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)

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO2 concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO2 concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO2 concentration caused bronchial relaxation, while decreasing the CO2 concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonist relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.
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PMID:Halothane alters the response of isolated airway smooth muscle to carbon dioxide. 156 97

Awake, adult male rats (some with chronically indwelling femoral artery catheters) were exposed for up to 7 days to one of three environments: a) normoxia (PIO2 = 155 Torr), b) hypoxic hypocapnia (PIO2 = 90 Torr), and c) hypoxic normocapnia (PIO2 = 73 Torr, PICO2 = 32 Torr), and arterial blood gas and acid-base status were documented. After 1 hour to 7 days, rats were sacrificed, and the time courses of the brain levels and turnovers of norepinephrine (NE), dopamine (DA) and serotonin (5-hydroxytryptamine or 5HT) were determined in each condition. The transient decrease in monoamine levels seen on exposure to acute hypoxia was absent if normocapnia was maintained; 7 days hypoxia with or without hypocapnia resulted in increased monoamine levels. Normocapnia also prevented an immediate, sustained decrease in 5HT turnover and a delayed decrease in DA turnover which were observed in hypoxic hypocapnia. A delayed increase in 5HT turnover appeared to be due to hypoxia independent of PaCO2. Therefore, the initial, transient loss of mental acuity and some ventilatory adaptations observed during prolonged hypoxia may be a result of the decrease in PaCO2 rather than the decreased oxygen concentration.
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PMID:Separate effects of low carbon dioxide and low oxygen content on rat brain monoamine metabolism during hypoxemia. 312 46

The aim of this study was to examine the influence of ketanserin, a 5-hydroxytryptamine antagonist antihypertensive agent, on the relationship between cerebral blood flow (CBF) and middle cerebral artery flow velocity (Vmean MCA) and to compare Doppler-sonographic indices of downstream resistance (pulsatility index, PI; resistance index, RI) with calculations of cerebrovascular resistance (CVR) in 17 male patients under fentanyl/midazolam anesthesia. CBF was measured with the Kety-Schmidt technique using argon as a tracer. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and jugular bulb pressure. Measurements of Vmean MCA and determinations of PI and RI were performed by use of a 2-MHz transcranial Doppler ultrasound device. All variables were measured at normo- and moderate hypocapnia before and after intravenous (i.v.) bolus administration of 0.3 mg/kg ketanserin followed by an infusion of 0.06 mg.kg-1.h-1. Ketanserin changed neither average CBF nor Vmean MCA. The CO2 reactivity of Vmean MCA was significantly lower than the CO2 reactivity of CBF (P < 0.01); however, ketanserin did not change the relationship between CBF and Vmean MCA. During hypocapnia, CVR as well as PI and RI significantly increased (P < or = 0.01), indicating consistent directional changes in arteriolar resistance and flow velocity pulsatility. In contrast, after i.v. administration of ketanserin, CVR decreased (P < 0.05), whereas both Doppler-derived indices increased (P < 0.01). These results suggest that ketanserin in a clinically relevant dose does not alter the validity of serial Vmean MCA measurements as an index of global CBF and that ketanserin does not change the diameter of middle cerebral arteries (MCAs). Doppler-derived indices of pulsatility and resistance, which are supposed to estimate changes in downstream resistance, reflect changes, after administration of ketanserin, in systemic hemodynamics rather than changes in CVR.
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PMID:Effect of ketanserin on global cerebral blood flow and middle cerebral artery flow velocity. 780 2

Alkalizing perivascular fluid constricts, whereas acidification dilates, cerebral arterioles. It is not known whether vascular smooth muscle cells (VSMCs), endothelium, or neuronal elements sense pH changes. We hypothesized that VSMCs themselves transduce extracellular pH (pHo) changes. We examined the motor responses of cultured adult rat middle cerebral arterial VSMCs during pHo and intracellular pH (pHi) changes. Motor responses were inferred from the deformation pattern of a silicone substratum, dimethylpolysiloxane, which wrinkles as cells contract. pHi was measured with 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Cultured VSMCs retained motor responses to vasoconstrictors (5-hydroxytryptamine and K+), and to sodium nitroprusside, which were typical of intact arterioles. VSMCs contracted with increasing and relaxed with decreasing pHo. Hypocapnia contracted VSMCs when the pHo increased, and hypercapnia relaxed VSMCs when the pHo decreased. However, at a constant pHo, changes in PCO2 caused opposite responses despite equivalent changes in pHi. Thus VSMCs contract with increased pHo and relax with decreased pHo just as intact arterioles do. These responses do not reflect changes in pHi or PCO2. pHi changes paradoxically alter VSMC tone in the direction opposite that caused by pHo changes.
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PMID:Motor responses of cultured rat cerebral vascular smooth muscle cells to intra- and extracellular pH changes. 924 19