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Biomedical subjects

J S Sarma

Publications and source records attributed to J S Sarma.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effect of ethanol on regional myocardial blood flow and hemodynamics, before and after coronary artery ligation in dogs.

The effects on regional myocardial blood flows (RMBF) and hemodynamics due to ethanol administered before and after acute coronary artery ligation (CAL) in 18 anesthetized dogs were studied. Ethanol was administered to seven dogs (group I) prior to CAL and to six dogs (group II) after CAL; five dogs (group III, control) received only saline before and after CAL. Uniform blood ethanol levels (180 +/- 30 mg/dl) were maintained in groups I and II after initial ethanol administration. In these groups the heart rate and rate-pressure product (which reflects myocardial oxygen consumption) remained stable, but pulmonary arterial pressures were elevated. Other hemodynamic parameters remained stable in all groups. Ethanol caused a significant transmural increase of RMBF (p less than 0.001) in both groups I and II. In group II the increase was significant in both nonischemic and ischemic tissues, with no apparent redistribution of flow among the myocardial layers. The percentage increase of RMBF due to ethanol was highest in group II nonischemic tissue (95-107%) compared to the corresponding ischemic tissue (57-60%) and the group I myocardial tissue (36-47%) prior to CAL (p less than 0.001). The observed differences between ethanol pre- and posttreatments suggest different interactions between ethanol and catecholamines. The results also confirm that vasodilatory reserve is present in the acutely ischemic myocardium and that the local availability of ethanol is important for coronary vasodilatation.

Animals↗
PubMed1987

Hysteresis in the human RR-QT relationship during exercise and recovery.

The present study was undertaken to test the hypothesis that the human RR-QT relationship during dynamic exercise differs markedly from that during the recovery phase. Fourteen subjects from the age of 16 to 71 years exercised on a treadmill according to the Bruce protocol. Electrocardiograms were recorded continuously on a magnetic tape, from 1 minute before exercise to 10 minutes into recovery. An exponential formula, proposed by us earlier, closely represented the exercise RR-QT data. However, it was not appropriate for the often S-shaped recovery curves which invariably deviated from the exercise curves, exhibiting hysteresis. Initially, all recovery QT intervals were shorter than the exercise values, but later in the recovery, some crossed the exercise curves from below, resulting in longer QT intervals. The recovery data were fitted by a third degree polynomial, and the hysteresis was calculated as the area between the exercise and recovery curves within a 150 ms range of the RR interval starting from its minimum value. The mechanisms for the occurrence of hysteresis are likely to involve the sympatho-adrenal activity in the early post-exercise period and the time course of QT interval adaptation to rapid changes in the RR interval.

Adolescent↗
PubMed1984

An exponential formula for heart rate dependence of QT interval during exercise and cardiac pacing in humans: reevaluation of Bazett's formula.

A new exponential formula to characterize the human RR-QT relation was evaluated in comparison with Bazett's formula in 16 subjects: 10 healthy, normal men (ages 18 to 30 years) who exercised on a stationary bicycle, and 6 patients (ages 50 to 80 years; 2 women and 4 men) with rate-programmable VVI pacemakers whose rates were changed by an external programmer. The RR and QT intervals for heart rate in the range of 50 to 180 beats/min were measured from electrocardiographic tracings recorded at a paper speed of 100 mm/s. The data from each subject were fitted separately by 4 formulas by an appropriate regression analysis using a statistical package program: (F1) QT = A1 - B1*Exp(-k1*RR); (F2) QT = A2[1-Exp-(-k2*RR)]; (F3) QT = A3* square root (RR) + B3; and (F4) QT = A4* square root (RR), where all A, B, and k are regression parameters. The relative goodness of fit of data by the 4 formulas was assessed by the mean-squared residual and the Akaike Information Criterion using Wilcoxon signed-ranks tests. This analysis confirmed that F1 is the best model among the formulas tested and F4 (Bazett's formula) is the least acceptable for both exercised and paced groups. The deviations from Bazett's formula were more striking for the paced group than for the exercised group, as reflected by the mean-squared residual values for F4 (715 +/- 86 for the paced group vs 384 +/- 41 for the exercised group, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Ventricular refractory periods in relation to rate and test-site VT intervals in anesthetized and conscious dogs: a canine model for conscious state measurements.

The functional relationship of ventricular effective refractory period (ERP) with basic cycle length (BCL) of stimulated ventricular depolarization and VT intervals of test-site unipolar ventricular electrograms were studied in five conscious and eight anesthetized (sodium pentobarbital, 30 mg/kg) open-chested dogs. The range of BCLs studied was 300 to 1000 ms, achieved through ventricular stimulation following chemically-induced complete AV block. In the conscious animal model developed for this study, two-to-four ventricular electrode leads were exteriorized and the ventricular rate was maintained by an implanted programmable VVI pacemaker. In all animals studied, the BCL-ERP relation was closely represented by the empirical equation ERP = A-B.Exp(-k.BCL), and the VT-ERP relation over the same range of BCLs was linear: ERP = C + D.VT. The correlation coefficients were in the range of 0.991 to 0.999. The mean values of the parameters in the above equations determined by the appropriate non-linear or linear regression analysis showed significant differences between the two groups of animals studied. In three conscious animals a strong linear correlation between the test-site VT intervals and simultaneously measured QT intervals measured from the lead II surface electrogram was demonstrated (r = 0.993 to 0.998). For a fixed site of stimulation, the morphology of ventricular depolarization complexes as well as the corresponding T-waves remained essentially unaltered with BCL for both myocardial and surface electrograms. The possible applications of developed canine model and the results of the present study include: (1) the study of the rate-dependent effects of cardioactive drugs on ventricular electrophysiology and, (2) the improved design of electronic refractory periods of rate programmable pacemakers.

Anesthetics↗
PubMed1981

A digital module for cardiac pacemaker assessment.

The accuracy of a digital pacemaker testing module incorporated into a digital recording electrocardiograph has been tested against two other methods of waveform recording. Measurements of rate (pulse interval), pulse width, pulse amplitude and ratio of trailing edge to the leading edge amplitude were found to be highly accurate. The pulse shapes were faithfully recorded. The practical clinical use of the method is discussed.

Electrocardiography↗
PubMed1980

Toxicity, pharmacokinetics, and cholesterol-inhibitory effect of 7-ketocholesterol.

The possible toxic effect of intravenous 7-ketocholesterol (7-KC), a steroid which has been shown to inhibit cholesterol flux in the arterial wall, was investigated in rabbits. The histology, hematology and blood chemistry were compared in 4 control animals, 3 animals receiving high doses (5.50 +/- 0.33 mg/kg/day) and 4 animals injected with lower doses 1.85 +/- 0.28 mg/kg/day) of the oxygenated sterol. Each animal received a total of 16 injections at the rate of 2 injections per day. Pharmacokinetic studies on the disappearance rate of [4-(14)C]7-KC were also carried out. Pathologic changes in the organs of animals injected with 7-KC were few. In one animal exposed to the higher concentration of 7-KC, some granulomatous angiitis in the lung was noticed. Changes in the liver were not significantly different from those observed in the control animals. Inhibition of arterial flux of cholesterol (inhibition of 55%) was noticed with high and low doses of the oxidized sterol. The disappearance curves of [14C]cholesterol in blood and plasma were characteristic of a 2-compartment model. The rate constant determining tissue uptake of 7-KC was higher than tissue efflux and there was no appreciable reflux into red cells. The results indicate that it is possible to reduce cholesterol flux in the arterial wall of rabbits without causing major toxic changes and that both red cells and tissue act as a reservoir for the oxygenated sterol.

Animals↗
PubMed1979

Inhibition of cholesterol uptake by the arterial wall in the intact animal.

This report presents evidence that 7-ketocholesterol effectively inhibits cholesterol uptake by the arterial wall in intact rabbits. The 7-ketocholesterol was administered to the animals by infusing isologous blood pre-incubated with the sterol. Each animal was used as its own control by the use of 3H and 14C-labelled cholesterols as tracers to measure the arterial cholesterol uptake during two successive infusions. The mean cholesterol uptake by the carotid and femoral arteries in the presence of 7-ketocholesterol was 18+/-3 nmoles/g, whereas the average of cholesterol uptake by these arteries was 53+/-5 nmoles/g when the animals were infused with isologous blood containing no 7-ketocholesterol. The mean concentration of 7-ketocholesterol in the animals blood ranged from 34 to 87 nmoles/ml. In preliminary experiments in vitro, pre-incubation of plasma with particulate 7-ketocholesterol caused inhibition of cholesterol uptake by perfused pig coronary arteries, although the particulate fraction of 7-ketocholesterol was removed prior to perfusion. The mean cholesterol uptake by the arteries perfused with plasma containing 7-ketocholesterol (240+/-20 nmoles/ml) was 96+/-21 nmoles/g, whereas the mean cholesterol uptake of the paired controls was 324+/-86 nmoles/g. The 7-ketocholesterol was found to bind to the lipoproteins and with higher affinity to red cells.

Animals↗
PubMed1978

The effect of alcohol on active and passive stiffness, and on isometric contractions of glycerinated heart muscle in rats.

The response of the contractile and the series elastic elements to ethanol was studied isometric contraction and quick release methods after measuring the passive length-tension relationship in glycerinated heart muscle fibers of rats at resting state. In rats consuming 30% ethanol for an average of 5 weeks, maximal developed tension (P0), the maximal rate of tension development (dp/dtmax) and Vmax were significantly depressed, the time to peak tension (t0) was not changed. As in fresh papillary muscle the modulus of elasticity of active glycerinated muscle increased in proportion to load. The stiffness of the series elastic element showed significant elevation in rats receiving ethanol. The passive stiffness in resting state revealed no significant difference between control and alcohol exposed rats. Therefore, increased stiffness of the series elastic element and diminished contractility are present following chronic alcohol consumption.

Animals↗
PubMed1977

The effect of indomethacin, 6-hydroxydopamine, saralasin, and hemorrhage on renal hemodynamics.

This report describes the response of the renal circulation to prolonged hemorrhagic hypotension and reinfusion of blood, and to the effect of a variety of drugs (saralasin, indomethacin, and 6-hydroxydopamine, 6-OH-DA). Plastic microspheres were used to measure blood flow perfusing the entire kidney and also the outer cortex, inner cortex, and medulla of the kidney. Cardiac output was determined with a Doppler flow probe, and total and regional flows were calculated. Redistribution of blood flow from outer cortex to inner cortex and medulla occurred during hemorrhage and after administration of saralasin and 6-hydroxy-dopamine, while indomethacin did not alter intrarenal flow distribution. Total renal flow increased after reinfusion of blood and saralasin, but decreased after indomethacin. It did not change after 6-hydroxydopamine. The results demonstrate that changes in total and intrarenal flow occur independently and are probably due to different mechanisms.

Angiotensin II↗
PubMed1977

Regional blood flow, contractility and metabolism in early myocardial infarction.

The effects of occlusion of the left anterior descending coronary artery on a variety of metabolic parameters was examined in both infarcted and noninfarcted areas of the dog heart. These included mitochondrial performance, glycolysis, in vitro contractility, and regional myocardial blood flow. Measurements were made at 1 and 3 h after onset of ischemia. Regional coronary blood flow was measured in infarcted, noninfarcted and borderline regions using radioactive microspheres. Blood flow through the ischemic area was reduced by an average of 69% after 1 h of ischemia, and 75% after 3 h. After 3 h the subendocardium of the borderline region also revealed a significantly reduced blood flow. Mitochondria isolated from the ischemic region of the heart exhibited a substantial decrease in the rate of respiration (QO2), and minor reductions in the coupling between oxidative phosphorylation and electron transport (RCI), and in the amount of ADP phosphorylated per oxygen reduced (ADP:O ratio). Levels of hexose monophosphates were elevated 1 and 3 h after ischemia was initiated. At the same time, the concentration of fructose-1,6-diphosphate declined markedly, reflecting inhibition of glycolysis at the phosphofructokinase level. Concentrations of the adenosine phosphate moieties, as well as creatine phosphate, were reduced, while levels of free fatty acids were elevated in ischemic tissue. The in vitro contractility of glycerinated ischemic muscle fibers was also depressed. Significant changes were found in maximal tension development (P0), maximal rate of tension development (dp/dtmax), time to peak tension (t0), and shortening velocity at zero load (Vmax).

Animals↗
PubMed1976

Mechanism of inhibition of cholesterol uptake by the arterial wall.

Experiments have been described dealing with lipid synthesis and cholesterol uptake in perfused human and pig coronary arteries, rabbit aortas, and with the inhibitory effect of 7-ketocholesterol on cholesterol uptake in these preparations and in rabbits in vivo. Human and pig coronary arteries failed to synthesize cholesterol in vitro. 7-ketocholesterol inhibited cholesterol uptake in human coronary arteries and aortas of pigs and rabbits in vitro and by rabbit aortas in vivo. The inhibitory effect in vivo could only be shown after repeated i.v. injections of 7-ketocholesterol after solubilizing the steroid with bile sale (Na-glycocholate). Although 7-ketocholesterol was absorbed from the G.I. tract, gastric feeding of the bile salt steroid complex was ineffective, probably because of inadequate blood levels of 7-ketocholesterol achieved. The metabolic fate of 7-ketocholesterol and the nature of its effect on cholesterol are discussed. It is not likely that inhibition of HMG-CoA reductase is responsible for the inhibition of cholesterol uptake. The possibility was discussed that both cholesterol and 7-ketocholesterol actively compete for identical and specific binding sites or that an increase in 7-ketocholesterol in plasma leads to an increase in intracellular concentrations of this steroid thus inhibiting cholesterol transfer across the cell membrane. However definite conclusions on the nature of inhibition must await further experimentation.

Acetates↗
PubMed1976

In vivo inhibition of cholesterol uptake in rabbit aortas by 7-ketocholesterol.

The iv injection of 7-ketocholesterol into rabbits, made soluble by combining with bile salts, inhibited cholesterol uptake by the aorta. However, the inhibition was not as marked or as uniform as previously demonstrated in in vitro experiments. This difference may have been the result of lower plasma concentrations of 7-ketocholesterol in the injected animals. Gastric feeding of 7-ketocholesterol failed to inhibit aortic cholesterol uptake, probably because of inadequate plasma concentrations of the inhibitory steroid. The results suggest that the mechanism of 7-ketocholesterol on aortic cholesterol uptake is through competitive inhibition.

Animals↗
PubMed1975

Lipid metabolism in perfused human and dog coronary arteries.

The paper represents a summary of our studies in which in vitro perfusion of human and animal coronary vessels was carried out. Formation and uptake of lipids in perfused human coronary arteries were studied under a vairety of experimental conditions, including exposure to carbon monoxide. The effect of collagenase on lipid synthesis and transport in carotid arteries of dogs was also studied. Human plasma with hydrogen-3-labeled cholesterol and carbon-14-acetate was used to perfuse human blood vessels. Autologous plasma was employed. Inhibition of cholesterol uptake was accomplished by the addition of 7-ketocholesterol (concentrations of 0.005 to 1 mum/ml) to the perfusate. Both atherosclerotic and normal human coronary arteries incorporated 14C-acetate into lipids but failed to synthesize either cholesterol of cholesterol esters. Similar results were obtained in human saphenous veins perfused at arterial pressure. Cholesterol uptake from the perfusion fluid was demonstrated in atherosclerotic and normal human coronary arteries as well as in human saphenous veins. Carbon monoxide increased permeability of the arterial wall to cholesterol uptake. In dog arteries exposed to collagenase marked increases in cholesterol uptake were found, but total lipid synthesis was reduced; the relative synthesis individual lipids remained unchanged. The addition of 7-ketocholesterol to the perfusate reduced cholesterol uptake by the vessel by 90 percent. Inhibition of cholesterol uptake was present in all species and was not due to oxidation of cholesterol to 7-detocholesterol in the perfusate. The results illustrate that human coronary arteries as well as human saphenous veins synthesize lipids but not cholesterol. Cholesterol flux into the artery is augmented by carbon monoxide and collagenase. The data also show that active inhibition of cholesterol uptake in the arterial wall can be accomplished by competitive inhibition with 7-ketocholesterol.

Acetates↗