Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases are reported in which respiratory arrest occured coincident with the intravenous administration of large doses of trimethaphan camsylate (Arfonad) to control hypertension. The mechanism of the respiratory depression is unknown, but it may have been related to a direct effect of trimethaphan on the respiratory center or to a curare-like effect of the drug. Close monitoring of ventilatory capacity should be maintained in all patients treated with trimethaphan.
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PMID:Respiratory paralysis during treatment of hypertension with trimethaphan camsylate. 93 75

Acute hypotension was produced in rats by using two experimental techniques: intravenous infusion of a ganglion-blocking agent (Arfonad), and venesection of a femoral vein. Horseradish peroxidase (HRP) was injected intravenously after each procedure, and subsequently observed in the inner ear by light and electron microscopy. In both experimental models, a large amount of tracer spread into the intercellular spaces, but it was halted by tight junctions bordering the stria vascularis. The endothelium exhibited a high distribution density of labelled vesicles, which suggested increased vesicular transport. There was no extravasation of HRP from capillaries in the spiral ligament in spite of the presence of some labelled pinocytotic vesicles. The present study was concerned with the discovery of enhanced capillary permeability of the stria vascularis under acute hypotension, as in the case of acute hypertension (Sakagami et al., 1984).
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PMID:Increased capillary permeability of the stria vascularis to HRP, induced by experimental acute hypotension in rats. 646 26

The effects of acute hyper- and hypotension on the stria vascularis and spiral ligament of the rat were studied electron microscopically with the horseradish peroxidase (HRP) tracer method. Acute hypertension was induced by i.v. infusion of methoxamine chloride (Mexan), and acute hypotension by i.v. infusion of a ganglion-blocker (Arfonad) and by venesection. In both acute hyper- and hypotensive experiments, a large amount of leaked HRP spread into the intercellular spaces until it was stopped by tight junctions bordering the stria vascularis. The stria capillary endothelium displayed a dense distribution of labelled vesicles, which suggests increased vesicular transport. There was no extravasation of HRP from capillaries in the spiral ligament, despite the presence of some labelled pinocytotic vesicles. The present paper deals with the discovery of enhanced capillary permeability of the stria vascularis under acute hyper- and hypotension, and makes comparison between acute hyper- and hypotension in order to define the function of the stria vascularis.
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PMID:Ultrastructural study of the effect of acute hyper- and hypotension on the stria vascularis and spiral ligament. 659 6

The authors sought to develop a model for assessing in vivo regulation of cerebral vasoregulation by nitric oxide (NO), originally described as endothelial-derived relaxing factor, and to use this model to establish the role of NO in the regulation of cerebral blood flow (CBF) in primates. By using regional intraarterial perfusion, the function of NO in cerebral vasoregulation was examined without producing confounding systemic physiological effects. Issues examined were: whether resting vasomotor tone requires NO; whether NO mediates vasodilation during chemoregulation and autoregulation of CBF; and whether there is a relationship between the degree of hypercapnia and hypotension and NO production. Twelve anesthetized (0.5% isoflurane) cynomolgus monkeys were monitored continuously for cortical CBF, PaCO2, and mean arterial pressure (MAP), which were systematically altered to provide control and experimental curves of chemoregulation (CBF vs. PaCO2) and autoregulation (CBF vs. MAP) during continuous intracarotid infusion of 1) saline and 2) an NO synthase inhibitor (NOSI), either L-n-monomethyl arginine or nitro L-arginine. During basal conditions (PaCO2 of 38-42 mm Hg) NOSI infusion of internal carotid artery (ICA) reduced cortical CBF from 62 (saline) to 53 ml/100 g/per minute (p<0.01), although there was no effect on MAP. Increased CBF in response to hypercapnia was completely blocked by ICA NOSI. The difference in regional (r)CBF between ICA saline and NOSI infusion increased linearly with PaCO2 when PaCO2 was greater than 40 mm Hg, indicating a graded relationship of NO production, increasing PaCO2, and increasing CBF. Diminution of CBF with NOSI infusion was reversed by simultaneous ICA infusion of L-arginine, indicating a direct role of NO synthesis in the chemoregulation of CBF. Hypotension and hypertension were induced with trimethaphan camsylate (Arfonad) and phenylephrine at constant PaCO2 (40 +/- 1 mm Hg). Autoregulation in response to changes in MAP from 50 to 140 mm Hg was unaffected by ICA infusion of NOSI. In primates, cerebral vascular tone is modulated in vivo by NO; continuous release of NO is necessary to maintain homeostatic cerebral vasodilation; vasodilation during chemoregulation of CBF is mediated directly by NO production; autoregulatory vasodilation with hypertension is not mediated by NO; and increasing PaCO2 induces increased NO production.
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PMID:Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates. 861 39