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Biomedical subjects

R T Wall

Publications and source records attributed to R T Wall.

29 records · Page 2Linked to original sources
PubMed1981

Platelet activation in clinical coronary artery disease and spasm.

Current concepts of atherogenesis, based on animal models, suggest a role for platelets in the development of atherosclerotic lesions, possibly through the release of alpha granule constituents. Platelets may also contribute to the development of vascular spasm through thromboxane A2 production. Platelet activation in the coronary circulation in patients with coronary artery disease (CAD) should occur if these hypotheses apply clinically. We measured aortic and coronary sinus plasma levels of the platelet alpha granule constituent beta-thromboglobulin (B-TG) and thromboxane B2 (TX B2) by radioimmunoassay in 15 patients with severe atherosclerotic CAD, seven patients with angiographically normal coronaries, and five patients undergoing evaluation for coronary artery spasm (CAS). Compared with the controls, CAD patients had significantly greater transmyocardial release of B-TG (11.1 +/- 8.1 ng/ml, mean +/- SEM vs 62.5 17.2, p less than 0.05 by rank sum test); TX B2 gradients showed a similar trend but the difference was not statistically significant (-0.08 +/- 0.03 ng/ml vs 0.22 +/- 0.02, 0.05 less than p less than 0.10). Three of the five patients studied developed CAS which was associated with acute elevation in coronary sinus TX B2; the two non-CAS patients with drug provocation had undetectable coronary sinus TX B2. We conclude that abnormal platelet activation takes place in the coronary circulation of CAD patients, and that production of acute myocardial ischemia by CAS occurs with increased coronary sinus TX B2.

Angina Pectoris↗
PubMed1981

Studies on the cellular basis of atherosclerosis: the effects of atherosclerosis risk factors on platelets and the vascular endothelium.

Thrombosis is a well-recognized complication of atherosclerosis and may be a factor in initial lesion formation. Experimental endothelial cell injury results in activation of the coagulation mechanism and therefore may be a critical aspect of the pathogenesis of occlusive vascular disease. If this is so, then risk factors for atherosclerosis should affect the endothelium either by causing cell injury, inhibiting repair mechanisms, or altering its thromboresistant properties. To test this, we studied the effect of several risk factors on endothelial cell behavior in vitro. Since the smooth muscle cell is the major cellular component of human atherosclerotic plaque and since a primary smooth muscle cell lesion is suggested by the clonal nature of human plaque, we also studied the effect of risk factors on arterial smooth muscle behavior. We have found that homocysteine directly injures human endothelium, which may account for the premature arterial disease in homocystinuria. Serum from patients with familial hypercholesterolemia inhibits the critical function of endothelial cell migration, as well as arterial smooth muscle cell migration. Moderate hypoxia has no effect on endothelial cell or smooth muscle cell viability, proliferation, or migration. Platelet factors are shown to affect human smooth muscle cell proliferation and both endothelial cell and smooth muscle cell migration. Preliminary study of platelet activation in diabetes with retinopathy suggests a relation to glucose control, but might reflect underlying vessel disease rather than direct platelet effect.

Arteriosclerosis↗
PubMed1980

Binding and release of factor VIII/von Willebrand's factor by human endothelial cells.

The uptake and release of factor VIII/von Willebrand's protein by cultured human umbilical vein endothelial cells have been examined using highly purified 125I-factor VIII possessing von Willebrand's factor activity. 125I-factor VIII/vWF was taken up by the cells, reaching maximum binding within 4 h with a t1-2 of binding of 15 min. Endothelial cell binding of 125I-factor VIII/vWF reached saturation at a concentration of 1.5 mg/l. Binding was inhibited by coincubation of excess unlabelled factor VIII/vWF. Most of the cell-associated radioactivity was released by treatment of the cells with trypsin. Internalization of bound protein was evidenced by the incorporation into the cells of radioactivity which could not be released by trypsin. Human vascular smooth muscle cells did not bind 125I-factor VIII/vWF. Addition of 0.1 microM epinephrine to the 125I-factor VIII/vWF labelled endothelial cultures induced the release of cell bound, protein-associated radioactivity into the medium. Propranolol inhibited completely epinephrine-induced release, whereas phenylephrine had no effect. Endothelial cells maintained in medium partially depleted of factor VIII/vWF by tricalcium citrate cellulose treatment of plasma did not release factor VIII antigen into the culture medium during subsequent incubation. Although [3H]proline was incorporated into proteins released by endothelial cells under these experimental conditions, specific incorporation of label into factor VIII/vWF antigen was not detectable by a sensitive solid-phase immunoradiometric assay. We conclude that factor VIII/vWF binds to endothelial cells and that this cell-bound protein is mobilized by epinephrine through beta-adrenergic stimulation.

Antigens↗
PubMed1978

Factors influencing endothelial cell proliferation in vitro.

The relative roles of blood cell products and plasma factors on endothelial cell proliferation were evaluated by studying the proliferative response of human umbilical vein endothelial cells to cell free plasma derived serum (CFPDS), whole blood serum (WBS), platelet released factors, fibroblast growth factor and macrophage conditioned medium in vitro. Human adult arterial smooth muscle cells were treated in a similar manner for comparison. The rate of endothelial cell proliferation was directly related to the concentrations of both WBS and CFPDS. Grwoth rate in WBS was marginally greater than that observed in CFPDS during early culture, however, similar confluent densities were achieved. The addition of platelet released factors to CFPDS did not further stimulate endothelial cell proliferation. In contrast smooth muscle cells were quiescent in CFPDS despite increasing serum concentrations, but proliferated actively in response to platelet released factors. Both human macrophage conditioned medium and fibroblast growth factor increased endothelial cell proliferation significantly when compared with CFPDS alone. It is concluded that endothelial cell proliferation in preconfluent cultures is dependent on plasma factors while human vascular smooth muscle cells also require cell derived mitogens such as platelet growth factor to proliferate. The release of a substance by human macrophages mitogenic for endothelial cells may be involved in endothelial cell proliferation in vivo.

Blood↗
PubMedDate not supplied

Anesthetic considerations in patients with chronic granulomatous disease.

Chronic granulomatous disease (CGD) is a rare, genetically transmitted disorder characterized by recurrent, life-threatening infections with catalase-positive micro-organisms and excessive inflammatory reactions that lead to granuloma formation. Long-term prophylactic antimicrobial agents and aggressive surgical management are the mainstays of therapy. The authors provided anesthetics for 17 patients with CGD undergoing 55 surgical procedures. These patients presented to surgery with multiple organ system involvement and were at significant risk for complications in the perioperative period. Granulomatous lesions of the gastrointestinal (GI) tract may predispose such patients to regurgitation and aspiration.

Adolescent↗
PubMedDate not supplied

Monitored anesthesia care for laparoscopies in oncology patients.

A retrospective chart review was conducted on 241 oncology patients who received monitored anesthesia care for laparoscopy. A review of perioperative analgesic and sedative requirements, and perioperative complications is included. The authors conclude that laparoscopy for diagnostic and staging purposes can be accomplished successfully with monitored anesthesia care.

Adolescent↗