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Biomedical subjects

J A Colwell

Publications and source records attributed to J A Colwell.

At least 109 records · Page 6Linked to original sources
PubMed1976

Use of oral agents in treating diabetes mellitus a perspective.

A comprehensive study by the University Group Diabetes Program compared the effects of therapy with oral antidiabetic agents, insulin, and placebo in patients with adult-onset diabetes mellitus. Results showed an increased number of deaths, particularly due to cardiovascular diseases, among patients receiving oral agents. In spite of these findings, therapeutic recommendations have changed only slightly. An FDA proposal recommends moderate labeling changes. When possible, control of diabetes with diet alone should be attempted. If this is unsuccessful, an oral sulfonylurea should be added to the regimen. If glucose and lipid levels remain high after six months of such therapy, insulin should be used.

Administration, Oral↗
PubMed1976

Glucose and insulin responses in sheep subjected to a second episode of hemorrhagic shock.

These studies indicated that the responses of the sheep beta cell parallel mnay of those seen in man. Regulation by pH, potassium, and epinephrine and suggested, as is the existence of a two-pool system for insulin synthesis and release which is responsive to glucose. Differences in glucose and insulin responses following a second episode of shock are noted. It is shown that the addition of hypertonic glucose to a resuscitation regimen is associated with a response to a second episode of shock that is more nearly like that to a first episode of shock.

Animals↗
PubMed1976

Altered platelet function in diabetes mellitus.

An increased sensitivity of platelets to aggregation from ADP and epinephrine is described in diabetics with or without vascular disease. This sensitivity correlates with elevated levels on von Willebrand factor (vWF), which, in turn appears to be influenced by growth hormone. VWF activity correlates with previously described "plasma factor" activity. Platelets from diabetic subjects are more sensitive than platelets from normal subjects to arachidonic acid-induced aggregation. This sensitivity is abolished by aspirin, which is a prostaglandin synthetase (cyclo-oxygenase) inhibitor. Platelets from diabetc subjects synthesize increased amounts of PGE2-like material (iPGE) in response to ADP, epinephrine, collagen, and arachidonic acid. The latter finding suggests that a fundamental mechanism for increased platelet aggregation in diabetes is increased prostaglandin synthetase activity. Therapeutic endeavors that would lower growth hormone levels, vWF activity, and/or prostaglandin synthetase activity may be of benefit in the prophylaxis of diabetic vascular disease. Prospective studies are needed to explore these hypothesis, as are more studies on the precise mechanisms and platelet aggregation in diabetes mellitus.

Adenosine Diphosphate↗
PubMed1975

Inhibition of labile aggregation-stimulating substance (LASS) and platelet aggregation in diabetes mellitus.

Irreversible second-phase aggregation of platelets in diabetic patients is prevented in vitro by 5, 8, 11, 14-eicosatetraynoic acid (TYA), a competitive inhibitor of the labile aggregation-stimulating substance (LASS) which is formed from arachidonic acid. Thus, inhibition of prostaglandin synthesis inhibits platelet aggregation in diabetic subjects. These findings indicate that platelets from diabetics are subject to control by intracellular mechanisms operative in the regulation of platelet function in normal individuals.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1975

Increased platelet aggregation in early diabetus mellitus.

In view of the tendency toward vascular disease in diabetes mellitus, we studied platelet aggregation in 15 normal, 7 prediabetic, 12 latent, and 20 frankly diabetic subjects. Platelets from latent and frank diabetics showed increased platelet aggregation 4 minutes after adding adenosine 5'-diphosphate (60% verus 29% at 1.0 mu-M), epinephrine (46% versus 14% at 0.25 mu-M), and collagen (72% versus 17% at 0.25 mu-g/ml). Three prediabetics had increased platelet aggregation. Platelet sensitivity to aggregating agents was most marked in frank diabetics, intermediate in latent diabetics, and least in prediabetics. Second-phase platelet aggregation was reversed with acetylsalicylic acid, intravenous tolbutamide, and oral glucose administration. We conclude that platelet aggregation may be increased early in diabetes mellitus and may be involved in the genesis of diabetic microangiopathy. Prospective studies on the effect of therapeutic agents such as acetylsalicylic acid on the natural course of diabetic vascular disease are indicated.

Adenosine Diphosphate↗