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Biomedical subjects

R Zelis

Publications and source records attributed to R Zelis.

At least 199 records · Page 11Linked to original sources
PubMed1970

Effect of respiration on venous return and stroke volume in cardiac tamponade.

Measurements have been made of pressure and blood velocity in venae cavae and aorta in a patient with severe cardiac tamponade in whom there was pulsus paradoxus. The characteristic pressure changes of pulsus paradoxus were associated with variations in peak blood velocity in the ascending aorta and stroke output. Maximum filling of the right side of the heart occurred during inspiration, and was associated in time with minimum left ventricular stroke volume. These findings point to competition for space by the ventricles in the distended pericardial sac as being the major factor in the production of pulsus paradoxus.

Adult↗
PubMed1970

The role of skin and muscle resistance vessels in reflexes mediated by the baroreceptor system.

The role of skin and muscle vascular beds in baroreceptor-mediated alterations of peripheral vascular resistance was evaluated in six normal subjects in whom the skin circulation in one forearm was temporarily suppressed by epinephrine iontophoresis. Baroreceptor activity was enhanced by application of negative pressure to the neck (neck suction) and inhibited by application of lower body negative pressure. Forearm blood flow was measured simultaneously in both arms with strain gauge plethysmographs. Since blood flow in the treated arm consisted entirely of muscle flow, skin flow was calculated from the difference between total forearm flow in the intact arm and muscle flow in the treated arm. Vascular resistances were calculated as the ratio of mean arterial pressure to the blood flow of each vascular bed. During neck suction, mean arterial pressure decreased from an average of 89 to 75 mm of Hg (P < 0.005), heart rate decreased from an average of 60 to 55 beats/min (P < 0.005), and total skin and muscle flows remained essentially unchanged. Cutaneous vascular resistance decreased from an average of 75 to 49 mm of Hg/ml per 100 g per min (P < 0.05), muscle vascular resistance from 68 to 51 (P < 0.005), and total forearm vascular resistance from 36 to 24 (P < 0.025). During lower body negative pressure, heart rate increased from an average of 59 to 69 beats/min (P < 0.005), mean arterial pressure did not change significantly, and significant decreases occurred in forearm blood flow from 5.4 to 2.7 ml/100 g per min, in skin blood flow from 3.1 to 1.4, and in muscle blood flow from 2.3 to 1.3. Cutaneous vascular resistance increased from an average of 47 to 110 mm of Hg/ml per 100 g per min (P < 0.05), muscle vascular resistance from 43 to 72 (P < 0.005), and total forearm vascular resistance from 20 to 38 (P < 0.001). These results demonstrate that both the skin and muscle resistance vessels participate in reflex changes initiated by alterations in baroreceptor activity.

Adult↗
PubMed1970

Effects of hyperlipoproteinemias and their treatment on the peripheral circulation.

The purpose of this study was to determine the effect of familial hyperlipoproteinemia (HLP) on peripheral vascular disease (PVD) and the extent to which the vascular disease (PVD) and the extent to which the vascular disease is modified by treatment of the lipoprotein disorder. PVD was detected plethysmographically by observing a diminished peak reactive hyperemia blood (PRHBF) following ischemia. The value for PRHBF in the extremity demonstrating the lowest response in 32 normal subjects (age 19-50 yr) was 39.6+/-1.5 SEM, ml/min per 100 g. Patients with untreated HLP. who had PRHBF below the lower limit of normal, were 2 of 11 type II, 9 of 12 type III, 1 of 10 type IV. As a group, patients with type III HLP showed diminished PRHBF (26.6 +/-3.0 ml/min per 100 g, P <0.01). In view of the high incidence of PVD and the striking reduction in serum lipids and complete resorption of xanthomas observed in type III HLP with therapy, six patients were studied before and after 3-6 months of treatment with a therapeutic diet and clofibrate. PRHBF in the most severely affected extremity increased markedly, from 20.4 +/-1.6 to 31.9 +/-1.8 ml/min per 100 g (P<0.01), indicating a dramatic increase in maximum blood flow to this extremity. In two type III patients with PVD not treated, no change in PRHBF occurred over 5 months. In two other type III patients the PRHBF increased 17% during the first 25 days of therapy concomitant with a 30% reduction in whole blood viscosity. Over the next 120 days, blood viscosity decreased only an additional 4.6% whereas the PRHBF increased 57%, indicating that the observed changes seen in the PRHBF with therapy of type III patients can be only minimally accounted for by changes in the viscosity of the blood. Thus, patients with type III HLP are particularly susceptible to the development of PVD and objective improvement of PVD can occur with medical treatment of this lipid transport disorder.

Adult↗
PubMed1970

The hyperlipoproteinemias. A simplified classification and approach to therapy.

It is now clear that the various hyperlipidemias represent a heterogenous group of disorders, each having various clinical and laboratory characteristics, prognosis and treatment. The three disorders commonly associated with premature atherosclerotic vascular disease are Type II (hyperbetalipoproteinemia), Type III ("broad beta" or "floating beta" disease) and Type IV (hyperprebetalipoproteinemia or, endogenous hypertriglyceridemia). The diagnosis of each of these three disorders can be suggested by the fasting serum cholesterol level and the appearance of the fasting serum after it has remained overnight in a refrigerator. Type II disease is characterized by a clear serum and a pronounced to moderate hypercholesterolemia. It is treated by reducing dietary cholesterol and saturated fats, increasing dietary polyunsaturated fats, and cholestyrmine. Type IV disease is characterized by a turbid serum indicating hypertriglyceridemia and a normal or only slightly elevated serum cholesterol level. It is treated with weight reduction, a low carbohydrate diet and clofibrate. Type III disease is characterized by both a turbid serum and increased cholesterol levels. It is treated with weight reduction, a low cholesterol diet and clofibrate. With the treatment of all disorders the lipid values should improve; however, with the treatment of Type III disorder both triglyceride and cholesterol levels return to normal, xanthoma resorb and there is an improvement in the peripheral blood flow, indicating that there has been amelioration of the atherosclerotic process.

Blood Protein Disorders↗