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Biomedical subjects

M A Pfeffer

Publications and source records attributed to M A Pfeffer.

At least 181 records · Page 10Linked to original sources
PubMed1976

Pumping ability of the hypertrophying left ventricle of the spontaneously hypertensive rat.

Cardiac pumping ability was assessed during the natural development of left ventricular hypertrophy by elevating venous pressure by infusing Tyrode's solution intravenously to produce peak cardiac output. This experiment was performed on spontaneously hypertensive rats (SHR) of three age groups (11, 24, and 83 weeks). From 11 to 24 weeks, peak cardiac output of SHR increased in direct proportion to the abnormally increased ventricular mass; Thus peak cardiac output per gram of left ventricle (LV) remained stable. Similar results were obtained for two strains of normotensive rats at each of the same three age groups. Thus, in the normotensive animal peak cardiac output per gram of LV remained stable over a wide range of ages and varying left ventricular weights. However, with progressive elevation of arterial pressure in aging SHR (83 weeks), we observed severe ventricular hypertrophy (100% increases in left ventricular to body weight ratio). In this oldest SHR group, unlike age-matched normotensive rats, there was a marked reduction in the pumping ability per gram of LV. Thus, during the natural development of left ventricular hypertrophy SHR demonstrated both a stable stage of hypertrophy in which the increased left ventricular mass maintained its pumping ability, and a later stage of deterioration in which there was a loss of the normal relationship between ventricular mass and pumping ability.

Animals↗
PubMed1975

Mechanism of immediate hemodynamic effects of chlorothiazide.

The mechanism of the immediate hemodynamic effects of intravenous chlorothiazide (25 mg. per kilogram) was studied in 22 anesthetized open-chest dogs. Within 20 minutes after administration, cardiac output and stroke volume significantly fell; this was associated with decreased central venous and left ventricular end-diastolic pressures. That these hemodynamic effects were caused by, and dependent upon, volume loss through diuresis (eightfold increase in urine volume) was shown: by a return of these measurements to control levels when the volume loss (by diuresis) was corrected with 6 per cent Dextran; by prevention of the hemodynamic changes in chlorthiazide-treated dogs previously prepared with ureterocaval anastomosis; and by confirming these same hemodynamic effects by quantitatively equivalent hemorrhage. Thus, the immediate diuresis produced by chlorothiazide resulted in a contracted plasma volume (increased hematocrit and serum protein concentration) which, in turn, diminished cardiac venous return, central filling pressures, stroke volume, and cardiac output. There was no evidence demonstrated to indicate any direct myocardial effect or peripheral venodilation induced by thiazide.

Animals↗
PubMed1975

Adrenergic mechanisms in human hypertension and in spontaneously hypertensive rats.

1. The role of adrenergic neuronal mechanisms in the development of early hypertension in man and the spontaneously hypertensive rat has been explored. 2. In both, a hyperkinetic circulatory state is associated with reduced parasympathetic and increased adrenergic cardiac influences. 3. Spontaneously hypertensive and normotensive control rats were treated with propranolol from conception until 12 weeks. Although heart rate and output remained reduced, there was no difference in growth or elaboration of pressure with respect to their untreated controls. 4. After another series of spontaneously hypertensive and control rats received cardiac autonomic blockade (atropine and timolol), they sequentially received alpha-adrenergic blockade (phenoxybenzamine), ganglionic blockade (trimethaphan) and smooth-muscle vasodilatation (hydralazine). These studies revealed only a small pressure differential between the two groups before hydralazine and still less thereafter; unlike the control rats, pressure in spontaneously hypertensive rats fell markedly after ganglionic blockade as a result of reduced output, indicating greater adrenergic control mediated through venoconstriction. 5. These findings indicate: increased cardiovascular adrenergic control in young spontaneously hypertensive rats, the hyperkinetic circulation merely reflecting one aspect of increased total cardiovascular input. Structural alterations seem to participate minimally. 6. These experimental observations closely, resemble findings in early hypertensive man, and it is suggested that altered total cardiovascular adrenergic input is responsible for the elaboration, development, and maintenance of essential hypertension in man.

Animals↗
PubMed1975

Hemodynamic effects of mebutamate in spontaneously hypertensive rats.

The acute hemodynamic effects of the antihypertensive agent mebutamate were evaluated in spontaneously hypertensive and normotensive Wistar rats. Arterial and venous pressures and cardiac output (electromagnetic flowmeter) were recorded in artificially ventilated, open-chest, ether-anesthetized animals before and after varying doses of mebutamate were injected intravenously. In both normotensive and hypertensive rats mebutamate produced a moderate decrease in arterial pressure which was associated with a reduction in both heart rate and cardiac output; total peripheral resistance remained unchanged. These data suggest that mebutamate may have therapuetic value in reducing arterial pressure in mild to moderately severe hypertensive patients.

Animals↗
PubMedDate not supplied

Cardiac hypertrophy and performance of Dahl hypertensive rats on graded salt diets.

The relationship between arterial pressure and left ventricular (LV) functional capacity and LV mass during the natural development of cardiac hypertrophy was assessed in Dahl-resistant (R) and -sensitive (S) hypertensive rats maintained on three dietary NaCl regimens (0.4%, 4.0%, and 8.0% for 9 weeks, then 4.0%) from 5 until 20 weeks of age. In R rats, arterial pressure and LV mass were unaffected by diet. In contrast, S rats demonstrated levels of arterial pressure and LV hypertrophy that were graded according to dietary NaCl. Hemodynamic studies on rats under ether anesthesia demonstrated that the graded pressure elevation in S rats was produced by corresponding increases in total peripheral resistance, as cardiac output did not vary. During acute volume loading, the S rats on all diets achieved the same maximum stroke volume as did R rats, despite the marked increase in the arterial pressure of S rats. An analysis of the ejection fraction/afterload relationship demonstrated preserved contractile state. The ability of the left ventricle to generate pressure was increased in S rats in direct proportion to the degree of LV hypertrophy. Thus, in young adult S rats, cardiac performance was well compensated since pump and contractile functions were maintained and pressure-generating capacity was increased in relation to the degree of LV hypertrophy.

Animals↗
PubMedDate not supplied

Selection bias in the use of thrombolytic therapy in acute myocardial infarction. The SAVE Investigators.

OBJECTIVE: To determine whether clinical selection for thrombolytic therapy for acute myocardial infarction results in a skewed population for subsequent adverse cardiovascular events. DESIGN: A comparison of the clinical features of the patients in the Survival and Ventricular Enlargement Study who either had or had not received thrombolytic therapy was conducted in both univariate and multiple logistic regression analyses. SETTING: Hospitalized patients experiencing acute myocardial infarction from 112 broadly representative, private, academic, and government hospitals in the United States and Canada. PATIENTS: All patients in the Survival and Ventricular Enlargement Study had had a recent myocardial infarction (less than 16 days) and had a left ventricular ejection fraction of 40% or less. INTERVENTION: Thrombolytic therapy was administered to 733 patients and was not given to 1498. MAIN OUTCOME MEASURES: The comparisons with respect to use of thrombolytic therapy were formulated after the completion of enrollment and indicated that the majority of patients did not receive thrombolytic therapy. RESULTS: The 1498 (67.1%) patients who did not receive thrombolytic therapy were at higher risk (older age, lower functional capacity, greater likelihood of a history of prior myocardial infarction, angina, diabetes, and hypertension) for subsequent cardiovascular events and, as anticipated, were more likely to have concomitant gastrointestinal and neurological diseases. A multiple logistic regression analysis indicated that older age, prior myocardial infarction, impaired functional status, employment status, diabetes, and neurological diseases were predictors of use of thrombolytic therapy. CONCLUSION: Although the Survival and Ventricular Enlargement Study population was selected for left ventricular dysfunction, the majority of patients who currently are judged clinically as unsuitable for thrombolytic therapy have a higher risk for adverse cardiovascular events.

Captopril↗