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)

The brains of nine cats were subjected to bitemporal electric convulsive treatment. The current (AC, 220 V, 50 Hz, ca. 500 mA, 500 ms) was applied two to five times. Pial vessels were observed through a skull window. Immediately after current application, some pial arteries exhibited segmental spastic constriction which usually did not disappear until the animals were killed. Before sacrificing the animals, 20 min after convulsive treatment they were perfused with a carbon suspension. In some cortical areas blackening was impaired indicating that perfusion was not complete. Electron-microscopic investigation revealed that spasm also occurred in arterioles of the brain parenchyma. Many arterial vessels, some of them possessing only one muscular cell sheat, had collapsed so that the lumen was merely a small cleft. The spasms were irregularly distributed and confined to small segments of the vessel. Small arteriolar vessels were more affected than large pial arteries. Arterial spasms continued for 20 min. In a total of 39 control animals spastic constriction was observed only once; this animal had been subjected to prolonged hypocapnia.
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PMID:Spastic constriction of cerebral vessels after electric convulsive treatment. 93 91

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.
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PMID:Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. 332 39

A 42 year old woman with long standing Raynaud's disease, unresponsive to medical and surgical treatment, was noted to have a typical history of the hyperventilation syndrome. Rewarming of the hands following cold challenge was markedly prolonged in the presence of hypocapnia. It is suggested that hyperventilation may have an aetiological role in maintaining digital artery spasm in Raynaud's disease, which would benefit from recognition and treatment.
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PMID:Hyperventilation and Raynaud's disease. 367 Dec 72

The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.
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PMID:Cerebrovascular reactivity in patients with ruptured intracranial aneurysms. 391 94

Examination of 28 agitated, hyperventilating patients with fetal tachycardia showed that the mothers were in a hyperventilation-related state of hypocapnia and alkalosis. The mean maternal pCO2 was 17.48 +/- 6.79 mm Hg, the pH 7.54 +/- 0.14, which caused a reflex spasm of the umbilical veins, fetal acidosis and fetal tachycardia. Additional experiments on sheep revealed a similar correlation between maternal hyperventilation, hypocapnia, respiratory alkalosis and fetal tachycardia while the flow volume of the uterus showed no change.
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PMID:Maternal hyperventilation as a possible cause of fetal tachycardia sub partu. A clinical and experimental study. 642 85

The impedance of a hemodynamic system is defined as the ratio of each harmonic component of blood pressure to that of flow. Calculation of impedance cures has been extensively performed in the systemic circulation, leading to the recognition of reflected pressure and flow waves and clarifying the shape of ultrasound waveforms. Impedance in the human cerebral circulation has not been measured primarily because of the relative inaccessibility of simultaneous flow and pressure data in the human cerebral circulation. We defined an impedance index using the transcranial Doppler waveform for that of flow and a noninvasive applanation measure of the carotid artery pressure waveform. Middle cerebral artery velocities and carotid artery pressure waveforms were simultaneously recorded in 16 vessels from 10 normal volunteers, 42 vessels in 14 patients with aneurysmal subarachnoid hemorrhage, and 14 vessels in 7 subjects during conditions of hypocapnia, normocapnia and hypercapnia. Impedance was calculated by dividing the harmonic associated with pressure divided by that of flow, and averaging 10 to 20 such calculations. Relative impedance curves were calculated by dividing by the impedance at the first harmonic. Impedance was also studied in an electrical model consisting of a Windkessel element containing inductance in series with a second Windkessel to model the large vessel and vascular bed, respectively. Model parameters were taken from the literature for these calculations. For the normal subjects, the shape of the impedance index curve was similar to those found in the systemic circulation. The impedance index curves for patients in vasospasm (middle cerebral velocity was greater than 180) showed a peak at the second or third harmonic, which appeared more frequently than the nonspasm group (p < 0.01). Furthermore, the ratio of the second harmonic to the first harmonic was significantly > 1.0 in the spasm group but significantly < 1.0 in the normal group (p < 0.05). Calculations from the electrical model replicated the appearance of these peaks at the second or third harmonic for vasospasm parameters. A statistically significant peak appeared at the second or third harmonic in the impedance index curves for patients in vasospasm, which was replicated quantitatively by our electrical model. Although such peaks can be explained in the systemic circulation by the presence of reflected waves, the distance to the reflection site is larger than expected for the cerebral circulation. This suggests the importance of the inertia of blood as a stenosis worsens and as the origin for the observed changes in the impedance index curves.
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PMID:An impedance index in normal subjects and in subarachnoid hemorrhage. 1105 55

We present a woman with heterozygous carnitine palmitoyl transferase 2 (CPT-2) deficiency who in the last 6 months suffered from episodic dyspnea and choking. Symptoms could not be attributed to her muscular energy defect, since heterozygous CPT-2 deficiency is usually asymptomatic or causes only mild muscle fatigability. Myopathy is usually triggered by concurrent factors, either genetic (additional muscle enzymes defects) or acquired (metabolic stress). The patient was referred to our respiratory clinic for suspect bronchial asthma. Spirometry showed mild decrease in inspiratory flows. Methacholine challenge was negative. Dyspnea was triggered by hyperventilation-induced hypocapnia, which produced marked decrease in airflow rates, particularly in inspiratory flows, consistent with laryngospasm. Nutritional assessment of the patient showed low serum level of calcium and vitamin D, attributable to avoidance of milk and dairy products for lactose intolerance and to insufficient sunlight exposure. After calcium and vitamin D supplementation episodic laryngospasm disappeared and hypocapnic hyperventilation test induced very mild change in airflow rates. Calcium and vitamin D deficiency may favour laryngeal spasm mimicking asthma, particularly in subjects with underlying myopathy.
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PMID:Laryngeal spasm mimicking asthma and vitamin d deficiency. 2484 4