Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anoxia and KC1 have been used to inactivate peripheral nerves by depolarization conduction block. Investigation of the inactivation patterns in isolated sciatic nerves of healthy and alloxan-diabetic rats suggests that the paranodal gap substance of healthy nerve behaves as an effective periaxonal diffusion barrier. In diabetic nerve the permeability of this barrier is significantly increased. A marked reduction in the K' binding capacity of the nodal gap substance has been demonstrated in myelinated nerves of human diabetics and alloxan diabetic rats.
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PMID:Nodal gap substance in diabetic nerve. 427 85

Anoxia (during 2 minutes after decapitation) produced a significant elevation of cAMP contents (up to 410%) in mouse brain cells. This effect was abolished by an intraperitoneal injection of alloxan (A), morphine (M), and ethanol (E) 30 minutes before decapitation, and after a 2 minutes diethyl ether (DE) inhalation. It was found that anoxia produced some decrease in phosphodiesterase (FDE) activity. A preliminary injection of A and E produced an activation of FDE; M and DE did not change FDE significantly. Mechanisms of action of all the four agents on the cAMP content under anoxia are different. A and E produced a rapid cAMP hydrolysis on stimulating the activity of FDE, M and DE inhibited apparently adenylate cyclase. The activation of adenylate cyclase due to anoxia is considered as one of the initial steps in the cell injury extention.
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PMID:[Increase in the cAMP content of mouse brain cells in ischemia and inhibition of this effect by certain biologically active compounds]. 626 87

An isolated perfused working rat heart preparation was used to assess the effect of alloxan-induced diabetes on myocardial performance. Ventricular performance was assessed under different aortic afterload, isoproterenol-stimulated and anoxic conditions. Basal left ventricular pressure development and rate of rise of ventricular pressure were depressed in hearts from diabetic animals. Neither coronary flow nor cardiac output were affected by diabetes. The dose and temporal responses to an infusion of isoproterenol were unaltered in diabetic hearts. Isoproterenol increased coronary flow by 50% and elevated ventricular pressure, dP/dt, and cardiac output by two- to threefold. Anoxia depressed ventricular pressure to below 20% of control within 5 min in both diabetic and normal hearts. Reoxygenation after 10 min of anoxia produced equivalent recovery in both groups working against a 52-mmHg aortic afterload, whereas recovery after 20 or 30 min of anoxia, was depressed in diabetic hearts. Elevating aortic afterload decreased performance of diabetic hearts and decreased their ability to recover from a 10-min anoxic exposure. Many of these observed differences in mechanical performance of diabetic hearts can be overcome by high glucose or insulin in the perfusion media.
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PMID:Performance of diabetic rat hearts: effects of anoxia and increased work. 700 27