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 (95% N2 + 5% CO2) potentiated the contractile response to KCl 20 mmol/L, histamine (His) 5 mumol/L and acetylcholine (ACh) 0.5 mumol/L in isolated porcine coronary arterial rings. Calcium antagonists m-nisoldipine (m-Nis) and nisoldipine (Nis) 0.4-250 nmol/L produced a concentration-dependent decrease in both KCl, His and anoxia-potentiated KCl2 His or ACh-induced contractions. Chlorpheniramine 10 mumol/L but not cimetidine 10 mumol/L and atropine 10 mumol/L abolished contractions induced by His and ACh respectively. All 3 agents did not affect KCl response and the anoxia facilitation. Indomethacin 10 mumol/L markedly attenuated the further increase in tension by anoxia but failed to inhibit the response by these vasoconstrictors.
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PMID:Effects of m-nisoldipine on anoxia-potentiated histamine and acetylcholine-induced contractions of the porcine isolated coronary artery. 213 Jun 15

Experiments were designed to determine the role of the endothelium in the responsiveness of the arterial wall to anoxia. Paired rings of canine femoral arteries were mounted for isometric tension recording in organ chambers filled with aerated Krebs-Ringer bicarbonate solution (37 degrees C). One ring served as control; in the other the intimal layer was removed mechanically. Anoxia was induced by gassing the organ chamber with 95% N2/5% CO2. In control rings anoxia augmented contractile responses to noradrenaline, KCl and BaCl2. On return to O2 the contractile responses were transiently depressed. Removal of the endothelium reduced the anoxic augmentation, but did not affect the post-anoxic inhibition. Indomethacin did not affect the response to anoxia. Anoxia abolished the endothelium-dependent inhibitory effect of acetylcholine and thrombin, reduced that of adenosine triphosphate, but augmented that of arachidonic acid. These experiments indicate that endothelial cells may contribute to anoxic facilitation of the responsiveness of the canine arterial wall.
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PMID:Anoxia and endothelium-dependent reactivity of the canine femoral artery. 687 96

Bovine coronary arterial strips (BCA) exhibiting spontaneous tone, relax in response to a decrease in the pO2 of the bathing medium. Experiments were performed to determine if prostaglandins (PGs) mediate the oxygen-induced changes in tension. BCA were equilibrated in Krebs-bicarbonate solution at 37 degrees C gassed with 95% O2, 5% CO2 and tension was measured isometrically. When the pO2 of the bathing medium was decreased, BCA exhibited reversible reductions in tension. Switching from 95% O2, 5% CO2 to 95% N2, 5% CO2 (anoxia) elicited an initial relaxation followed by a contraction. In contrast, a change to 5% O2, 5% CO2, 90% N2 (hypoxia) was followed by a sustained relaxation. Re-introduction of O2 to anoxic strips produced a biphasic response: relaxation followed by contraction. Indomethacin or eicosatetraynoic acid (EYA) increased tone and inhibited the relaxation produced by anoxia or hypoxia. Indomethacin or EYA did not inhibit the relaxation of anoxic strips during re-introduction of O2, but did inhibit the contraction partially. Relaxation of arterial strips to arachidonic acid (AA) was similar to relaxation to prostacyclin (PGI2). Anoxia limited the relaxation to AA but not to PGI2. We conclude that PG synthesis contributes to the basal tone and the hypoxia-induced relaxation of BCA. In addition, hypoxia, unless severe, does not prevent the conversion of AA to PGI2.
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PMID:Prostacyclin (PGI2) mediates hypoxic relaxation of bovine coronary arterial strips. 701 74