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Biomedical subjects

D Shepro

Publications and source records attributed to D Shepro.

At least 181 records · Page 10Linked to original sources
PubMed1978

Humorally mediated alterations in cardiac performance as a consequence of positive end-expiratory pressure.

Two experimental designs were used to study the mechanism of the decreased cardiac output associated with the use of positive end-expiratory pressure (PEEP). In the first study of nine dogs the application of 15 cm H2O PEEP led to a decrease in cardiac output (CO) from 2.68 +/- 1.05 to 2.01 +/- 1.26 liters/min (+/- SD) (p less than 0.05) concomitant with an increase in transmural central venous pressure of 5.2 +/- 0.9 to 8.4 +/- 2.7 mm Hg (p less than 0.05) and a slight increase in transmural left atrial pressure of 6.8 +/- 3.3 to 7.3 +/- 3.6 mm Hg (p less than 0.1). These data are consistent with altered ventricular performance. In a second study nine pairs of dogs were cross-circulated. Application of 15 cm H2O PEEP to one member of the experimental pair led to a decrease in the CO of the other member from 2.71 +/- 0.98 to 2.21 +/- 0.81 liters/min (p less than 0.001). This decrease returned toward baseline with the removal of PEEP (p less than 0.02). Results indicate that one mechanism whereby PEEP reduces the cardiac output is through the action of a humoral agent.

Animals↗
PubMed1977

Calcium electrode--a method for the continuous monitoring of the platelet release reaction.

The calcium electrode is a convenient, inexpensive, and non-traumatic method for measuring changes in the extracellular calcium which accompanies a platelet release reaction. With this instrument, the temporal pattern of release by platelets in a buffered-saline medium following thrombin stimulation was observed as follows: an initial time lag phase, followed by a maximum release phase, and finally a slow release phase.

Blood Platelets↗
PubMed1976

Similarities between platelet contraction and cellular motility during mitosis: role of platelet microtubules in clot retraction.

The effects of inhibitors of mitosis, energy metabolism and protein synthesis on clot retraction were investigated. The results show that (1) Incubation of colchicine (0-01-0-1 mM) with platelet-rich plasma (PRP) inhibits the subsequent retraction of clots derived from diluted PRP. (2) Inhibition of clot retraction by high concentrations of colchicine (up to 40 mM) can be overcome by increasing the platelet concentration in the system. (3) Incubation of clots in colchicine or 80% D2O solutions inhibits their retraction. Exposure of partially retracted clots to these agents is without effect. (4) Hydrostatic pressure retards clot retraction. (5) Incubation of PRP with either 2-deoxy-D-glucose or antimycin alone does not affect clot retraction, but a combination of these agents is inhibitory. (6) Clot retraction is not inhibited by puromycin or cycloheximide. (7) Platelets in retracting clots have constricted regions containing microfilaments and pseudopods containing microtubules. Fibrin strands are progressively condensed around the constricted regions as retraction advances. (8) The development of platelet constriction, platelet pseudopods and the intracellular microfilaments are delayed in colchicinized clots, corresponding to the retardation of retraction. Following the initial delay of retraction colchicinized clots, like controls, show condensation of fibrin strands adjacent to these constricted areas of platelets containing microfilaments. The formation of pseudopods is impaired and no microtubules are found in platelets in the presence of colchicine. The above results suggest that the thrombin-induced platelet contraction during clot retraction is a coordinated movement, which, under optimal conditions involves both microtubules and microfilaments. The contraction of microfilaments produces the constriction of platelets and brings about clot retraction by reducing the angle between fibrin strands. Platelet microtubules are related to the development of pseudopods and play a supplementary role in facilitating microfilament-mediated cellular constriction. The similarities between platelet contraction and cellular motility in mitosis is discussed.

Antimycin A↗
PubMed1975

Endothelial injury induced by bacterial endotoxin: effect of complement depletion.

The role of complement activation in the pathogenesis of endothelial injury caused by bacterial endotoxin was investigated in the rat. DNA synthesis in aortic endothelium was compared 48 hours after an intravenous injection of endotoxin (50 - 500 mug) in normal rats and in rats depleted of haemolytic complement by purified cobra venom factor. At the time of endotoxin administration the rats treated with cobra venom factor had less than 3% of the normal haemolytic complement level, their fibrinogen level was increased and clot retraction was impaired. Endotoxin stimulated endothelial DNA synthesis to the same degree in normal and in complement-depleted rats. Cobra venom factor alone did not stimulate endothelial DNA synthesis. The complement-depleted rats given 500 mug endotoxin were less thrombocytopenic than normal rats at the time of sacrifice, but the difference was not statistically significant. We conclude that the injurious effect endotoxin has on endothelium is not mediated by activation of late components of complement.

Animals↗
PubMed1975

Aggregation and release in thrombocytes of the duck.

Avian thromboyctes are aggregated by a number of substances that cause platelet aggregation, and evidence suggests that this response is related to the release of serotonin (5-hydroxytryptamine, 5-HT) from intracellular granules. In this study duck thrombocytes released 5-HT during collagen-induced aggregation, but thrombocytes incubated with 14C-labeled adenine did not release radioactive adenine nucleotides. These results indicate the existence of a metabolic pool of adenine nucleotides that is separate from released constituents of the cell. No unlabeled adenine compounds were detected in the supernatants of aggregated thrombocytes indicating either the rapid alteration of released nucleotides or the absence of a specific release pool of adenine nucleotides. Finally there is no release of the intracellular enzyme markers, lactate dehydrogenase, beta-glucuronidase, and acid phosphatase, during collagen-induced aggregation. These findings suggest that avian thrombocytes exhibit a specific release reaction and that serotonin acts as the functional counterpart of ADP in platelet aggregation.

Adenine↗
PubMed1975

Serotonin transport by cultured bovine aortic endothelium.

Endothelial cells isolated from bovine aortas without prior treatment with enzymes were cultured in RPMI 1640 medium containing 17% fetal calf serum and antibiotics. The endothelial cells at confluency (7 days) were similar to endothelium in situ or to freshly isolated endothelial cells from blood vessels as seen by light, scanning, and electron microscopy. Cultured and freshly isolated indothelial cells exposed to labeled serotonin, even in the presence of iproniazid (5 x 10-4M), took up approximately 125 and 250 pmoles 14C-serotonin/mg protein, respectively, in 3 hours. Imipramine (10-4M) reduced uptake for both cell groups. Cold (4 degrees C) and metabolic inhibitors sharply reduced serotonin uptake by both freshly isolated and cultured endothelial cells. Ouabain (10-5M) almost completely blocked serotonin transport. Six analogues of serotonin at concentrations ten times above experimental serotonin concentrations did not affect serotonin transport in the cultured endothelial cells but did reduce it in the freshly isolated endothelial cells by 50%. The data on transport suggest that serotonin uptake is not unique to pulmonary endothelium, as has been suggested previously. In addition, using cultured indothelial cells to study serotonin transport is compatible with using other serotonin model systems such as platelets, lung, or brain. Lastly, serotonin uptake by endothelial cells may involve an active transport mechanism similar to that described for the pulmonary circulation, platelets, and insect salivary glands.

Animals↗