation. There were several minor peaks between these two prominent peaks. The elevation near both ends may be due to the presence of covalently bound sugars near both N- and C- ends of the helical part of type I collagen alpha chains. The AFM images of SLS presented here indicate that the type I collagen molecule is not uniform in diameter and has two bulged parts within its triple helix.     

Role of nitric oxide in vascular hyper-responsiveness to norepinephrine in hypertensive Dahl rats

OBJECTIVE: To determine whether the abnormal vascular responses observed in salt-sensitive hypertension are caused by an impairment in vascular nitric oxide function. DESIGN: Isometric tension was measured in aortic rings isolated from Dahl salt-sensitive and salt-resistant rats fed a regular-salt (0.4% NaCl) or a high-salt (8% NaCl) diet, with and without inhibition of endogenous nitric oxide synthesis. METHODS AND RESULTS: Systolic arterial pressure, measured weekly by the tail-cuff method, increased markedly in DS rats with a high-salt diet but did not increase in the other groups. In aortic rings, norepinephrine evoked dose-dependent contractions which were significantly increased in rings from DS rats with a high-salt diet Pretreatment with Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, increased the norepinephrine-induced contraction in all groups and abolished differences in contractile responses between high-salt DS rats and the other groups. Acetylcholine induced endothelium-dependent relaxation, which was significantly depressed in high-salt DS rats. L-NAME attenuated the acetylcholine-induced relaxation in all groups and abolished the difference in relaxation response between high-salt DS rats and the other groups. Sodium nitroprusside-induced relaxation was significantly depressed in high-salt DS rats. CONCLUSIONS: Vascular hypercontractile responses to norepinephrine in DS hypertensive rats can, in part, be explained by an impairment in endothelial nitric oxide production.     

Prostaglandin I2 contributes to the vasodepressor effect of baicalein in hypertensive rats

Lipoxygenase inhibitors reduce blood pressure in hypertensive rats. The vasodepressor effect of lipoxygenase inhibitors may be related to increased production of prostaglandin (PG) I2 since lipoxygenase-derived fatty acid hydroperoxides inhibit PGI2 synthase. This hypothesis was examined in rats made hypertensive by infusion of angiotensin II (200 ng/min i.p.) for 12 to 14 days. In hypertensive but not in normotensive rats, the lipoxygenase inhibitor baicalein (60 mg/kg s.c.) increased (P<.05) the conversion of exogenous PGH2 to PGI2 by aortic segments, the release of 6-keto-PGF1alpha by aortic rings, the concentration of 6-keto-PGF1alpha in blood, and the renal excretion of 6-keto-PGF1alpha. Treatment with baicalein did not affect the blood pressure of normotensive rats but decreased the blood pressure of hypertensive rats from 177+/-8 to 133+/-9 mm Hg after 120 minutes (P<.05). Also, the lipoxygenase inhibitor cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (8 mg/kg s.c.) was without effect on the blood pressure of normotensive rats but decreased the blood pressure of hypertensive rats from 182+/-4 to 139+/-8 mm Hg (P<.05). However, the blood pressure of hypertensive rats pretreated with indomethacin (5 mg/kg i.v.) was affected by neither baicalein nor cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate. Moreover, in hypertensive rats in which baicalein had decreased blood pressure to 148+/-6 mm Hg, the administration of rabbit serum containing antibodies against 5,6-dihydro-PGI2 (0.3 mL i.v.) partially reversed the response to baicalein, increasing blood pressure to 179+/-7 mm Hg within 20 minutes (P<.05). The antibodies also were shown to block the vasodepressor effect of PGI2 but not of PGE2. Collectively, these data suggest contribution of PGI2 to the acute antihypertensive effect of baicalein in rats with angiotensin II-induced hypertension.     

Role of nitric oxide in the modulation of the vascular response to angiotensin II in hypertensive rats

Studies of phagocytic efficiency in cells of the macrophage lineage have assumed additional importance since the discovery that HIV infection of these cells impairs their immune function. A rapid method has been developed for measuring phagocytosis of the opportunistic pathogen Mycobacterium avium complex by human monocytes. Fluoresceinated M. avium complex (F-MAC) was incubated with whole blood at 37 degrees C and the fluorescence of extracellular F-MAC was quenched using a vital blue stain. Monocytes were then stained with a monoclonal antibody (mAb) to human CD14 conjugated to phycoerythrin (PE) red cells were lysed, and the percentage of monocytes which had phagocytosed F-MAC was measured by flow cytometry. The results were reproducible in samples of blood taken from individual donors over a period of 1 or 2 weeks, and optimum F-MAC concentrations and an optimum incubation time were determined by experiment. This method has the advantages of requiring only a small volume of blood, not necessitating manipulation of cells before testing, and using a phagocytic target relevant to the pathogenesis of HIV infection.     

Compliance with antihypertensive treatment in consultation rooms for hypertensive patients

Compliance with antihypertensive therapy was examined by a questionnaire in 124 essential hypertension patients in an outpatient hypertension clinic. It was found that antihypertensive drugs were used regularly by only 62% of patients, with forgetting and feeling of well-being without therapy the principal reasons given for irregular drug taking. Treatment of hypertension is reported to have a deleterious effect on physical and mental activity, routine activities, sexual activity, memory, athletics and family life in only 2% of patients. Patients who were aware that increased BP reduces life span used the prescribed drugs more regularly and came regularly for checkups compared with patients lacking the relevant information. Patients over 60 years of age and smokers exhibited the worst compliance. No significant differences were found for sex or duration of treatment. With regard to nonpharmacological measures, most patients were willing to begin a programme of regular physical exercise, reduce weight, learn relaxation techniques and reduce alcohol intake: smokers, however were unable to stop the habit.     

Vasopressor effect of lysophosphatidic acid on spontaneously hypertensive rats and Wistar Kyoto rats

Early endothelial injury may play a role in the development of transplant arteriosclerosis. The present study documents early endothelial changes using a rat aortic graft model. Abdominal aortic allografts from PVG rats were orthotopically transplanted to DA rats. Controls were DA to DA transplants. Endothelial cell (EC) injury, regeneration, and leukocyte infiltration in the intima were evaluated using scanning electron microscopy and histological and immunocytochemical techniques. Nontransplanted aortic segments showed partial loss of ECs after 1 or 2 hr of preservation. Control isografts demonstrated extensive EC denudation and neutrophil adherence to residual ECs at 1 day post-transplantation. After 3 days, isografts showed continued regeneration of ECs in the central area and ingrowth of endothelium from both clamped sites in the recipient aorta. Reendothelialization was complete by day 14. Allografts showed similar findings to isografts up to day 3. In contrast to isografts, however, there was a secondary EC loss beginning at day 7. Monocytes/macrophages and T cells were noted to be adherent to residual ECs in 7- and 14-day allografts. At 20 days, ECs were absent from the luminal surface in the center of allografts. Endothelium did extend from clamped sites toward the midgraft region as in isografts. By 60 days allografts were completely reendothelialized. These results demonstrate that in both isografts and allografts there is initial EC loss due to mechanical trauma and ischemia/reperfusion injury, followed by partial reendothelialization. This latter process continues unabated in isografts, whereas in allografts the secondary EC loss occurs due to an allogenic response. This is followed by complete reendothelialization that occurs during the concurrent development of significant intimal hyperplasia.     

Role of macrophage overactivation in the development of acute pancreatic injury in rats

PURPOSE: To report quantitative changes in the anterior chamber configuration after small-incision cataract surgery with implantation of a posterior chamber intraocular lens by means of ultrasound biomicroscopy. METHODS: We examined the anterior chamber configuration of 20 eyes of 20 patients before and 3 months after small-incision cataract surgery (phacoemulsification and aspiration plus foldable intraocular lens implantation through a 3.0- to 4.0-mm self-sealing wound) by means of ultrasound biomicroscopy. The following variables were measured: the anterior chamber depth at the center of the cornea, the angle-opening distance 250 microns from the scleral spur (AOD250), the angle-opening distance 500 microns from the scleral spur (AOD500), and the trabecular-iris angle. RESULTS: The anterior chamber depth at the center of the cornea, AOD250, AOD500, and trabecular-iris angle increased significantly after surgery. The preoperative anterior chamber depth at the center of the cornea and trabecular-iris angle were negatively correlated with the differences between the postoperative and preoperative values (P < .01). The preoperative values of all variables examined were negatively correlated with the ratios of the postoperative value to the preoperative value (P < .002). CONCLUSIONS: The present results showed that small-incision cataract surgery significantly deepened the anterior chamber and widened its angle. The more shallow the preoperative anterior chamber was, the greater the postoperative change of the chamber was; and the more narrow the preoperative angle was, the greater the postoperative change of the angle was.