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)

We investigated cerebral blood flow and metabolism, and cerebral vascular response in 9 patients with cerebrovascular Moyamoya disease or unilateral Moyamoya phenomenon using positron emission tomography (PET). The subjects consisted of 5 men and 4 women, and were from 9 to 60 years old. Five patients had bilateral occlusion in the carotid fork with Moyamoya vessels (fulfilled the criteria of cerebrovascular Moyamoya disease), and four patients had unilateral Moyamoya phenomenon. The PET scanner used was the HEADTOME III, of which spatial resolution in clinical use was 10 mm full width at half-maximum (FWHM) in the image plane. Cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), cerebral oxygen extraction fraction (OEF), and cerebral blood volume (CBV) were measured in resting state by the 15O-labelled gases steady state method in every patient and 22 normal controls (17 men and 5 women, and from 26 to 64 years old). Consecutively cerebral vascular responses were measured by H215O autoradiographic method in resting state, hypercapnia, hypocapnia, and hypertension. Forced hypercapnia, hypocapnia, and hypertension were achieved by 7% CO2 inhalation, hyperventilation, and venous infusion of angiotensin II, respectively. CMRO2 of the whole brain was significantly lower in patients than in normal controls (p less than 0.05), and CBV of the lentiform nucleus significantly increased in patients (p less than 0.01). This reflected Moyamoya vessels in the basal ganglionic regions. In 3 of 5 patients with bilateral Moyamoya vessels, CBF and CMRO2 in the symptomatic cerebral hemisphere were lower than that in the nonsymptomatic hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vascular responses in cerebrovascular "Moyamoya" disease--evaluated by positron emission tomography]. 251 9

Several authors have observed that nitrous oxide increases cerebral blood flow (CBF) and/or intracranial pressure (ICP) in experimental situations and in humans. However, the effects of hypocapnia on the cerebrovascular responses to N2O have not been investigated. Therefore, six New Zealand White rabbits were anesthetized with approximately equal to 1.0 MAC halothane (mean end-tidal concentration 1.26%) and surgically prepared for recording of ICP, the EEG, and both cortical and global CBF (by the H2-clearance method). After preparation was complete, measurements were obtained during ventilation with 70% nitrogen (in O2), and after the inspired gas mixture was changed to 70% N2O (still with 1.0 MAC halothane). Two such data pairs (N2-N2O) were obtained, one during hypocarbia (PaCO2 approximately equal to 20 mm Hg) and the other during normocarbic (PaCO2 approximately equal to 40 mm Hg) conditions. Mean arterial pressure (MABP) was held constant within each data pair by infusing angiotensin II as needed. Nitrous oxide resulted in a consistent increase in EEG frequency and decrease in amplitude as compared with N2, and produced small (approximately equal to 1 mm Hg) but statistically significant increases in ICP during both hypo- and normocarbic conditions. Nitrous oxide administration also increased CBF as measured both in frontal cortex and globally, with similar changes seen during hypo- and normocarbic conditions, e.g., cortical CBF increased from 42 +/- 8 to 59 +/- 15 ml.100 gm-1.min-1 during hypocarbia, and from 61 +/- 13 to 75 +/- 15 ml.100 gm-1.min-1 during normocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of PaCO2 on the cerebrovascular response to nitrous oxide in the halothane-anesthetized rabbit. 311 86

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

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
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PMID:A study of profound hypothermia by surface cooling. 677 40

1 Because they affect isolated cerebral arteries, some calcium antagonists have been studied on the intact cerebral circulation of the rat.2 Global cerebral blood flow ((133)Xe clearance technique) was measured in anaesthetized rats. Neither perhexiline (0.1 mug/kg to 1.0 mg/kg, i.v.) nor diltiazem (0.06-0.6 mg/kg, i.v.) had any significant effect on resting cerebral blood flow when measured 5 min after each dose. A high dose of nifedipine (1.0 mg/kg, i.v.) was administered during induced hypocapnia. Nifedipine failed to modify the hypocapnic vasoconstriction of the cerebral vasculature when compared to vehicle-treated rats.3 The possibility of discrete changes in regional cerebral blood flow was investigated. Local cerebral blood flow was measured in a number of brain regions by the [(14)C]-ethanol technique 15 min after the administration of nifedipine (20 or 100 mug/kg, i.v.). Nifedipine had no apparent effect on regional blood flow in the rat brain.4 Acute arterial hypertension increases protein leakage into the brain, a phenomenon susceptible to drugs that act on endothelial pinocytosis which is known to be calcium-dependent. The increase in protein extravasation, induced by the intravenous administration of either angiotensin II or adrenaline, was unchanged in rats previously treated with either nimodipine (20 mug/kg, i.v.) or nifedipine (50 mug/kg, i.v.) when dissolved in ethanol alone. However, nifedipine (20 mug/kg, i.v.) when dissolved in a solution of polyethylene glycol and ethanol further enhanced the hypertension-induced increase in brain albumin permeability.5 In conclusion, we have been unable to demonstrate any apparent effects of various calcium antagonists on the intact cerebral circulation of the rat, despite the number of different experimental models used.
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PMID:Calcium antagonists: effects on cerebral blood flow and blood-brain barrier permeability in the rat. 687 38