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Biomedical subjects

R J Bing

Publications and source records attributed to R J Bing.

At least 109 records · Page 6Linked to original sources
PubMed1981

Quantitative capillary topography and blood flow in the cerebral cortex of cats: an in vivo microscopic study.

In 50 anesthetized cats the microcirculation in intermediate and deeper layers of the cerebral cortex was visualized in vivo by microtransillumination, and documented by high-speed microcinephotography. The viability of the preparation was verified in a series of experiments demonstrating spontaneous vasomotion and responsiveness to chemical stimulation of pial arterioles and small arteries. Stereological methods for quantitative analysis of projected images of capillaries in a comparatively large tissue volume were employed to determine morphometric and topographical parameters of the asymmetric, highly tortuous intracortical capillary network. Capillary diameters (5.1 +/- 0.84 micrometer), radii of curvature (median 57 micrometer), total capillary lengths per tissue volume 939 +/- 338.2 mm/cu.mm), capillary volume fractions (2.1 +/- 0.51%), total capillary surface areas per tissue volume (15.3 +/- 4.85 sq.mm/cu.mm), and intercapillary distances (median 24.2 micrometer) showed significant interregional differences. The frequency distribution of the lengths of capillary segments (median 108 micrometer) was best described by a Weibull distribution. On the average 90% of all capillaries were continuously perfused. Capillary red cell flow (median velocity 1500 micrometer/sec) was predominantly unidirectional and conspicuously irregular. The variance of capillary red cell velocities (CRCVs) was significantly correlated (tau = 0.48) with capillary tortuosity. An extreme value distribution best described the observed frequency distribution of CRCVs. Flow irregularities represented both white noise and a significant stochastic periodicity at frequencies between 40 and 90 Hz.

Animals↗
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↗
PubMed1980

The effect of regional myocardial ischemia on series elastic and contractile elements of glycerinated heart muscle in dogs.

The response of the contractile and the series elastic elements to ischemia was studied with isometric contraction and quick release methods after measuring the passive length-tension relationship in glycerinated heart muscle fibers of dogs at resting state. Myocardial infarction was induced by ligating left coronary artery. Muscle fibers taken from the ischemic area three hours after ligation demonstrated reduction in maximal developed tension (P0), the maximal rate of tension development (dp/dtmax) and Vmax. The time to peak tension (t0) was increased. 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 elevated significantly in ischemic muscle fibers. The passive stiffness in resting state showed a decrease in the slope accompanied by an increase in the intercept in ischemic heart muscle. Therefore, increased stiffness of the series elastic element and diminished contractility are present following acute myocardial infarction.

Animals↗
PubMed1980

Lipoprotein uptake in perfused arteries: inhibition by 7-ketocholesterol.

The effect of 7-Ketocholesterol (7-KC), an oxygenated sterol (OS) on the uptake of low density lipoproteins (LDL) by artificially perfused porcine carotid arteries was studied. The perfusate consisted of Dulbecco's modified Eagle medium, supplemented with albumin and pure 125I-LDL. Prior exposure to 7-KC significantly inhibited LDL uptake (from 2.47 to 1.92 micrograms LDL p/gr artery). The degree of inhibition of LDL uptake was less than that previously observed for arterial influx of cholesterol.

Animals↗
PubMed1980

Action of anti-anginal drugs on cardiac metabolism.

Diltiazem, a calcium antagonist, was found to lessen the effect of ischemia resulting from coronary occlusion in dogs. For example, this agent preserves the high energy phosphate reservoir and decreases the inhibition of glycolytic flux at the phosphofructokinase level caused by myocardial ischemia. Diltiazem produced a marked reduction in ischemia-induced damage to the contractile elements. Increased tissue levels of lactate and free fatty acids attributable to ischemia were lowered by diltiazem. Although diltiazem increased contractility of isolated ischemia heart muscle fibers, it did not lessen the effect of ischemia on mitochondrial respiration or mitochondrial calcium binding. On the other hand, diltiazem was found to counteract the effects of ischemia followed by reperfusion on mitochondrial oxygen consumption and calcium binding.

Angina Pectoris↗
PubMed1979

Effect of diltiazem, a calcium antagonist, on myocardial ischemia.

In line with studies on the metabolism of the ischemic myocardium, the effectiveness of diltiazem hydrochloride, a potent calcium antagonist, in reducing the effects of ischemia was evaluated. Nonischemic and ischemic tissue samples were examined in two groups of dogs--Group I, dogs receiving no drug and killed after 60 minutes of regional ischemia, and Group II, dogs given diltiazem after 10 minutes of ischemia and killed 50 minutes later. Administration of diltiazem proved beneficial in several ways: The decrease in adenosine-5'-triphosphate in the ischemic region was halved, inhibition of anaerobic glycolysis was reduced, tissue levels of lactic acid and free fatty acids were lowered and the contractility of glycerinated heart muscle fibers was improved. However, administration of the drug did not influence mitochondrial function. Mitochondrial oxygen consumption and respiratory control were reduced by equal amounts in both groups, as was mitochondrial calcium ion binding. These observations demonstrate that diltiazem is capable of minimizing the consequences of acute ischemic, although the beneficial effects do not extend to all aspects of myocardial metabolism.

Adenosine Diphosphate↗
PubMed1979

The relationship of regional coronary blood flow to mitochondrial function during reperfusion of the ischemic myocardium.

The relationship of changes in regional coronary flow to the nature and degree of biochemical disturbances during occlusion of branches of the left anterior descending coronary artery and following reestablishment of flow was investigated in two groups of dogs: group I, moderate ischemia before reflow, and group II, severe ischemia prior to reflow. Regional coronary blood flow was determined before ligation, after 60 min of ischemia and after 15 min of reflow using labelled microspheres. Hearts made ischemic for 60 min but not reperfused served as controls. Groups I and II were distinguished by the following features. Group II showed a marked exacerbation of biochemical damage on reperfusion of the ischemic region (reduced levels of ATP, impairment of mitochondrial oxygen consumption and mitochondrial calcium binding). This was accompanied by significant subendocaridial hyperemia. Reperfusion in group I, on the otherhand, partially reversed these changes (increased level of ATP in the ischemic-reperfused region, improved mitochondrial oxygen consumption and calcium binding). Mitochondrial calcium uptake and oxidative phosphorylation (ADP/O ratio) were not affected in any group. These data illustrate that the degree of biochemical damage following reperfusion of the ischemic myocardium is determined by the degree of ischemia, and suggest that interference with ATP production by the mitochondria is not responsible for the damage.

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

Cardiac metabolsim: its contributions to alcoholic heart disease and myocardial failure.

Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and its interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca++-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the dimunition in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.

Acetaldehyde↗
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↗