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Biomedical subjects

R R Beck

Publications and source records attributed to R R Beck.

7 recordsLinked to original sources
PubMed1991

Portal venous compliance in canine endotoxin shock.

The response of the small intestinal vascular bed to endotoxin and ibuprofen was determined in mongrel dogs under pentobarbital anesthesia. Blood flow was measured in the superior mesenteric artery and pressures in the artery and portal vein. Venous compliance was calculated from the rate of pressure rise in the occluded portal vein at a constant arterial inflow. The response to endotoxin was followed for 1 hr, ibuprofen was given, and the response was followed for a second hour. Arterial pressure and mesenteric flow decreased after endotoxin, accompanied by an increase in venous compliance and in the compliance/resistance ratio. Treatment with ibuprofen increased arterial pressure but did not improve blood flow; however, it effectively reversed the changes in compliance. The results indicate a loss of arterial vasomotor tone in response to endotoxin which is not shared by the portal venous system. This may result in fluid loss into the intestinal bed. Ibuprofen restored arterial tone and released the venous constriction, but did not significantly alter the metabolic responses to endotoxin.

Animals↗
PubMed1989

Influence of ibuprofen on renal function in acutely endotoxemic dogs.

Dogs were anesthetized with pentobarbital and instrumented to measure renal function. An inulin infusion was started; after an appropriate equilibration period one group was infused with endotoxin only (ETOX), a second group was pretreated with ibuprofen before (PRET) endotoxin, and a third group was post-treated with ibuprofen after (POST) endotoxin. Renal blood flow decreased in all animals, but renal vascular resistance increased only in the POST group animals. Urine flow and osmolar clearance decreased and free water clearance increased in the post-treated animals. Glomerular filtration rate as well as electrolyte excretion decreased in both the ETOX and POST group animals. Renal glucose output was unchanged in the ETOX and POST groups, but in the ibuprofen-pretreated animals there was significant net uptake, indicating increased utilization. Ibuprofen alone had no significant effect on blood flow, renal resistance, filtration rate, or solute and water handling. However, when ibuprofen was given 30 min after the induction of endotoxemia, the changes brought about by endotoxin alone were further intensified.

Animals↗
PubMed1988

Canine peripheral vascular response to endotoxin shock at a constant cardiac output.

The peripheral vascular response to Escherichia coli endotoxin (1 mg/kg/i.v.) was measured for 2 hr in the pentobarbital anesthetized dog. Total venous return was collected and returned by a pump to the right atrium to maintain a constant cardiac output. Occlusion of the venous lines permitted estimation of venous compliance in the systems drained by the superior (SVC) and inferior vena cavae (IVC). After endotoxin administration, arterial pressure and total peripheral resistance rapidly dropped and remained low for 2 hr. IVC compliance was decreased at 10-30 min and SVC compliance at 10 min after endotoxin. The decrease in compliance is interpreted as venous dilation and probably venous pooling. The latter may account for a substantial portion of the total venous pooling reported in early endotoxin shock. After 30 min, compliance increased and by 60 min was equal to control. Left ventricular relaxation ability decreased as indicated by maximal negative dp/dt. Ibuprofen, 10 mg/kg, was administered at 120 min or earlier, depending on the state of the animal; rapid recovery of arterial pressure and ventricular function occurred without a significant change in venous compliance.

Animals↗
PubMed1987

Effect of ibuprofen on the course of canine endotoxin shock.

Four groups of dogs were anesthetized, instrumented for measurement of blood pressures and flows across the liver, and, except for the control group, injected with 1 mg/kg endotoxin. The control group received only saline. One group received endotoxin only (ETOX) while animals in the other two groups received 10 mg/kg ibuprofen either 30 min before (PreIBU) or 30 min after endotoxin (PostIBU). Blood pressure, hepatic arterial and portal flow decreased after endotoxin injection in the ETOX and Post IBU animals but not in the PreIBU-injected animals. Pressure and flows returned to normal within 15 min after ibuprofen in the PostIBU animals but remained significantly lower in the ETOX animals. There was a transient increase in blood glucose concentration in the ETOX and PostIBU animals immediately after endotoxin injection, but not in the PreIBU group. Glucose then steadily decreased in all three experimental groups for the remainder of the experiment in spite of the fact that glucose production was elevated. Blood lactate and glycerol concentration increased in all three groups throughout the experiment. Ibuprofen was able to correct the pressure and flow changes caused by endotoxin, but did not prevent the hypoglycemia or accumulation of lactate and glycerol in plasma.

Animals↗
PubMed1986

Role of calcium ion in hormone-stimulated lipolysis.

Using the flask-incubated fat cell system, the effects of Ca2+ removal from the incubation medium on the lipolytic system were studied. The removal of Ca2+ resulted in a total abolition of the lipolytic response and the increased cyclic AMP accumulation produced by ACTH. The lipolytic response to isoproterenol and forskolin were reduced approximately 40% by Ca2+ removal, but cyclic AMP accumulation was not altered in the presence of either of these agents using a Ca2+-free medium. The lipolytic response to the dibutyryl analog of cyclic AMP was also reduced by omission of Ca2+ from the incubation medium. It is concluded the Ca2+ is required for the interaction of ACTH with its receptor and the resultant activation of adenylate cyclase. Ca2+ also is required at some step in the lipolytic process distal to cyclic AMP.

Adipose Tissue↗