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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been postulated that a coronary vasoconstriction during hypocapnia might be opposed by a compensating coronary vasodilatation due to impaired myocardial oxygen supply. The present study was performed first to examine whether a maximal decline in coronary sinus (CS) oxygen content was reached during hypocapnia. During hypercapnia a myocardial "over perfusion" has been demonstrated. The second purpose of the present study was to examine whether a myocardial "over perfusion" is essential to maintain a sufficient myocardial tissue oxygen supply during hypercapnia. Closed-chest dogs were anesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Nitrogen gas and carbon dioxide could both be added to the inspiratory gas to create arterial hypoxemia (arterial SO2 65%) and hypercapnia, respectively. Arterial hypoxemia during hypocapnia increased myocardial blood flow (MBF) by 50%, while CS SO2 decreased significantly. The decrease in CS SO2 demonstrates a reserve capacity of myocardial oxygen extraction during hypocapnia, thereby ruling out any major coronary vasoconstriction during hypocapnia. Hypercapnia during normoxemia increased MBF, myocardial oxygen delivery, and CS SO2 substantially, but this was not observed when hypercapnia was created during arterial hypoxemia. From the present results we conclude that hypocapnia does not cause any major coronary vasoconstriction, while hypercapnia results in a myocardial "over perfusion," which is a luxury perfusion not essential to maintain sufficient myocardial oxygen supply during hypercapnia.
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PMID:Myocardial oxygen supply during hypocapnia and hypercapnia in the dog. 309 94

Ammonia intoxication, which results in astrocytic edema and glutamine accumulation, blocks cerebral vasodilation during hypercapnia but not during hypoxia. Ammonia's effect on blood flow during hypocapnia is unclear, with some brain regions showing a paradoxical increase in flow. Here, we studied the responses to hypocapnia of pial arterioles not surrounded by astrocytic end feet to avoid mechanical compression by local edema. Blood flow was measured by microspheres in pentobarbital sodium-anesthetized rats equipped with closed cranial windows that permitted intravital microscopy. The normal pial arterial constriction in hypocapnia (12 +/- 1%; mean +/- SE) was blocked (2 +/- 1%) during a 6-h intravenous infusion of ammonium acetate, with some regions (cerebrum, midbrain) showing increased flow during hypocapnia. After pretreatment with methionine sulfoximine (MSO), which inhibits glutamine synthesis, the normal hypocapnic constrictor response was retained in pial arterioles (11 +/- 2%) during hyperammonemia. The increase in the calculated cerebrovascular resistance also was retained. An analog of MSO that does not block glutamine synthesis (buthionine sulfoximine) was ineffective in maintaining hypocapnic reactivity. In a sodium acetate-treated control group, MSO did not alter the pial arteriolar response. Normal vasoconstrictive ability was shown during ammonium infusion in response to U-46619, a thromboxane analog. We conclude that the inhibition of hypocapnic responsivity induced by ammonium is not due to paralysis of the pial arteriolar smooth muscle or to vascular compression by swollen astrocytes but is in some way due to glutamine metabolically produced from the ammonium.
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PMID:Preserved hypocapnic pial arteriolar constriction during hyperammonemia by glutamine synthetase inhibition. 995 Aug 45

We investigated ventillatory responses to a plasma alkaloids and hypocapnia,a nd the basis for the ventilatory response to sodium bicarbonate (NaHCO3) infusion in rainbow trout. Plasma alkalosis and hypocapnia created by infusion of sodium hydroxide (NaOH) did not cause hypoventilation, whereas infusion of hydrochloric acid (HCl) caused vigorous hyperventilation, associated with an acidosis, a reduction in blood O2 content (CaO 2) and a release of circulating catecholamines. Infusion of NaHCO3 stimulated ventilation and caused an increase in plasma pH, total carbon dioxide content (CaCO 2) and catecholamine levels, and a reduction in oxygen tension (PaO 2). Infusion of ammonium bicarbonate (NH 4HCO3) caused hyperventilation and was associated with an increase in CaCO 2 and plasma total ammonia (Camm) and ammonia gas (NH3) concentration. Infusion of sodium chloride (NaClI) and Cortland's saline had no effect on ventilation. The results indicate that trout do not exhibit the ventilatory sensitivity to pH seen in terrestrial vertebrates. Ventilatory responses to NaHCO3 appear to have been a result of reductions in PaO 2, a release of catecholamines and an increase in CaCO 2 whereas responses to NH4HCO3 appear to have been a result of increases in CaCO 2 and Camm.
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PMID:Effects of changes in plasma pH, CO2 and ammonia on ventilation in trout. 2421 51