PubMed Health⌕ Search

Biomedical subjects

R D Goldfarb

Publications and source records attributed to R D Goldfarb.

At least 37 records · Page 2Linked to original sources
PubMed1982

Cardiac mechanical performance in circulatory shock: a critical review of methods and results.

The article reviews studies which have focused upon the changes in cardiac contractile behavior induced by shock states. The major hypothesis tested experimentally was that cardiac contractility is depressed by shock states. The conclusions drawn by the cited articles are diverse, equally divided between confirming and rejecting the above hypothesis. The thesis of this article is that these diverse conclusions may have been caused by the limitations of the methods employed to assess cardiac contractility. The concepts of cardiac function curves, cardiac work and efficiency, parameters of shortening and the analysis of the end systolic pressure volume relationship (EES) are examined for their suitability to determine changes in cardiac contractility during shock states. Only the EES methodology appears to be able to assess cardiac contractility in shock states due to its insensitivity to altered conditions of cardiac contraction.

Animals↗
PubMed1982

Cardiac dynamics following shock: role of circulating cardiodepressant substances.

This article seeks to answer the questions "Is cardiac function depressed in shock states, and if so, what is the mechanism for this depression?" The behavior of cardiac contractile function in shock states covers two broad areas of investigation: cardiac function and the cardiovascular response to shock. The major techniques used to examine cardiac function in shock have included pump function vs. end diastolic volume, indices of cardiac work and efficiency, parameters of shortening rate, and the end systolic pressure-volume relationship. The results obtained from these studies, especially those which employed the former three technologies, have yielded divergent results. The main thesis of this article is that the confusion concerning the effects of circulatory shock upon cardiac dynamics is due in large part to the failure of most technologies to distinguish between shock-induced alterations in peripheral vascular function and shock-induced alterations in cardiac dynamic function. However, recent evidence obtained from the end systolic pressure volume relationship, which appears to be sensitive to changes in cardiac dynamic function but independent of changes in peripheral vascular function, indicates that cardiac dynamic function is indeed depressed following endotoxin administration. Several possible mechanisms for this depression are reviewed.

Animals↗
PubMed1981

The effect of leucine on plasma insulin following endotoxin shock in the rat.

We have previously documented the ability of exogenous L-leucine to accelerate the endotoxin shock syndrome. In this report we have tested the hypothesis that the mechanism for this action of leucine was via an induction of pancreatic insulin hypersecretion. Pentobarbital-anesthetized rats were injected with 1 mg/100 gm S. enteritidis endotoxin (LD90) or vehicle and infused with either Krebs Henseleit vehicle or 0.153 M leucine to a dose of 7.6 mmole/kg. Following leucine administration, plasma concentrations of leucine decayed at an exponential rate in both endotoxin-treated and sham-treated groups. The extrapolated initial leucine concentration in the endotoxin-treated rats was significantly higher than the sham rats, indicating a lower circulating blood volume in the endotoxin-treated group. In the vehicle and endotoxin-treated group, insulin levels exhibited a biphasic response, significantly lower at 30 minutes and significantly higher at three hours. In the leucine- and endotoxin-treated groups, insulin levels were markedly higher 0.5, 2, and 3 hours after leucine infusion. In the two non-endotoxin treated groups, no significant changes in insulin levels were noted after infusion. Therefore, the shock accelerating action of leucine may be due to a direct stimulation of insulin secretion inducing a prolonged hyperinsulinemia.

Animals↗
PubMed1981

Microembolization induced oxygen utilization impairment in the canine gracilis muscle.

Impaired peripheral oxygen utilization coinciding with an elevated cardiac index, venous oxygen tension, and serum lactate with the loss of reactive hyperemic response have been observed in a large series of resuscitated trauma patients. We tested the hypothesis that these clinical findings were due to an alteration of the microcirculation caused by embolization of intravascular particulate matter. To test this hypothesis, we used the bilateral pump-perfused, isolated canine gracilis muscle preparation which we subjected to microembolization with 15 micrometers polystyrene spheres. Prior to microembolization, oxygen consumption was flow-limited up to 6 ml min-1 (r = .928) and at higher flows, oxygen consumption was independent of flow. Following microembolization, the relationship of oxygen consumption and blood flow remained correlated (r = .893), but there was less oxygen consumption at any given flow rate (P less than .05). Imidazole, 30 mg kg-1, IP administered to prevent platelet aggregation, resulted in the return of oxygen utilization to the preembolization value. PVO2 of the microembolized muscle was significantly higher than in the contralateral muscle, which was abolished after imidazole administration. These data suggest that microembolization leads to an oxygen utilization defect similar to that observed in the resuscitated trauma patient. Since this defect was reversed by imidazole administration, a humoral mechanism in the microcirculatory bed may act to restrict oxygen utilization following microembolization and trauma.

Animals↗
PubMed1980

Effect of shock on calcium accumulation by cardiac sarcoplasmic reticulum.

Earlier work has suggested that the decreased cardiac performance in shock is due to negative inotropic substances that alter the Ca++ metabolism of the myocardium. We investigated this possibility by examining the Ca++-dependent ATPase activity and the Ca++-uptake ability of cardiac sarcoplasmic reticulum (microsomes) from normal hearts and endotoxin-shocked hearts. Both the ATPase activity and the accumulation of Ca++ by microsomes from shocked hearts were lower than for microsomes from normal hearts. In the presence of serum from shocked dogs, the ATPase activities and Ca++-uptake of both microsome preparations were reduced from those measured in modified Krebs-Henseleit, but this was not considered significant because the same extent of depression was seen with serum from normal dogs. These findings could not attribute the depressed ATPase activities and Ca++-uptake abilities to a shock-induced circulating cardio-depressant material but did demonstrate that calcium metabolism in cardiac tissue was altered in the shock state.

Adenosine Triphosphatases↗
PubMed1979

Oxygen consumption in canine skeletal muscle following massive saline infusion.

To study the effect of interstitial edema on tissue oxygen transport, we infused buffered isotonic saline solution at a rate of 200 ml/kg/hr into mongrel dogs for two hours, measuring oxygen delivery and consumption in a skinned, innervated hindlimb. Hematocrit dropped gradually to 10.8 +/- 3.9%. Muscle water content increased 13% (P less than 0.05). However, oxygen consumption did not change significantly from control of 0.228 +/- 0.029 ml/min/100 gm. Femoral venous oxygen tension fell from control of 62.6 +/- 2.6 mm Hg to 31.4 +/- 2.3 mm Hg. Mean arterial flow increased to nearly twice the control level of 12.5 +/- 1.1 ml/min/100 gm and fell gradually, with the sustained 50% drop in vascular resistance largely explained by expected decreases in blood viscosity. We conclude that interstitial edema did not cause a significant defect in canine skeletal muscle oxygen utilization.

Animals↗
PubMed1978

The effect of indomethacin on cardiovascular and lysosomal mechanisms during experimental myocardial ischemia.

The present study evaluated the effects of indomethacin (INDO) on cardiovascular and lysosomal mechanisms during experimental myocardial ischemia (MI). INDO (5 mg/kg) was infused IV prior to MI, and the results were compared to vehicle-treated and sham-operated dogs. INDO induced a slight hypertension after MI. Additionally, INDO attenuated the decline in coronary blood flow in the non-ischemic myocardium after MI. Myocardial lysosomes (biopsied three hours post-MI) were more labile in ischemic than in nonischemic tissue, and INDO had a stabilizing effect on lysosomes from ischemic tissue. Plasma activity of cathepsin was increased following MI, and INDO attenuated this increase. In the myocardium (biopsies three hours post-MI) prostaglandin A + E levels were suppressed 60% in both ischemic and nonischemic tissue with INDO treatment; prostaglandin F2 alpha levels were lower with INDO treatment but not significantly so. These results suggest that INDO has a stabilizing effect on lysosomes in vivo, possibly involving an endogenous prostaglandin mechanism, and this protective effect may attenuate lysosomal damage to the cardiovascular system during MI.

Animals↗
PubMed1977

The chemical nature of a pancreatic cardiodepressant factor.

The presence of a cardiodepressant factor of pancreatic origin has been reported in the plasma of experimental animals and man in a variety of shock states. It has been suggested that the depression of developed tension of the isolated cat papillary muscle may be caused by excess NaCl in the bathing medium rather than a specific cardiodepressant peptide. Incubated pancreatic homogenate was used as a source of this factor, and after protein precipitation, ultrafiltration (10,00 and 1,000 MW), dialysis and lyophilization, the residue was applied to a Sephadex G-10 column in order to ensure the removal of all salts. The protein effluent of the Sephadex column contained all the cardiodepressant activity of the filtered, dialyzed pancreatic homogenate and none of the salt content. To further isolate this cardiodepressant factor, the active residue was applied to a cellulose column and eluted with butanol: glacial acetic acid: water (25:26 v/v/v). This elution gave 8 distinct peptide peaks, one of which, peak 4, contained significant depressant activity. Thus, a cardiodepressant peptide of approximately 250-1,000 MW exists in pancreatic homogenates and this compound is not excess NaCl in the assay system.

Animals↗