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Biomedical subjects

J N Cohn

Publications and source records attributed to J N Cohn.

At least 325 records · Page 18Linked to original sources
PubMed1980

Effect of prazosin on renal function in congestive heart failure.

Prazosin improves hemodynamics promptly in patients with congestive heart failure (CHF), but tolerance to repeated doses may develop rapidly. To determine if the kidneys play a role in this attenuation of effect, we studied renal responses in nine CHF patients treated with prazosin (5 mg three times a day for 3 days) preceded and followed by 3 days of placebo. Prazosin decreased mean arterial blood pressure from 87.0 +/- 2.2 (mean +/- SEM) to 84.0 +/- 2.0 mm Hg (p < 0.05) with no change in heart rate (73.1 +/- 3.3 bpm on placebo and 73.6 +/- 3.5 bpm on prazosin). The change in creatinine clearance from 81.6 +/- 8.7 to 96.3 +/- 10.4 ml/min with prazosin was not statistically significant, but the slight increase in urine volume from 2.33 +/- 0.22 to 2.51 +/- 0.23 1/24 hr was (p < 0.01). There were no significant changes in serum sodium, potassium, chloride, CO2, blood urea nitrogen, osmolality or glucose, urinary excretion of sodium or potassium, or sodium balance. The data were analyzed for changes within each period but there were no significant changes from day to day. Plasma renin activity rose from 3.93 +/- 0.69 to 4.96 +/- 0.84 ng/ml/hr during prazosin (p < 0.02). Significant alterations in renal function are not likely when patients with CHF are treated with prazosin, and any attenuation of effect of prazosin after repeated doses is not likely due to mechanisms involving alterations in renal function.

Aged↗
PubMed1980

Progressive myocardial dysfunction associated with increased vascular resistance.

To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 +/- 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 +/- 8.5 to 84.0 +/- 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 +/- 0.8 mmHg at control and rose to 11.8 +/- 1.4 mmHg at 1 mo and 14.9 +/- 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 +/- 0.1 at control to 3.8 +/- 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.

Animals↗
PubMed1979

Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart.

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.

Animals↗
PubMed1979

Effect of isosorbide dinitrate on response to submaximal and maximal exercise in patients with congestive heart failure.

Isosorbide dinitrate is an effective vasodilator that improves resting left ventricular performance in patients with congestive heart failure, but little is known of the effect of the drug on the response to exercise. Bicycle exercise to symptomatic maximum was performed by 18 patients with class II to IV congestive heart failure before and 90 minutes after administration of isosorbide dinitrate, 40 mg orally. Although resting pulmonary wedge pressure and systemic vascular resistance were significantly reduced after isosorbide dinitrate, exercise duration was not altered and maximal oxygen consumption was not significantly changed (13.6 +/- 1.3 [SEM] standard error of the mean versus 13.8 +/- 1.2 ml/kg per min). At peak exercise pulmonary wedge pressure of 37.1 +/- 1.7 mm Hg, cardiac index of 4.19 +/- 0.35 liters/min per m2, and systemic vascular resistance of 14.7 +/- 1.3 units were not significantly different after nitrate administration. However, at submaximal loads, pulmonary wedge pressure was reduced from 33.6 +/- 1.7 to 27.9 +/- 1.8 mm Hg (P less than 0.01), and systemic resistance from 16.5 +/- 1.5 to 13.7 +/- 1.0 units (P less than 0.01) after administration of isosorbide dinitrate. Thus, short-term administration of nitrates does not improve maximal exercise capacity or left ventricular performance at maximal exercise in patients with congestive heart failure, but it does appear to improve pump function at submaximal work loads and may therefore enable patients to perform limited exercise more comfortably.

Administration, Oral↗
PubMed1979

Effect of dilation of the distal coronary bed on flow and resistance in severely stenotic coronary arteries in the dog.

Studies were performed to evaluate the hemodynamic response of severely stenotic coronary arteries to dilation of the distal coronary bed. A critical stenosis was produced with an adjustable wire snare on the left anterior descending or circumflex arteries of open chest dogs. Coronary flow, distal coronary pressure and aortic pressure were measured. In one group of experiments, coronary arteriolar dilatation was induced by transient occlusion of the artery distal to the stenosis. After the release of a transient occlusion in vessels without a critical stenosis, flow increased (from 33 +/- 4 to 85 +/- 8 ml/min, P less than 0.01), distal pressure decreased slightly (from 86 +/- 4 to 80 +/- 4 mm Hg, P less than 0.01), and large vessel resistance did not change significantly (from 0.06 +/- 0.02 to 0.08 +/- 0.03 units). After the release of a transient occlusion in vessels with a critical stenosis, flow decreased (from 23 +/- 3 to 12 +/- 2 ml/min, P less than 0.01), distal pressure decreased to persistently low levels (from 63 +/- 2 to 29 +/- 2 mm Hg, P less than 0.01), and large vessel resistance increased (from 1.4 +/- 0.3 to 6.7 +/- 1.8 units, P less than 0.01). In a separate group of experiments, radio-opaque contrast medium was used to dilate the distal coronary bed. In these studies dilation of the distal coronary of arteries with a critical stenosis again resulted in a decrease in coronary blood flow (from 35 +/- 4 to 19 +/- 3 ml/min, P less than 0.01), a decrease in distal coronary pressure (from 84 +/- 6 to 35 +/- 6 mm Hg, P less than 0.01) and an increase in large arterial resistance (from 1.0 +/- 0.2 to 5.5 +/- 1.2 units, P less than 0.02). Therefore, in coronary vessels with severe stenosis, dilation of the distal coronary bed may result in a paradoxical decrease in coronary blood flow.

Animals↗
PubMed1979

Immediate effects of hydralazine-isosorbide dinitrate combination on exercise capacity and exercise hemodynamics in patients with left ventricular failure.

Resting hemodynamics improve during vasodilator administration in patients, with congestive heart failure (CHF), but the effects of these agents on exercise is unknown. Twenty-two patients with class II or III CHF performed bicycle exercise to symptomatic maximum before and 90 minutes after random double-blind administration of oral hydralazine (100 mg) and isosorbide dinitrate (40 mg) (11 patients, group 1) or placebo (11 patients, group 2). Exercise duration was unchanged after treatment in either group. Maximal oxygen consumption changed insignificantly in both groups, from 12.6 +/- 1.2 (SEM) to 13.6 +/- 1.6 ml/kg/min in group 1, and from 11.7 +/- 1.4 to 13.4 +/- 1.7 ml/kg/min in group 2. Maximal cardiac index was unchanged in both group 1 (4.00 +/- 0.33 to 4.41 +/- 0.29 l/min/m2) and group 2 (4.11 +/- 0.43 to 4.14 +/- 0.42 l/min/m2). Systemic vascular resistance at peak exercise was also unchanged in both group 1 (14.1 +/- 1.6 to 11.8 +/- 1.0 units) and group 2 (14.7 +/- 1.6 to 13.5 +/- 1.6 units). at submaximal exercise (300 kilopond-meters/min), however, cardiac index after treatment increased in group 1 (0.51 +/- 0.18 l/min/m2, p less than 0.05) and systemic vascular resistance decreased (-3.3 +/- 1.3 units, p less than 0.05), but were unchanged in group 2. Thus, although vasodilators do not improve maximal exercise capacity acutely, they can improve hemodynamics at lower work loads which may, therefore, be better tolerated in patients with CHF.

Adult↗
PubMed1979

Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates.

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.

Blood Pressure↗
PubMed1979

Nitroprusside.

Sodium nitroprusside has proved to be the most effective and best-tolerated vasodilator drug available for the management of acute hypertension, heart failure, and other vasoconstricted states as well as for the induction of controlled hypotension during surgery. It dilates both arteries and veins, has a rapid onset and offset of action, and is almost uniformly effective in achieving the desired degree of dilation by careful dosage titration. The need for close monitoring of its intravenous administration and the potential toxicity of prolonged infusions limit its general use from periods of hours to a few days, but its unique and usually well-maintained vascular actions make it an ideal agent for short-term therapy and a potentially useful model for development of new, orally effective vasodilator drugs.

Aortic Dissection↗
PubMed1979

Splanchnic hemodynamic factors in cirrhosis with refractory ascites.

Splanchnic and systemic hemodynamic observations in eight patients with cirrhosis and refractory ascites were compared to those of 25 patients with cirrhosis and responsive ascites. The refractory ascitic group was characterized by less portasystemic shunting from both the superior mesenteric and splenic vascular beds, a lower cardiac output, a higher systemic vascular resistance, a wider arterial-hepatic venous oxygen difference, and a tendency for a lower HBF and higher postsinusoidal resistance. Portal pressures assessed from hepatic vein catheterization were similar in the two groups. The absence of a well-developed portasystemic collateral bed in patients with refractory ascites could in part be caused by the tense ascites but could also be an important factor in the mechanism of refractory ascites.

Adult↗
PubMed1978

Nitrate therapy for congestive heart failure.

A randomized double-blind crossover trial included 16 patients with severe congestive heart failure who received isosorbide dinitrate or placebo for eight weeks, and then the opposite treatment for eight more weeks. All patients received their usual maintenance therapy with digitalis and diuretics. Seven morbid events occurred during 85 patient-weeks of isosorbide dinitrate therapy compared with 17 during 76 patient-weeks of placebo. Severity of congestive heart failure improved in all eight patients who received isosorbide dinitrate compared with two patients who showed improvement and five whose symptoms became worse with placebo. No significant differences in physical findings, cardiac dimensions, or resting hemodynamics were observed. Maximal exercise duration increased significantly by 2.54 minutes with isosorbide dinitrate therapy, and rose insignificantly by 1.24 minutes with placebo. This preliminary trial suggests that long-term vasodilator therapy may be clinically beneficial in congestive heart failure.

Adult↗