Comparison of angiotensin converting enzyme and renin inhibition in rats following myocardial infarction

Renal and systemic hemodynamics were studied in rats 1 month after induction of myocardial infarction by ligation of the left coronary artery. The mean arterial pressure, heart rate, and cardiac index were not different from controls, but there were striking elevations in heart weight (p < 0.001), left ventricular end diastolic pressure (p < 0.002), and renal vascular resistance (p < 0.01). Renal blood flow and the percent of cardiac output perfusing the kidneys were reduced by 18% (p < 0.01) and 14% (p < 0.01), respectively. Acute angiotensin inhibition was studied at a dose of the converting enzyme inhibitor, enalapril, or the renin inhibitor, CP71362, that lowered the mean arterial pressure by 15 mm Hg in normal rats. In normal rats, enalapril and CP71362 were without effect on renal blood flow (RBF), renal vascular resistance (RR), and RBF as a percent of cardiac output. However, in rats with myocardial infarction, enalapril and CP71362 increased the RBF and RBF as a percent of cardiac output and lowered the RR to levels similar to normal controls (p < 0.02). Enalapril and CP71362 were equally effective in reducing the left ventricular end-diastolic pressure and total peripheral resistance in rats with myocardial infarction. These data demonstrate significant intrarenal vasoconstriction following myocardial infarction in the absence of detectable changes in mean arterial pressure or cardiac index. Converting enzyme inhibition or renin inhibition had similar beneficial effects on cardiorenal function, suggesting that both classes of compounds act by a similar mechanism to improve renal hemodynamics in congestive heart failure.     

Vasodilatory effects of propylthiouracil in patients with alcoholic cirrhosis

BACKGROUND/AIMS: An experimental study has shown that propylthiouracil increases portal blood flow in normal rats. Whether propylthiouracil has a similar effect in patients with alcoholic cirrhosis remains to be demonstrated. The aim of this study was to evaluate the effects of oral propylthiouracil (300 mg) on systemic and portal hemodynamics in patients with alcoholic cirrhosis. METHODS: Plasma propylthiouracil levels were also measured by high performance liquid chromatography in five patients with alcoholic cirrhosis. In eight patients with cirrhosis, mean arterial pressure, cardiac output and portal blood flow were evaluated before and after placebo and propylthiouracil administration. Hemodynamic measurements were performed by the Doppler technique. The plasma peak level of propylthiouracil was achieved at 1.4 +/- 0.1 h in patients with alcoholic cirrhosis. This time was chosen to express hemodynamic changes. RESULTS: Propylthiouracil administration caused a significant increase in portal blood flow (+16.5%, p < 0.05) in patients with alcoholic cirrhosis. This effect was associated with a mild and significant rise in cardiac output (from 5.8 +/- 0.2 to 6.1 +/- 0.3 l/min, p < 0.05) and a decrease in peripheral vascular resistance (from 1171 +/- 69 to 1070 +/- 67 dyn . s-1 . cm-5, p < 0.01). A significant correlation was observed between changes in portal blood flow and peripheral vascular resistance (r = 0.79, p < 0.05). No significant changes were observed after placebo. CONCLUSIONS: Our findings show that propylthiouracil has a vasodilatory effect in patients with alcoholic cirrhosis. We postulate that this effect could be the mechanism by which propylthiouracil decreases hypermetabolic state, and increases oxygen delivery to the liver, in patients with alcoholic liver diseases.     

Clinical, biological, and immunophenotypical characteristics of B-cell chronic lymphocytic leukemia with trisomy 12 by fluorescence in situ hybridization

Intra-aortic balloon pumping is frequently used in patients with cardiogenic shock when oliguria persists despite maximal pharmacologic support. The objective of this study was to measure the effect of intra-aortic balloon pumping on renal blood flow, renal oxygen delivery, and renal oxygen consumption in such patients. Central hemodynamics, renal blood flow, and oxygen transport were measured in 10 patients in low cardiac output states. Measurements were made with and without intra-aortic balloon counterpulsation. Renal blood flow was measured by continuous renal vein thermodilution. Small improvements were observed in cardiac output (3.1 +/- 0.8 vs 3.5 +/- 0.8 L/min, P < .01) and pulmonary capillary wedge pressure (22 +/- 5.6 vs 19 +/- 5.3 mmHg, P < .05), but mean arterial blood pressure was unchanged (69 +/- 11 vs 69 +/- 5 mmHg, not significant). Baseline renal blood flow was reduced to approximately 37%, renal oxygen delivery to 31%, and renal oxygen consumption to 60% of normal values. No significant improvement was seen in single-kidney renal blood flow (184 +/- 108 vs 193 +/- 107 mL/min), renal oxygen delivery (28 +/- 16 vs 30 +/- 16 mL/min), or renal oxygen consumption (4.9 +/- 2.0 vs 4.7 +/- 2.5 mL/min) in response to 1:1 counterpulsation. In comparison with measurements made during short-term suspension of counterpulsation, 1:1 aortic balloon pumping failed to result in an increase in renal blood flow, oxygen delivery, or oxygen consumption from the low levels observed in these patients.     

Cardiovascular, renal, and neurohumoral responses to single large-volume paracentesis in patients with cirrhosis and diuretic-resistant ascites

OBJECTIVE: Large volume paracentesis is an effective treatment for refractory ascites, but the need for routine infusion of albumin or other volume expanders remains controversial. The aim of this study was to assess the short term effects of a single 5-L paracentesis without albumin replacement on total central blood volume, systemic and renal hemodynamics, sodium homeostasis, and neurohumoral factors. PATIENTS AND METHODS: Twelve patients with biopsy-proven cirrhosis and tense, diuretic-resistant ascites were studied before and 48 h after a single 5-L paracentesis without albumin infusion. Systemic hemodynamics and total central blood volume were assessed using radionuclide angiography. Glomerular filtration rate and effective renal plasma flow were measured by inulin and para-aminohippurate clearances, respectively. Lithium clearance was used as an index of proximal tubular reabsorption of sodium. In addition, plasma concentrations of neurohumoral factors were determined. RESULTS: Total central blood volume was 2.41 +/- 0.33 L/m2 (mean +/- SEM) before and 2.34 +/- 0.18 L/m2 48 h after large volume paracentesis (p = 0.76). Similarly, no differences were detected in the cardiac index, glomerular filtration rate, effective renal plasma flow, urinary sodium excretion, hematocrit, plasma renin activity, or concentrations of plasma aldosterone, norepinephrine, or atrial natriuretic factor. CONCLUSIONS: A single large volume paracentesis without albumin replacement causes no disturbances in systemic and renal hemodynamics 48 h after the procedure. These results suggest that a single 5-L paracentesis without albumin infusion is a safe and satisfactory short term option for the management of patients with cirrhosis and tense, diuretic-resistant ascites.     

Genotyping of the CYP1A1 and GSTM1 genes in esophageal carcinoma patients with special reference to smoking

OBJECTIVES: Patients with cirrhosis and ascites have high plasma levels of atrial natriuretic peptide (ANP). Pharmacological doses of this hormone usually worsen systemic hemodynamics of cirrhotic patients. We assessed whether ANP influences cardiovascular homeostasis and renal function in patients with compensated cirrhosis at plasma levels comparable to those observed in patients with cirrhosis and ascites. METHODS: Radionuclide angiocardiography was performed in eight compensated cirrhotic patients during placebo (three periods of 15 min each) and ANP infusion (2, 4, and 6 pmol/kg.min for 15 min each), together with appropriate blood and urine sampling, to evaluate left ventricular diastolic, systolic, and stroke volume, heart rate, cardiac output, arterial pressure, peripheral vascular resistance, creatinine clearance, urinary sodium excretion, plasma renin activity, plasma aldosterone, norepinephrine and hematocrit. RESULTS: The infusion increased plasma ANP up to levels (52.03 +/- 2.29 pmol/L) comparable with those observed in 35 patients with ascites (46.42 +/- 1.57 pmol/ L). This increment was associated with significant reductions in left ventricular end diastolic volume, stroke volume, cardiac index (from 3.7 +/- 0.7 to 3.1 +/- 0.5 L/min.m2, p < 0.05) and mean arterial pressure (from 96.7 +/- 6.5 to 88.5 +/- 9.5 mmHg, p < 0.05), while heart rate and hematocrit significantly increased. Peripheral vascular resistance did not change. These hemodynamic effects occurred despite significant increases in plasma renin activity and norepinephrine. ANP also induced increases in creatinine clearance, urinary sodium excretion, and fractional sodium excretion. CONCLUSIONS: Low-dose ANP affected cardiovascular homeostasis and renal sodium handling in compensated cirrhosis, suggesting that this hormone may be involved in the pathophysiology of systemic hemodynamic and renal functional abnormalities of cirrhosis.     

Blood pressure tracking

Interactions between nitric oxide (NO) and angiotensin (ANG) II in renal vascular beds were examined in anesthetized dogs. The renal blood flow (RBF) response to an intrarenal arterial injection of ANG II was significantly augmented by intrarenal infusion of the NO synthase inhibitor N(G)-nitro-L-arginine (LNA, 50 microg/kg/min). The simultaneous intrarenal infusion of L-arginine (1 mg/kg/min) prevented the potentiating action of LNA. Similar potentiation was also seen in phenylephrine-induced renal vasoconstriction. Moreover, during simultaneous intrarenal infusion of sodium nitroprusside (SNP), an NO donor, the potentiating action of LNA on the renal vasoconstrictor action of ANG II disappeared. Under these conditions, the released NO stimulated by ANG II was still inhibited by LNA, if present, but basally released NO was resupplied by SNP, as indicated by the return of the RBF. During an infusion of phenylephrine, which produced an increase in renal vascular tone similar to that observed during the infusion of LNA, the renal vasoconstrictor action of ANG II was not augmented. These data suggest that basally released NO plays an important role in the regulation of renal hemodynamics by modulating the renal vasoconstrictor actions of ANG II and phenylephrine.     

Normal trachea during forced expiration: dynamic CT measurements

In order to understand the mechanism of acute renal failure frequently observed in severe acute pancreatitis, renal microcirculation and renal hemodynamics were investigated during experimental acute pancreatitis in dogs induced by autologous bile and trypsin mixture into the pancreatic duct. Renal tissue blood flow (hydrogen gas clearance method), renal arterial blood flow, and cardiac output (transonic blood flow meter) were each measured for 5 h after induction of pancreatitis. The effect on renal hemodynamics of a new synthesized protease inhibitor--E-3123; 4-(2-succinimidoethylthio)phenyl-4-quanidinobenzoate methane sulfonate--intravenously infused at the rate of 3 mg/kg/h was also investigated. The mean blood pressure and pulse pressure decreased after induction of pancreatitis. Renal microcirculation and renal artery blood flow decreased during the experiment. However, in dogs with treated by E-3123, renal microcirculation was preserved during the first hour of the experiment and decreased gradually afterward, but it was significantly higher than that of the dogs without E-3123 during 3-5 h. The mean blood pressure and pulse pressure were preserved nearly at preoperative levels during the experimental period. We concluded that renal microcirculation decreased concomitantly with a deterioration of acute pancreatitis, and that the new pancreatic protease inhibitor E-3123 may have some beneficial effect to improve renal hemodynamics in the early period of acute pancreatitis.     

The antiproteinuric action of angiotensin-converting enzyme inhibitors in chronic glomerulonephritis and diabetic nephropathy

Antiproteinuria effects of angiotensin-converting enzyme (ACE) inhibitors was studied in 23 patients with chronic nephritis (CN) and 32 patients with diabetic nephropathy (DN). CN patients received Capoten, DN patients were given enalapril. The drugs were also examined for the action on systemic arterial pressure, renal function and intrarenal hemodynamics. Significantly decreased urinary excretion of protein occurred in DN patients on the treatment month 1, in CN subjects on month 3. In both groups ACE inhibitors produced marked hypotensive effect, did not affect renal function, noticeably improved intraglomerular hemodynamics. Hypotensive and antiproteinuria activity of the drugs were unrelated. The mechanism of antiproteinuria action of ACE inhibitors works via normalization of intrarenal hemodynamics. Systemic arterial hypertension seems to be an additional factor aggravating disturbances of intrarenal circulation and provoking proteinuria.     

Effects of endoscopic variceal ligation on oxygen transport and the arterial lactate levels in patients with cirrhosis

OBJECTIVE: Despite the increased cardiac output and oxygen delivery, an impaired oxygen uptake has been noted in patients with cirrhosis. We recently observed that endoscopic variceal ligation decreased the cardiac output due to a reduction in the cardiac preload. It is thus possible that a variceal ligation decreases the oxygen delivery and thereby negatively influences tissue oxygenation in patients receiving such treatment. We thus investigated the effects of variceal ligation on oxygen delivery, oxygen uptake, and the arterial lactate levels. METHODS: There were 22 patients with compensated cirrhosis and risky esophageal varices (Child's class A:B=13:9). Twelve patients underwent an endoscopic variceal ligation and 10 patients received gastroscopy as a control. The cardiac function, blood gas status, oxygen delivery, and arterial lactate concentration were also assessed before and after variceal ligation. The oxygen uptake was calculated by the Fick equation. RESULTS: Following variceal ligation, there was an immediate decrease in the cardiac output and oxygen delivery. The reduction in oxygen delivery was associated with a slight but significant increase in the arterial lactate concentration. The decreased oxygen delivery was also associated with a concomitant decrease in the oxygen uptake. In the control subjects, gastroscopy did not alter the systemic hemodynamics, arterial oxygen status, or arterial lactate levels. CONCLUSION: We found a significant decrease in the oxygen delivery in patients undergoing an endoscopic variceal ligation. Such deteriorated tissue oxygenation may be serious especially in patients with a low oxygen transport ability such as in patients with variceal hemorrhage with anemia. However, the clinical significance of these changes remains unclear and further studies are therefore warranted.     

The development of x-ray imaging to study renal function

The well-established role of the kidney in control of blood volume and ultimately arterial blood pressure has been underscored by the demonstration of alterations in renal hemodynamics and function recognized as responsible for these and other regulatory mechanisms. Nevertheless, the spatial complexity of intrarenal structure and function has made evident the need to study these separately in different regions of the intact kidney. Because of the introduction of x-rays, assessment of renal function has indeed been one of their attractive applications. However, despite the appeal of their noninvasiveness, several limitations confounded the different x-ray techniques used, most of which remained unresolved until the development of computed tomography. Furthermore, the development of fast imaging, which allows repetitive analysis of the same region of interest during the transit of contrast medium, holds a great potential to estimate intrarenal distribution of blood flow and the dynamic characteristics of tubular fluid flow in individual nephron segments. This latter assessment requires the administration of filterable x-ray contrast medium, which is cleared from the plasma almost exclusively by glomerular filtration, and the generation of contrast dilution curves. A historical review of the development and progress of the various x-ray techniques used will help understand the past and present of x-ray imaging, and will make it easier to envision the importance of their future roles in the study of renal physiology and pathophysiology.     

Cerebral autoregulation in patients with cirrhosis and ascites. A transcranial Doppler study

BACKGROUND/AIMS: Patients with cirrhosis and ascites usually show alterations of systemic hemodynamics and are thus prone to develop arterial hypotension, which might result in cerebral hypoperfusion if cerebral autoregulation is impaired. METHODS: We evaluated cerebral autoregulation in 15 patients with cirrhosis and ascites and 15 healthy subjects by monitoring mean blood flow velocity in the middle cerebral artery and arterial pressure during supine rest and passive tilting. RESULTS: Tilt provoked a drop of arterial pressure in both groups. Control subjects had a prompt recovery of mean flow velocity and a progressive recovery of arterial pressure, so that, after 120 s, both parameters had returned to baseline: at 20 s the recovery of flow velocity was faster (p<0.01) than that of blood pressure. By contrast, patients with cirrhosis had a delayed and incomplete recovery of both parameters (p<0.01 vs healthy subjects). In eight patients, the recovery of mean flow velocity paralleled that of arterial pressure, indicating an impaired cerebral autoregulation. These patients had a worse liver function, a higher cardiac index and lower peripheral resistance. CONCLUSIONS: Cerebral autoregulation is often impaired in patients with cirrhosis and ascites. These patients can develop cerebral hypoperfusion if arterial pressure falls abruptly.     

Migrant health: a harvest of poverty

The aim of the study was to assess prestarium effects on central and renal hemodynamics, blood lipids in hypertensive subjects. Prestarium was given in a daily dose 4-6 mg to 30 patients with essential hypertension stage II free of cardiac decompensation and renal failure. Echocardiography, tetrapolar chest rheoplethysmography with assessment of hemodynamics, radionuclide tracing of renal blood flow, tests for cholesterol and blood electrolytes were made before treatment, on treatment weeks 2-3 and 12. It was found that prestarium lowers blood pressure and total peripheral vascular resistance. Myocardial conductivity was not affected, whereas renal circulation activated. Low-density lipoproteins cholesterol fell. No significant changes in electrolytes were seen. The drug was well tolerated. In view of good clinical effect and tolerance prestarium is recommended for treatment of essential hypertension stage II in the absence of cardiac decompensation and renal dysfunction.     

CD9, but not other tetraspans, associates with the beta1 integrin precursor

Insulin resistance is common in patients with angina pectoris, a positive exercise electrocardiogram, and normal coronary angiograms (syndrome X). It is still not known whether insulin resistance affects the cardiac muscle itself and, if so, whether insulin resistance involves myocardial hemodynamics and energy metabolism. We investigated hemodynamics as well as metabolite exchanges across the heart and the forearm in eight patients with syndrome X and eight control subjects during a baseline period after an overnight fast and during a hyperinsulinemic-euglycemic clamp. Myocardial hemodynamics and metabolism were studied at rest, during pace stress, and in the recovery period after pacing. Neither coronary sinus blood flow nor forearm blood flow differed between the groups before and during the clamp. Whole body insulin-stimulated glucose uptake was decreased in the patients (15.6+/-2.1 vs. 23.1+/-2.0 micromol x kg-1 x min-1). Insulin-stimulated glucose uptake in the forearm and the cardiac muscle was equally reduced in the patients (46+/-5 and 48+/-5%). Myocardial glucose uptake correlated with total arterial delivery in the control subjects (r = 0.63, P < 0.01), but not in patients (r = 0.22, P = 0.13). Carbohydrate and lipid oxidation was similar in the two groups at rest, and changes during the clamp were not different in control subjects and patients either at rest, during pacing, or in the recovery period. Patients with syndrome X exhibit myocardial insulin resistance, but cardiac energy metabolism remains unaffected. In patients with syndrome X, insulin-stimulated glucose uptake is independent from myocardial blood flow.     

Effect of subcutaneous administration of octreotide on endogenous vasoactive systems and renal function in cirrhotic patients with ascites

Splanchnic and systemic arteriolar vasodilation plays an important role in ascites formation in cirrhosis. Octreotide produces splanchnic vasoconstriction, but the effects on systemic hemodynamics and renal function are controversial. This study evaluated the effect of subcutaneous octreotide administration on systemic hemodynamics, endogenous vasoactive systems, and renal function in cirrhotic patients with ascites. Twenty patients were included: 10 received octreotide 250 microg/12 hr subcutaneously (for five days), and 10 did not. No statistically significant changes were found in mean arterial pressure and cardiac rate. Octreotide induced a statistically significant decrease in plasma renin activity (P < 0.01), plasma aldosterone (P = 0.01) and plasma glucagon (P < 0.05). No significant variations were observed in other systemic vasoactive substances (nitric oxide and prostacyclin). Renal function was not modified in either group. In conclusion, in cirrhotic patients with ascites, subcutaneous octreotide administration decreases plasma glucagon, renin activity, and aldosterone without changing in systemic hemodynamics or renal function.     

Cyclosporine therapy after cardiac transplantation causes hypertension and renal vasoconstriction without sympathetic activation

BACKGROUND: Hypertension frequently complicates the use of cyclosporine A (CyA) therapy, and it has been suggested that sympathoexcitation may be the underlying mechanism in this form of hypertension. METHODS AND RESULTS: To further investigate the possibility of a neurogenic mechanism for this hypertensive effect, we studied the effects of CyA on renal blood flow (n = 11), forearm blood flow (n = 8), and sympathetic nervous system activity, assessed by renal and whole-body radiolabeled norepinephrine plasma kinetics and muscle sympathetic nerve firing (using microneurography) in cardiac transplant recipients receiving CyA and a reference group of healthy age-matched control subjects (n = 17). In 11 cardiac transplant patients (2 hours after cyclosporine dose), renal blood flow was significantly lower than that in 8 control subjects (680 +/- 88 vs 1285 +/- 58 mL/min, P < .001). In 5 of these transplant patients, renal blood flow was measured before and for 2 hours after oral cyclosporine and fell progressively over this period, by 37% (P < .01). Total body and renal norepinephrine spillover rates in transplant patients were similar to those in control subjects (3070 +/- 538 vs 2618 +/- 313 pmol/min and 579 +/- 124 vs 573 +/- 95 pmol/min, respectively), and there was no progressive effect in the 2 hours after cyclosporine dosing. Forearm blood flow was increased 2 hours after CyA administration (1.74 +/- 0.31 to 3.12 +/- 0.50 mL x 100 mL-1 x min-1, P < .001), whereas mean arterial blood pressure and noninvasively determined cardiac output (indirect Fick method) were unchanged. Muscle sympathetic nerve discharge rates recorded in 6 of these transplant patients were not different from those in 9 healthy control subjects (37.9 +/- 10.1 vs 41.3 +/- 2.3 bursts per 100 beats per minute). During 90 to 120 minutes of recording after cyclosporine dosing, nerve firing rates remained unchanged. CONCLUSIONS: CyA therapy causes acute renal vasoconstriction without accompanying systemic hemodynamic effects. These renal effects are nonneural, not being attributable to sympathoexcitation.     

MDS and AML with trisomy 8 as the sole chromosome aberration show different sex ratios and prognostic profiles: a study of 115 published cases

There are few studies on the use of dihydropyridine calcium antagonists in hypertensive patients with moderate renal insufficiency. We undertook an open study on the effects on renal function, albumin excretion and blood pressure of the slow-onset, long-acting dihydropyridine calcium antagonist, lacidipine, in 14 patients with stable, chronic renal insufficiency (mean assessed GFR 0.78 ml/s, range 0.50-1.17 ml/s) and moderate hypertension. Following a 2 week washout phase, lacidipine was administered for 24 weeks in a dose of 2 mg/day with the dose being titrated at 2 weekly intervals to a maximum of 6 mg/day in order to achieve adequate blood pressure control. Frusemide was introduced if blood pressure was not controlled on the maximum lacidipine dose. Blood pressure, creatinine clearance, 24 h urinary albumin excretion and plasma creatinine and albumin concentrations were measured at regular intervals throughout the study. Isotopic GFR was determined at the end of the washout period and at week 24. Lacidipine was not very effective in controlling blood pressure and had an adverse effect on renal function. In 3 patients with an incipient nephrotic syndrome this necessitated withdrawal from the study. Mean GFR of the 10 patients who completed the study decreased from 0.69 ml/s/1.73 m2 at baseline to 0.56 ml/s/1.73 m2 at week 24 (p = 0.006) with a decline in GFR being observed in 9 of these patients. The decrease in GFR was greatest in patients with poorly controlled blood pressure. An insignificant increase in mean urinary albumin excretion occurred during the study with this increase being observed only in patients with albuminuria > 1 g/24 h at baseline. These findings indicated that systemic hypertension altered glomerular hemodynamics and that the vasodilatation of pre-glomerular vessels which followed introduction of the calcium antagonist may have exacerbated this situation. The withdrawal of an angiotensin converting enzyme inhibitor during the washout period may have contributed to these changes. We suggest that renal function should be monitored closely in patients with renal insufficiency when a calcium antagonist is being used to control blood pressure, particularly in those with either marginal blood pressure control, significant albuminuria or an incipient nephrotic syndrome.     

Acute renal failure in open heart surgery

A case-control study was performed to establish possible risk factors for acute renal failure (ARF) and mortality in patients undergoing cardiac surgery. A consecutive series of 704 patients were included in the study. A randomized sample of 255 patients was taken to analyze risk factors for ARF and mortality. Incidence of acute renal failure was 3.8% (27/704). Low cardiac output (LCO) was observed in all patients who developed ARF and in 72/255 without ARF (p < 0.0005). When LCO was isolated, no difference was found between groups. Association to prolonged perfusion time and sepsis increased the probability of developing ARF: 5/27 versus 0/255, p < 0.001; and 9/27 versus 0/255, p < 0.001, respectively. Overall mortality was 7.2% (51/704). Significant difference was found between ARF (55.6%, 15/27) and non-ARF patients (5.4%, 36/704), p < 0.005. Neither age nor sex was associated to outcome. Nonsurvivor patients were more oliguric (11/15 vs. 0/12, p < 0.005), required dialysis more frequently (7/15 vs. 0/12, p < 0.005), and were complicated with sepsis more often (9/15 vs. 0/12, p < 0.005), compared to survivors. We concluded that ARF was an uncommon complication in this group of patients, but mortality rate was dramatically high. This study identified LCO associated to prolonged perfusion time and sepsis as risk factors for ARF. Severity of ARF (oliguric forms and dialysis requirement) and postoperative events (sepsis) were associated with mortality.     

Effects of iced and room temperature injectate on cardiac output measurements in critically ill patients with low and high cardiac outputs

OBJECTIVE: To determine the effect of injectate temperature (iced or room temperature) on cardiac output values in critically ill adults with low and high cardiac outputs. DESIGN: Quasi-experimental. SETTINGS: Two multidisciplinary intensive care units in two large, metropolitan, private, nonprofit hospitals in Texas. SUBJECTS: A convenience sample of 21 critically ill men and women who averaged 61 years of age (range 31 to 82 years) and whose most recent cardiac output measured with room temperature injectate was low (< or = 3.5 L/min) or high (> or = 8.0 L/min). INTERVENTION: Iced injectate and room temperature injectate (randomly ordered) were used to measure cardiac output in each subject. OUTCOME MEASURES: Cardiac output value with iced injectate versus cardiac output value with room temperature injectate. RESULTS: We found significant differences between cardiac output measurements with room temperature and those with iced injectate in eleven critically ill patients with low cardiac outputs (< or = 3.5 L/min) and in ten critically ill patients with high cardiac outputs (> or = 8.0 L/min). In the low cardiac output group, cardiac outputs using room temperature injectate averaged 0.37 L/min (range 0.1 to 1.10 L/min) higher than cardiac outputs using iced injectate (p = 0.001). In the high cardiac output group, measurements with room temperature injectate averaged 1.17 L/min L/min (range 0.3 to 3.0 L/min) higher than cardiac outputs with iced injectate (p = 0.005). Percent differences between room temperature and iced injectate values averaged 13% (range 3% to 27%) in patients with low cardiac outputs and 11% (range 3% to 29%) in patients with high cardiac outputs. Seven (77%) of the patients in the low cardiac output group and four (40%) of the patients in the high cardiac group had a 10% or greater difference--which many clinicians describe as a clinically significant difference--between room temperature and iced injectate cardiac output values. CONCLUSION: Although research is clearly needed to substantiate these findings, we suggest that nurses use iced injectate in patients with low and high cardiac outputs (< or = 3.5 L/min or > or = 8.0 L/min) to ensure accurate measurement of cardiac output.     

Quality assessment and vascular disease: the analytic imperatives confronting vascular surgeons in the new era

Not much is known about the relationship between portal hemodynamics and the grades of cirrhosis. Using pulsed Doppler ultrasonography, we studied portal vein diameter, portal flow velocity, and portal blood flow rate in 37 patients with liver cirrhosis (11 Child's A, 13 Child's B, and 13 Child's C) and 10 healthy controls. There was no difference in the maximum inner diameter of the portal vein in cirrhotics and controls. However, there was a significant decrease in the portal flow velocity in patients with Child's C cirrhosis, as compared to controls and patients with Child's A and Child's B cirrhosis. The portal blood flow rate in Child's B and Child's C cirrhosis was also significantly less as compared to controls and patients with Child's A cirrhosis. Patients with ascites and encephalopathy had significantly lower portal flow velocities and blood flow rate as compared to those without ascites and encephalopathy, respectively. This study indicates that portal flow significantly decreased in cirrhotic patients with worsening Child's grade of cirrhosis.     

Molecular cloning and characterization of CDEP, a novel human protein containing the ezrin-like domain of the band 4.1 superfamily and the Dbl homology domain of Rho guanine nucleotide exchange factors

BACKGROUND/AIMS: Liver cirrhosis and portal hypertension are associated with hyperdynamic circulation. Portacaval shunts are widely used to prevent recurrent hemorrhage, but the hemodynamic effects caused by these procedures have not been well characterized in cirrhosis. We therefore compared the hemodynamic effects of both end-to-side and side-to-side portacaval shunts in normal and cirrhotic rats. METHODS: Sprague-Dawley rats were divided into six groups according to the operations they underwent. End-to-side or side-to-side portacaval shunts were performed in both rats with cirrhosis induced by bile duct ligation and sham-operated rats. Systemic and regional blood flows were measured by the radioactive microsphere method. RESULTS: Portal pressures in the shunted rats decreased significantly. Cardiac index in cirrhotic rats (557 +/- 27 ml.min-1.kg-1) was significantly higher than controls (455 +/- 21 ml.min-1.kg-1), but the two types of shunts did not further increase cardiac index in either the cirrhotic or the sham-operated rats. After shunting, hepatic arterial flows approximately doubled. Portal tributary blood flows in the end-to-side shunted sham (108 +/- 13 ml.min-1.kg-1) and cirrhotic (139 +/- 19 ml.min-1.kg-1 groups were significantly higher than their respective controls (62 +/- 8 and 76 +/- 5 ml.min-1.kg-1). Portosystemic shunting indices were > 99% in both the end-to-side and side-to-side shunted groups in cirrhotic and sham-operated rats. CONCLUSIONS: The hyperdynamic circulation in cirrhotic rats was not augmented by portacaval shunting operations (either end-to-side or side-to-side), despite essentially total portosystemic blood diversion. Compensatory increase in the hepatic arterial blood flow to the liver remained intact even in cirrhotic rats. A selective redistribution of cardiac output to the mesenteric vascular bed was observed after the shunting procedure. However, there were no significant differences in hemodynamics between the end-to-side and side-to-side shunted groups.