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Biomedical subjects

J M Pfeffer

Publications and source records attributed to J M Pfeffer.

71 records · Page 4Linked to original sources
PubMed1981

Attitudes of house-physicians towards self-poisoning patients.

Eighty-two house-physicians filled in a questionnaire concerning the care of self-poisoning patients with special emphasis on training and attitudes. These recently qualified doctors dealt with large numbers of such patients and expressed dissatisfaction with their training in this respect. Hostile attitudes towards these patients developed most clearly at those district hospitals where psychiatrists are rarely available. During their 6 months as a house-physician, doctors at the teaching hospital became more interested in making a full assessment of these patients whereas those at other hospitals became less so. Better training at both undergraduate and pre-registration level is needed to make house-physicians more able and more willing to fully assess these patients.

Attitude of Health Personnel↗
PubMed1981

Left ventricular diastolic pressure-volume relations in rats with healed myocardial infarction. Effects on systolic function.

To determine the effects of healed myocardial infarction on the diastolic compliance of the left ventricle, we studied 36 rats 26 days after left coronary artery ligation. Peak cardiac output and stroke volume were measured under ether anesthesia during volume loading, and peak left ventricular developed pressure was determined during occlusion of the ascending aorta. During a slow infusion of saline into the potassium-arrested left ventricle, diastolic pressure and volume were measured continuously over the pressure range -5 to 30 mm Hg. Infarct size was determined by planimetry of serial sections taken from each heart at 1-mm intervals from apex to base. In rats with healed infarcts, left ventricular volume was increased in proportion to infarct size and the diastolic pressure-volume relationship was shifted so that at pressures below 2.5 mm Hg volume was increased, resulting in an increased ventricular compliance in this low pressure range. Above this pressure, the slopes of the pressure-volume curves were similar in rats with and without infarctions. Peak cardiac output and pressure-generating capacity were impaired in proportion to infarct size. This impairment of cardiac performance correlated with the infarct size-related increase in diastolic volume, which served to offset the reduction in flow generating capacity caused by systolic dysfunction, while contributing directly to the impairment of pressure generating capacity.

Animals↗
PubMed1980

Myocardial infarction in experimental hypertension in rats: mechanism of the reduction in blood pressure.

1. Haemodynamic changes during graded methoxamine infusion have been measured in 16 spontaneously hypertensive rats with healed myocardial infarction produced by left coronary artery ligation and in 15 hypertensive rats without infarction. 2. Arterial pressure of the hypertensive rats was reduced to levels within the normotensive range in animals with moderate and large myocardial infarctions. 3. The peripheral vascular response to methoxamine was similar in rats with and without infarction. 4. The reduction in blood pressure resulted from a combination of lower heart rate and inability to maintain stroke volume at hypertensive pressures.

Animals↗
PubMed1979

Natural biventricular hypertrophy in normotensive rats. I. Physical and hemodynamic characteristics.

The Wistar-Kyoto strain of normotensive rats (WKY) is being used as a control animal for studies involving the spontaneously hypertensive rats (SHR). A subset of the WKY demonstrating an inheritable transmission of biventricular cardiac hypertrophy (BVH) has been identified. The cardiac enlargement is pronounced, with right and left ventricular weights greater than twice normal in some animals. This natural development of BVH appears to be in response to an increased cardiac output. Blood pressure is normal and, therefore, peripheral resistance is reduced. Left ventricular injection of 15-micrometer radioactively labeled microspheres demonstrated that WKY with BVH had a substantial shunt fraction of their cardiac output (45 +/- 7% radioactivity recovered in the lungs vs. 3 +/- 2% in normal WKY). This subset of WKY with BVH provides a natural model of volume-load hypertrophy. In addition, investigators using the WKY for comparison with SHR should exclude animals with BVH.

Animals↗
PubMed1979

Cardiac function and morphology with aging in the spontaneously hypertensive rat.

To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.

Aging↗
PubMed1979

Myocardial infarct size and ventricular function in rats.

To define the relationship between infarct size and ventricular performance, we performed hemodynamic studies in rats 21 days after left coronary artery occlusion. Ventricular performance was assessed under ether anesthesia by measurements of baseline hemodynamics and stressed performance as determined by the peak cardiac output and stroke volume obtained during intravenous volume loading and by the peak left ventricular developed pressure obtained during occlusion of the ascending aorta. Infarct size was determined by planimetry of the endocardial circumference of each of four histological slices of the left ventricle. Rats with small (4-30%) myocardial infarctions had no discernible impairment in either baseline hemodynamics or peak indices of pumping and pressure-generating ability when compared to the sham-operated, noninfarcted rats. Rats with moderate (31-46%) infarctions had normal baseline hemodynamics but reduced peak flow indices and developed pressure. Rats with infarctions greater than 46% had congestive heart failure, with elevated filling pressures, reduced cardiac output, and a minimal capacity to respond to pre- and after load stresses. The entire spectrum of postinfarction ventricular function was observed, from no detectable impairment to congestive failure. In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium.

Animals↗
PubMed1978

Tumour production of alkaline phosphatase in a patient with giant-cell carcinoma of bronchus.

A patient with a giant-cell carcinoma of the bronchus was found to have a raised serum alkaline phosphatase without any evidence of bone or liver involvement. After necropsy the excised tumour was found to be producing alkaline phosphatase. The alkaline phosphatase found in the serum during life was heat-labile but that in the tumour was heat-stable. The significance of this is unknown.

Alkaline Phosphatase↗
PubMed1978

Ventricular morphology and pumping ability of exercised spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) and two strains of normotensive Wistar rats were subjected to a 5 day/wk swimming program to determine whether the heart of the SHR could respond to an additional stimulus to cardiac growth. Swimming was tolerated well by all rats. Although body weight of the exercised groups was not significantly reduced, both the right and left ventricular weights of all exercised groups were increased. Left ventricular circumference and chamber volume were increased without a change in free wall thickness in all exercised groups. Ventricular performance was assessed by peak cardiac output and stroke volume attained during rapid intravenous volume loading, both before and after autonomic inhibition. After combined cholinergic and beta-adrenergic inhibition, all exercised rats had slower heart rates and higher peak stroke volume than respectively sedentary controls. Thus, exercised SHR had the same alterations in cardiac mass and performance as exercised normotensive rats. Despite the initial presence of left ventricular hypertrophy, the SHR responded appropriately to an additional stimulus for adaptive cardiac growth.

Animals↗
PubMed1978

The aetiology of the hyperventilation syndrome. A review of the literature.

The aetiology of the hyperventilation syndrome is reviewed with special emphasis on psychological aspects. Early reports linking overbreathing and the emotions can be found as far back as the 16th century. During the last 50 years research has been carried out into respiration in psychiatric disorders but as far as the hyperventilation syndrome is concerned there have been few psychiatric studies. Though many people believe that hyperventilation occurs as a response to anxiety, it has recently been suggested that it is due to a bad breathing habit. Whichever view should prove to be correct, most people would agree that the distressing symptoms produced by hyperventilation may themselves cause anxiety and exacerbate the hyperventilation, thus setting up a vicious circle. By the time the patient presents, this vicious circle has usually become established.

Emotions↗
PubMed1977

Development of SHR hypertension and cardiac hypertrophy during prolonged beta blockade.

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.

Adrenergic beta-Antagonists↗
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

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↗