Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilating action of a new calmodulin antagonist, 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)- 1-piperazinyl]methyl) isoquinoline (Ro 22-4839), was examined in anesthetized animals. In anesthetized dogs, Ro 22-4839 when given intra-arterially dilated various vessels in the potency order of vertebral greater than internal carotid greater than femoral = coronary much greater than renal vessels. Ro 22-4839 (0.1-1.0 mg/kg i.v.) produced brief increases in the cerebral parietal cortex, vertebral and coronary arterial blood flows more markedly than in femoral, mesenteric and renal arterial blood flows. The compound given intraduodenally decreased the vertebral vascular resistance more extensively than the femoral one in a dose-dependent (3-30 mg/kg) way. The effect of intraduodenal administration was longer-lasting than brief action after intravenous administration, and tended to decrease heart rate. Ro 22-4839 did not significantly change cerebral oxygen consumption regardless of its increase in cerebral oxygen supply, suggesting that its cerebral vasodilating effect was due to its direct relaxing effect on the vascular smooth muscle. Papaverine and ifenprodil produced a shorter-lasting decrease in vertebral vascular resistance and caused significant tachycardia. In the video camera system monitoring the constrictory response of feline pial small vessels of the parietal cortex to hypocapnia, Ro 22-4839 was found to reverse vasoconstriction of both pial arteries and veins at the dose of 0.3 mg/kg i.v./min, which did not dilate these vessels under normocapnia. The compound uniformly reduced the pressor responses to various stimuli (electrical stimulation, norepinephrine and angiotensin II) in pithed rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral vasodilating and vasospasmolytic action of the cerebral circulation improver 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)-1- piperazinyl]methyl)isoquinoline in experimental animals. 360 93

With the use of isolated perfused rabbit lungs (n = 152), roles of endothelium-derived relaxing factor (EDRF) in pulmonary vascular responses to hypocapnia and hypercapnia were studied. Lungs were ventilated with a gas mixture containing 1, 5, or 10% CO2 and 21% O2, adjusting the perfusate pH to 7.8, 7.4, or 7.1, respectively. Methemoglobin (MetHb), hemoglobin (Hb), methylene blue (MB), and L-argininosuccinic acid (L-ASA) were used as modulators of EDRF. To eliminate augmented shear stress, we used papaverine during hypercapnia. As a measure of EDRF, we spectrophotometrically examined nitric oxide (NO) metabolites in the perfusate. Hypocapnia and hypercapnia evoked, respectively, unsustainable vasodilatation and vasoconstriction. Hb, MB, and L-ASA, but not MetHb, produced an increase in baseline pulmonary arterial pressure (Ppa). These agents also exacerbated vasoconstriction during hypercapnia. Hypercapnia and hypocapnia caused an increase and decrease, respectively, in EDRF production. L-ASA suppressed EDRF production in hypercapnic lungs. Papaverine did not suppress EDRF production under hypercapnia. In conclusion, 1) the effects of pH on pulmonary circulation are transient, 2) the increase in Ppa caused by hypercapnia is modulated by EDRF, and 3) the pulmonary EDRF genesis is activated by hypercapnic acidosis but suppressed by hypocapnic alkalosis.
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PMID:Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs. 876 59