Decrease In Pressure Gradient Research Articles

Intraventricular early diastolic velocity profile during acute myocardial ischemia: A color M-mode Doppler echocardiographic study

The aim of the study was to investigate the effect of acute myocardial ischemia on the early diastolic mitral-to-apical velocity profile. Intraventricular filling velocities were measured by color M-mode Doppler echocardiography, which allows simultaneous measurements of velocities at multiple sites. Twenty patients were examined during angioplasty and eight dogs during transient coronary artery occlusion. Velocities at each 0.46 cm level from the mitral tip toward the apex were determined at the time of peak early transmitral velocity. Before angioplasty, early diastolic flow velocities decreased progressively from the mitral tip toward the apex. During angioplasty, intraventricular velocities showed a more abrupt decrease from the middle region toward the apex (p < 0.05). A similar change in the mitral-to-apical profile was found during myocardial ischemia in dogs (p < 0.05). Also, there was a decrease in peak early transmitral velocity (p < 0.01) and peak early transmitral pressure gradient (p = 0.06). Volume loading and constriction of the caval veins performed in the nonischemic ventricle did not appear to change the mitral-to-apical velocity profile. Regional myocardial ischemia was associated with a change in the mitral-to-apical velocity profile as measured by color M-mode Doppler echocardiography. The altered filling pattern could not be explained by changes in loading conditions and may reflect impaired relaxation of the ischemic ventricle.

Unsteady axial viscoelastic pipe flows

The main objective of this work is to examine in detail basic unsteady pipe flows and to investigate any new physical phenomena. We take the viscoelastic upper-convected Maxwell fluid as our non-Newtonian model and consider the flow of such a fluid in pipes of uniform circular cross-section in the following three cases: 1. (a) when the pressure gradient varies exponentially with time; 2. (b) when the pressure gradient is pulsating; 3. (c) a starting flow under a constant pressure gradient. In the first problem we looked separately at the pressure gradient rising exponentially with time and falling exponentially with time, i.e. the pressure gradient is proportional to e ± α 2 τ . The behaviour of the flow field depends to a large extent on β where β 2 = α 2(1 ± Hα 2) with H being the quotient of the Weissenberg and Reynolds numbers. In both cases for small | βη|, η being the radial distance from the axis, the velocity profiles are seen to be parabolic. However, for large | βη| the flows are vastly different. In the case of increasing pressure gradient the flow depicts boundary-layer characteristics while for decreasing pressure gradient the velocity depends on the wall distance. The case of a pulsating pressure gradient is investigated in the second problem. Here the pressure gradient is proportional to cos nτ. Again the flow depends to a large extent on a parameter β ( β 2 = i n − n 2 H). For small values of | βη| the velocity profile is parabolic. However, it is found that, unlike Newtonian fluids, the velocity distribution for the upper-convected Maxwell fluid is not in phase with the exciting pressure distribution. In the case of large | βη| the solution displays a boundary-layer characteristic and the phase of the motion far from the wall is shifted by half a period. The final problem examines a flow that is initially at rest and then set in motion by a constant pressure gradient. A closed form solution has been obtained with the aid of a Fourier-Bessel series. The variation of the velocity across the pipe has been sketched and comparison made with the classical solution.

Balloon angioplasty for postoperative pulmonary artery stenosis in transposition of the great arteries

Objectives. This study was designed to assess the success rate and determinants of success or failure of balloon angioplasty for postoperative pulmonary stenosis in patients with transposition of the great arteries.Background. Previous reports have suggested that pulmonary stenosis that develops after the arterial switch operation is not likely to be dilated.Methods. Twenty-eight patients with transposition of the great arteries underwent 39 balloon angioplasty procedures after the arterial switch operation. The mean age at dilation was 4.5 ± 2.2 years (range 0.7 to 9.8), and the interval between operation and balloon dilation was 3.6 ± 1.8 years. The criterion of successful dilation was a ≥50% increase in predilation diameter or a ≥50% decrease in predilation pressure gradient. If the right ventricular/ aortic pressure ratio decreased by ≥0.2, so that the ratio became <0.68, reoperation was thought to be not indicated.Results. The success rate of balloon angioplasty for pulmonary artery stenosis was 51% (20 of 39 dilations). The mean age at dilation in the group with successful dilation (3.6 years) was significantly younger than that in the group with unsuccessful dilation (5.4 years). The interval between operation and dilation in the successful dilation group (2.4 years) was significantly less than that in the unsuccessful dilation group (4.6 years). In 13 patients who underwent balloon angioplasty <3.5 years after operation, balloon dilation was successful in 92%. The balloon/artery ratio was significantly greater in the successful than in the unsuccessful dilation group. A right ventricular/aortic pressure ratio ≥ 0.68 was observed in 20 patients, and reoperation was not indicated in 10 patients (50%). There was no death, but one pulmonary artery rupture that did not require surgical intervention occurred. Aneurysmal dilation of the pulmonary artery was observed in three patients.Conclusions. These data indicate that although the success rate of balloon angioplasty for pulmonary artery stenosis after the arterial switch operation is low (≈50%), balloon angioplasty can be the first therapeutic choice owing to the low complication rate and the potential benefit of the procedure. The success rate can be high if angioplasty is performed <3.5 years after operation and a balloon of adequate size is used.

Detection of Bursts in a Favorable Pressure Gradient with the VITA Technique.

The variable-interval time averaging (VITA) tchnique is applied to detect bursts in the turbulent boundary layer at favorable pressure gradients generated by a two-dimensional asymmetric contraction. Three averaging periods based on (1) the Eulerian micro-time scale, (2) the inner time scale and (3) the outer time scale are used to obtain conditionally averaged streamwise velocities with the VITA technique. The first of these scales is derived from the auto-correlation of the streamwise-fluctuating velocity component, and the second and third scales are obtained from the inner and the outer variables of boundary layers, respectively. Results of experiments show that when the Eulerian micro-time scale at Y+=15 is used as the averaging period in the VITA technique, the conditional averages at Y+=15 are similar and independent of the pressure gradient. On the other hand when the averaging periods based on the inner or the outer time scales are used, the conditional averages become irregular as the pressure gradient decreases.

Mitral balloon valvuloplasty with transesophageal echocardiography without using fluoroscopy.

Balloon mitral valvuloplasty with Inoue technique was performed in two group of patients. In group I (n = 40) valvuloplasty was performed under fluoroscopy without using echocardiography, whereas in group II (n = 13) valvuloplasty was performed under the guidance of transesophageal echocardiography alone, without using fluoroscopy. Patients in two groups were comparable with regard to clinical variables and hemodynamic parameters. Two female patients in group II were pregnant. Transmitral pressure gradient decrease did not differ significantly between two groups (pressure gradient: 17 +/- 5 to 4 +/- 1 in group I and 15 +/- 4 to 3 +/- 1 mm Hg in group II). Mitral valvular area increase was also not different in two groups (1.09 +/- 0.2 cm2 to 2.3 +/- 0.5 cm2 in group I and 0.9 +/- 0.2 to 2 +/- 0.3 cm2 in group II). In 14 cases from group 1 and 2 cases from group II mitral regurgitation increased after valvuloplasty (p < .05). Left atrial perforation occurred in one patient from group 1 and 2 patients from group II. In conclusion, mitral balloon valvuloplasty under transesophageal echocardiographic guidance alone is a safe and effective procedure in the treatment of mitral stenosis.

Closed transventricular dilation of discrete subvalvular aortic stenosis in dogs.

Discrete subvalvular aortic stenosis with peak systolic pressure gradients of more than 60 mm Hg was treated by closed transventricular dilation in six young dogs. Peak systolic pressure gradients were measured by direct catheterization before surgery, immediately after dilation, and 3 months after surgery. Maximum instantaneous pressure gradients were measured by continuous wave Doppler echocardiography before surgery and 6 weeks to 9 months after surgery. All dogs survived the procedure, and two dogs were clinically normal after 9 and 14 months. Two dogs died at week 6 and month 7. One dog was receiving medication for pulmonary edema 15 months after surgery. One dog underwent open resection of the subvalvular ring at month 3, and was clinically normal 6 months after the second procedure. Complications included intraoperative ventricular fibrillation in one dog, and mild postoperative aortic insufficiency in one dog. Closed transventricular dilation resulted in an immediate 83% decrease in the peak systolic pressure gradient from a preoperative mean of 97 +/- 22 mm Hg to a mean of 14 +/- 15 mm Hg. However, systolic pressure gradients measured by direct catheterization at month 3 (77 +/- 26 mm Hg), and by Doppler echocardiography at week 6 to month 9 (85 +/- 32 mm Hg) were not significantly different from preoperative values, which suggested recurrence of the aortic stenosis. Closed transventricular dilation should not be considered a definitive treatment for discrete subvalvular aortic stenosis in dogs, but may be useful in young dogs with critical aortic stenosis as a bridge to more definitive surgery.

Balloon angioplasty of the aorta in Takayasu's arteritis: Initial and long-term results

Percutaneous transluminal balloon angioplasty for stenosis of the aorta was performed in 36 patients with Takayasu's arteritis (age range, 8 to 36 years; mean, 19.1 ± 7.7 years). Balloon dilatation was successful in 34 patients and resulted in a decrease in the mean peak systolic pressure gradient (PSG) from 75.2 ± 29.1 mm Hg to 24.8 ± 19 mm Hg ( p < 0.001) and a mean increase in the diameter of the stenosed segments from 4.5 ± 2.2 mm to 9.6 ± 3.8 mm ( p < 0.001). Hemodynamic and angiographic restudy, which was performed in 20 patients at a mean follow-up period of 7.7 ± 4.1 months (range, 3 to 24 months), showed a further decrease in PSG (≥ 15 mm Hg) in seven patients (from 40.0 ± 11.2 mm Hg to 15.7 ± 10.2 mm Hg; p < 0.01), no significant change in PSG in 12 patients (17.1 ± 13.6 mm Hg vs 16.6 ± 12.7 mm Hg; p = NS, and an increase in PSG from 15 mm Hg to 85 mm Hg in one patient. The patient who showed restenosis underwent successful redilatation. Six patients who underwent late recatheterization and angiography at 36 to 60 months (mean, 43 ± 9.4 months) show continued relief of stenosis (mean PSG, 8.8 ± 7.8 mm Hg). Patients with short-segment (< 4 cm) stenosis experience more relief than patients with long-segment (≥ 4 cm) stenosis (residual PSG, 18.6 ± 8.2 mm Hg vs 40 ± 16 mm Hg; p < 0.01). All successfully treated patients experienced improvement in their symptoms and hypertension. There were no significant complications. No patient showed evidence of an aneurysm immediately after percutaneous transluminal balloon angioplasty or during follow-up aortography. Percutaneous transluminal balloon angioplasty for stenosis of the aorta in patients with Takayasu's arteritis is safe and highly effective and produces sustained improvement.

Impact of leftward septal shift and potential role of ischemia in its production during experimental right ventricular pressure overload

To determine whether leftward septal shifting mediates primary changes in left ventricular (LV) preload and diastolic function, seven animals were studied after instrumentation with right ventricular (RV) and LV Millar microtip pressure transducers and RV and LV segment length crystals. This allowed assessment of LV preload and LV diastolic pressure segment length relationships before and after the pulmonary artery pressure was first doubled, then tripled by embolizing the pulmonary circulation with glass beads, and then after an additional injection of glass beads reduced the cardiac output by 30%. Echocardiographic images were also acquired to assess LV size and septal configuration. To determine whether reversal of the transseptal pressure gradient and leftward septal shifting during acute pulmonary hypertension is associated with RV ischemia, transmural biopsies of the right ventricle for adenosine triphosphate and creatine phosphate analysis were performed at each stage. We determined that doubling and tripling of the pulmonary artery pressure was not associated with RV ischemia or alteration in septal configuration or diastolic function of the left ventricle. However, LV preload, measured by both segment length crystals and echo-derived areas and circumferences, was decreased when the pulmonary artery was tripled. When cardiac output was decreased 30% there was depletion of adenosine triphosphate and creatine phosphate, a reversal of the transseptal pressure gradient, and reduction of the LV shape and eccentricity indices consistent with leftward septal shift. The LV diastolic pressure/ segment length relationships were not consistently altered. We conclude that (1) LV preload decreases before the transseptal pressure gradient decreases and the septum shifts leftward, (2) LV distensibility does not appear to be altered by leftward septal shift when it occurs provided the pericardium is opened, and (3) RV ischemia likely contributes to the reversal of the transseptal pressure gradient and shifting of the septum leftward.

The effects of chronic endoscopic variceal sclerotherapy on portal pressure in cirrhotics

The effect of obliterating esophageal varices by endoscopic sclerotherapy on portal pressure was prospectively studied in 11 cirrhotic patients with variceal hemorrhage. Portal venous pressure gradient, determined as the difference between transhepatic portal and hepatic vein pressure, increased by a mean of 31.1% ± 14.5% in 8 (73%) and decreased by a mean of 30.1% ± 11.7% in 3 (27%) patients, with no statistically significant change overall (P = 0.1). These changes in portal venous pressure gradient occurred despite an improvement in the laboratory and clinical parameters of hepatic function. Deep abdominal sonography with color flow imaging at variceal obliteration showed patent paraumbilical veins in 6 (55%) patients, 3 of whom had decreases in portal venous pressure gradient (29%, 19%, 42.5%) at variceal obliteration. In 5 (45%) patients without patent paraumbilical veins, a statistically significant increase in portal venous pressure gradient between initial endoscopic variceal sclerotherapy and variceal obliteration was noted (P = 0.008). Rebleeding (single episode in all 4 patients, before obliteration in 3 patients) occurred in those with an increase in portal venous pressure gradient; all patients with portal venous pressure gradient decreases were nonbleeders. No correlation between changes in portal venous pressure gradient and time to variceal obliteration, number of sclerotherapy treatments, or rebleeding episodes was observed. Thus, an increase in portal venous pressure gradient was noted in the majority of patients at variceal obliteration. Although the portal venous pressure gradient decrease may be explained by a patent paraumbilical vein, the mechanism of portal venous pressure gradient increase is not clear. It is speculated that this portal venous pressure gradient increase may be caused by an increase in collateral resistance or flow or a combination of both, resulting from obliteration of esophageal varices by endoscopic sclerotherapy.

Propranolol and haemodynamic response in cirrhosis

In the present study, we compared cirrhotic patients who had a decrease in the hepatic venous pressure gradient after propranolol intake to patients without a decrease. Twenty patients with cirrhosis and oesophageal varices were investigated during hepatic vein catheterization before and 90 min after an oral dose of 80 mg propranolol. The hepatic venous pressure gradient decreased by 12.6% (19.0 +/- 4.7 to 16.3 +/- 3.6 mm Hg, p less than 0.05). Eight (40%) out of 20 patients had a decrease of less than 10% in protal pressure (non-responders). Responders had a higher baseline cardiac index than non-responders (3.79 +/- 0.74 vs. 2.83 +/- 0.53 1.min-1.m-2; p less than 0.01). No difference in the effect of propranolol on portal pressure was observed between patients with or without ascites, or between Child-Turcotte A, B, and C class patients. Our results suggest that cirrhotic patients who respond to oral propranolol with a decrease in portal pressure are more hyperdynamic than those without a significant fall in portal pressure.

Predictors of Event-Free Survival after Balloon Aortic Valvuloplasty

Balloon aortic valvuloplasty was developed as an alternative to aortic-valve replacement in selected elderly patients with aortic stenosis. The use of this procedure is limited, however, by a high incidence of restenosis. Between December 1985 and April 1989, valvuloplasty was performed in 205 patients. We evaluated 40 demographic and hemodynamic variables as univariate predictors of event-free survival by Cox regression analysis and identified independent predictors of event-free survival by stepwise multivariate analysis. Early hemodynamic results indicated a decrease in the peak transaortic-valve pressure gradient from 67 +/- 28 to 33 +/- 15 mm Hg after valvuloplasty and an increase in aortic-valve area from 0.6 +/- 0.2 to 0.9 +/- 0.3 cm2 (P less than 0.001 for both comparisons). The rate of event-free survival (defined as survival without recurrent symptoms, repeated valvuloplasty, or aortic-valve replacement) was 18 percent over the mean (+/- SD) follow-up period of 24 +/- 12 months (range, 1 to 47). Significant predictors of event-free survival included the left ventricular ejection fraction and the left ventricular and aortic systolic pressure before valvuloplasty, and the percent reduction in the aortic-valve pressure gradient; the pulmonary-capillary wedge pressure was inversely associated with event-free survival. Although the predicted event-free survival rate for the entire patient group was 50 percent at one year (95 percent confidence interval, 43 to 57 percent) and 25 percent at two years (95 percent confidence interval, 19 to 31 percent), the probability of event-free survival at one year varied between 23 and 65 percent when patients were stratified according to three independent predictors: the aortic systolic pressure, the pulmonary-capillary wedge pressure, and the percent reduction in the peak aortic-valve gradient. The most important predictors of event-free survival after balloon aortic valvuloplasty were related to base-line left ventricular performance. The best long-term results after valvuloplasty were observed among patients who would also have been expected to have excellent long-term results after aortic-valve replacement.

Propranolol in the prevention of the first hemorrhage from esophagogastric varices: A multicenter, randomized clinical trial

To assess the effectiveness of propranolol in the prevention of initial variceal hemorrhage, a doubleblind, randomized trial was carried out in three centers. Patients with cirrhosis (78% alcoholic), hepatic venous pressure gradients greater than 12 mm Hg and endoscopically proven esophageal varices were randomly assigned to propranolol (51 patients) or placebo (51 patients). Of the 102 patients, 58% were Child's class A, 34% were Child's class B and 8% were Child's class C. Daily dosage was determined by the administration of progressively increasing doses of propranolol with the hepatic vein catheter in place to achieve a 25% decrease in hepatic venous pressure gradient, a decrease in hepatic venous pressure gradient to less than 12 mm Hg or a decrease in resting heart rate to less than 55 beats/min. During a mean follow-up period of 16.3 mo, 11 patients in the placebo group (22%) bled from esophageal varices compared with 2 in the propranolol group (4%) during a mean period of 17.1 mo (p < 0.01). Three additional patients (6%) in the placebo group bled from portal hypertensive gastropathy compared with none in the propranolol group. Propranolol appeared effective in preventing bleeding from large varices. Eleven deaths (22%) occurred in the placebo group compared with eight deaths (16%) in the propranolol group (NS). The mean dose of propranolol was 132 mg/day, and the median dose was 80 mg/day. Using a compliance index (pill count, clinic attendance, alcohol and propranolol levels and alcohol history), 81% of the propranolol patients and 77% of the placebo patients were considered compliant. Complications severe enough to require cessation of therapy occurred in eight patients (16%) in the propranolol group and four in the placebo group (8%) (NS). We conclude that propranolol effectively prevents the first variceal hemorrhage in patients with alcoholic cirrhosis and large esophageal varices but does not improve survival. (HEPATOLOGY 1991;13:902–912.)

Propranolol in the prevention of the first hemorrhage from esophagogastric varices: A multicenter, randomized clinical trial

To assess the effectiveness of propranolol in the prevention of initial variceal hemorrhage, a double-blind, randomized trial was carried out in three centers. Patients with cirrhosis (78% alcoholic), hepatic venous pressure gradients greater than 12 mm Hg and endoscopically proven esophageal varices were randomly assigned to propranolol (51 patients) or placebo (51 patients). Of the 102 patients, 58% were Child's class A, 34% were Child's class B and 8% were Child's class C. Daily dosage was determined by the administration of progressively increasing doses of propranolol with the hepatic vein catheter in place to achieve a 25% decrease in hepatic venous pressure gradient, a decrease in hepatic venous pressure gradient to less than 12 mm Hg or a decrease in resting heart rate to less than 55 beats/min. During a mean follow-up period of 16.3 mo, 11 patients in the placebo group (22%) bled from esophageal varices compared with 2 in the propranolol group (4%) during a mean period of 17.1 mo (p less than 0.01). Three additional patients (6%) in the placebo group bled from portal hypertensive gastropathy compared with none in the propranolol group. Propranolol appeared effective in preventing bleeding from large varices. Eleven deaths (22%) occurred in the placebo group compared with eight deaths (16%) in the propranolol group (NS). The mean dose of propranolol was 132 mg/day, and the median dose was 80 mg/day. Using a compliance index (pill count, clinic attendance, alcohol and propranolol levels and alcohol history), 81% of the propranolol patients and 77% of the placebo patients were considered compliant. Complications severe enough to require cessation of therapy occurred in eight patients (16%) in the propranolol group and four in the placebo group (8%) (NS). We conclude that propranolol effectively prevents the first variceal hemorrhage in patients with alcoholic cirrhosis and large esophageal varices but does not improve survival.

Effect of Disopyramide on Systolic and Early Diastolic Time Intervals in Patients with Hypertrophic Cardiomyopathy

The present study clarified the effect of disopyramide on left-ventricular function in patients with hypertrophic cardiomyopathy (5 obstructive type: HOCM, 21 non-obstructive type: HNCM). The systolic and early diastolic time intervals were assessed 3 hours after a single oral administration of 100-mg disopyramide. The following parameters were evaluated at rest and after administration of disopyramide: 1) left-ventricular ejection time index (LVETI), 2) pre-ejection period index (PEPI), 3) the interval from aortic component of the second heart sound to mitral valve opening (IIA-MVO), and 4) the interval from MVO to O point of apexcardiogram (MVO-O). LVETI in HNCM did not change after disopyramide but that in HOCM was significantly shortened (P less than .05). PEPI in both HOCM and HNCM was significantly prolonged after administration of disopyramide. IIA-MVO time in both HOCM and HNCM was not influenced by disopyramide. MVO-O time in both HOCM and HNCM was significantly shortened after disopyramide. These results suggest that 1) shortening of LVETI in HOCM after disopyramide seemed to be due to the decrease in pressure gradient, 2) PEPI prolongation after disopyramide reflected the decrease in myocardial contractility, and 3) shortening of MVO-O time after disopyramide indicated the improvement of left-ventricular filling. The authors conclude that disopyramide may be an important new therapeutic agent in the treatment of patients with hypertrophic cardiomyopathy.

Hyposensitivity to vasopressin in patients with hepatitis B-related cirrhosis during acute variceal hemorrhage

It has been suggested that vasopressin given during hemorrhage may be less effective than when given during a stable state in a portal-hypertensive rat model. This study was designed to evaluate the hemodynamic response to vasopressin infusion in 25 HBsAg-positive cirrhotic patients. Nine patients had active variceal hemorrhage before vasopressin infusion, and the other 16 patients were in a stable condition at the time of infusion. The two groups of patients were similar in baseline values except that a higher heart rate was found in patients with hemorrhage (96 +/- 20 vs. 73 +/- 10 beats/min, mean +/- S.D., p less than 0.01). Thirty minutes after vasopressin infusion (0.66 units/min), hepatic venous pressure gradient significantly decreased in both bleeding and stable patients (from 21 +/- 9 to 18 +/- 9 mm Hg, p less than 0.05; and from 18 +/- 4 to 8 +/- 3 mm Hg, p less than 0.0001, respectively). However, the decrease of hepatic venous pressure gradient was less obvious in bleeding patients as compared with stable patients (4 +/- 3 vs. 9 +/- 2 mm Hg, p less than 0.0001). A significant reduction of hepatic venous pressure gradient after vasopressin infusion was found in five bleeding patients without shock (from a median of 16 mm Hg [range = 12 to 26] to 11 mm Hg [range = 6 to 18], p less than 0.05), but not in four bleeding patients with shock (from 28 [range = 15 to 36] to 25 [range = 18 to 33] mm Hg, p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Carotid artery approach for balloon dilation of aortic valve stenosis in the neonate: A preliminary report

Balloon valvuloplasty in neonates with severe aortic valve stenosis is limited by difficulties in catheter manipulation around the arch and across the valve and by the risk of femoral artery complications. A right common carotid artery cutdown was utilized for balloon aortic valvuloplasty in five neonates 1 to 20 days of age, weighing 3.1 to 3.9 kg. Standard balloon valvuloplasty was performed through a 6F sheath inserted in the right carotid artery. The arteriotomy was repaired at the end of the procedure.Mean left ventricular systolic pressure was reduced from 142 to 97 mm Hg, with a decrease in mean peak systolic pressure gradient from 76 to 33 mm Hg. Only one patient developed mild aortic regurgitation. One patient with a hypoplastic left ventricle died, and one patient required open valvotomy. All four survivors have a normal carotid pulse and no neurologic sequelae. Two of these patients required repeat balloon dilation to treat residual aortic valve stenosis at 8 and 10 months of age, respectively. Balloon valvaloplasty using a carotid artery approach is feasible and was safe in five neonates with severe aortic valve stenosis.

Acute and subacute prostaglandin and ANG II inhibition on glomerulotubular dynamics in rats

Prostaglandins (PG) and angiotensin II (ANG II) contribute to regulation of glomerular microcirculation. Acute vs. chronic physiological alterations of glomerular hemodynamics that result from inhibition of either PG or ANG II, or both, and their interaction were examined. Four groups of Munich-Wistar rats were submitted to the following micropuncture studies in euvolemic conditions for measurements of glomerular hemodynamics and tubular fluid reabsorption: 1) an untreated control group, 2) 4- to 6-day inhibition of both PG and angiotensin-converting enzyme activity with meclofenamate and MK-421 (enalapril), 3) 4- to 6-day treatment with enalapril followed by acute PG inhibition in the second measurement period, 4) 4- to 6-day PG inhibition followed by acute enalapril treatment in the second period. Dual 4- to 6-day treatment decreased single-nephron filtration rate (SNGFR, 24 +/- 2 vs. 33 +/- 2 nl/min in control; P less than 0.05) as a result of decreases in single-nephron plasma flow (SNPF) and glomerular hydrostatic pressure gradient (delta P). Treatment with enalapril alone for 4-6 days did not reduce SNGFR and SNPF; however, delta P decreased. Acute addition of meclofenamate did not alter these factors. SNGFR was decreased with 4- to 6-day treatment of meclofenamate from 33 +/- 2 in control to 25 +/- 1 nl/min (P less than 0.05). Acute treatment with enalapril in the 4- to 6-day meclofenamate-treated rats increased SNGFR to values not different from control. The results demonstrated that glomerular hemodynamic alterations consequent to inhibition of ANG II and PG systems differ between chronic and acute treatments. Therefore, interpretation of the role of individual hormonal systems in the control of glomerular hemodynamics should be approached with caution, since effects may be altered by duration of treatment and involvement of other vasoactive systems.

Hemodynamic Evaluation of Molsidomine: A Vasodilator With Antianginal Properties in Patients With Alcoholic Cirrhosis

Organic nitrates were reported to reduce portohepatic venous pressure gradient in patients with cirrhosis. However, these drugs lower arterial pressure and are well known to induce tolerance. The aim of the present study was to assess the hemodynamic effects of molsidomine, an antianginal agent, which does not induce tolerance and has little effect on arterial pressure in patients with normal liver, in 13 patients with alcoholic cirrhosis. Wedged hepatic vein pressure (-11%, p less than 0.01), portohepatic venous pressure gradient (-15%, p less than 0.005), hepatic blood flow (-17.4%, p less than 0.005), mean arterial pressure (-13.5%, p less than 0.01) and cardiac output (-17%, p less than 0.001) were significantly reduced by molsidomine. Free hepatic vein pressure, intrinsic hepatic clearance indocyanine green, heart rate and systemic vascular resistances were not significantly modified. There was no correlation between the decrease in portohepatic venous pressure gradient and the reduction in mean arterial pressure on one hand and the decrease in cardiac output on the other hand. We therefore conclude that in patients with cirrhosis, molsidomine has effects similar to nitrates on systemic and splanchnic hemodynamics.

Improvement in mitral flow dynamics during exercise after percutaneous transvenous mitral commissurotomy. Noninvasive evaluation using continuous wave Doppler technique.

Evaluation of mitral flow dynamics during exercise is critically important in patients who receive percutaneous transvenous mitral commissurotomy (PTMC) because limited mitral flow during exercise provokes hemodynamic deterioration and involves cardiogenic symptoms in patients with mitral stenosis. To examine mitral flow dynamics during exercise, we applied continuous wave Doppler technique in 20 patients with mitral stenosis. Exercise Doppler study was performed 2 days before and 5 days after PTMC. PTMC increased mitral valve area from 1.0 +/- 0.3 (mean +/- SD) to 1.9 +/- 0.5 cm2 and decreased mean transmitral pressure gradient from 8 +/- 2 to 4 +/- 1 mm Hg at rest. Moreover, PTMC decreased mean transmitral pressure gradient from 21 +/- 6 to 11 +/- 4 mm Hg at submaximal exercise. The extent of an increase in mitral valve area by PTMC correlated with a decrease in the mean transmitral pressure gradient at the submaximal exercise (r = -0.76, p less than 0.01) and that at rest (r = -0.52, p less than 0.05). Heart rate after PTMC during exercise was significantly lower than that before PTMC, indicating that the compensatory mechanism (tachycardia) to increase cardiac output during exercise is less necessary after PTMC. Thus, we conclude that the mitral flow dynamics during exercise is improved, as well as the resting mitral flow dynamics 5 days after PTMC, and that exercise Doppler study enabled us to make a noninvasive evaluation of the mitral flow dynamics in patients who receive PTMC.

Effects of volume loading during experimental acute pulmonary embolism.

Volume loading is used to treat hemodynamically compromised patients with acute pulmonary embolism despite data to suggest that volume loading after embolism might cause a leftward shift of the ventricular septum with a subsequent decrease in left ventricular (LV) end-diastolic volume and stroke work. We studied 10 closed-chest, anesthetized, and ventilated dogs to assess the effects of volume loading after pulmonary embolism caused by autologous clot. LV, right ventricular, and right atrial pressures as well as LV anteroposterior, septum-to-right ventricular, and septum-to-LV free wall diameters (sonomicrometry) were measured. Pericardial pressure was measured with flat, liquid-containing balloons. The effects of volume loading were assessed before embolism, after one episode of embolization, and after repeated embolizations. The LV area index (as a reflection of LV volume) increased during volume loading before embolism (2,870 +/- 430 to 3,080 +/- 520 mm2; p less than 0.05), did not change significantly during infusion of fluid after one embolization (2,850 +/- 470 to 2,860 +/- 500 mm2; p = NS), and decreased significantly during volume expansion after repeated embolizations (2,760 +/- 440 to 2,660 +/- 420 mm2; p less than 0.01). An index of LV stroke work increased (188 +/- 85 to 260 +/- 101 mm Hg x mm2; p less than 0.05), did not change significantly (188 +/- 39 to 203 +/- 52 mm Hg x mm2; p = NS), and decreased markedly (133 +/- 64 to 45 +/- 27 mm Hg x mm2; p less than 0.001) before embolism, after one embolization, and after repeated embolizations, respectively. The decrease in LV area index during volume loading after repeated embolizations was associated with an increase in septum-to-right ventricular free wall diameter (31 +/- 8 to 34 +/- 8 mm; p = 0.001) and a decrease in the septum-to-LV free wall diameter (44 +/- 5 to 42 +/- 5 mm; p less than 0.001), whereas the LV anteroposterior diameter did not change (62 +/- 5 to 63 +/- 5 mm; p = NS). This is compatible with a leftward septal shift being partially responsible for the decrease in LV end-diastolic volume; such a shift would be expected with the observed decrease in transseptal end-diastolic pressure gradient (-3 +/- 2 to -5 +/- 2 mm Hg; p = 0.001). In addition, after repeated embolizations, LV transmural pressure decreased in response to the volume load reflecting a marked increase in pericardial pressure.(ABSTRACT TRUNCATED AT 400 WORDS)