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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.
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PMID:EEG and spectral analysis in acute hyperventilation. 241 22

Hypocapnia and induced hypotension have been claimed by some to cause cerebral hypoxia because of insufficient perfusion. Regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCMRglc) were measured simultaneously in the same animal subjected to hypocapnia or hypocapnia combined with induced arterial hypotension. The rCMRglc was measured with (3H) deoxyglucose and the rCBF with (14C) iodoantipyrine with the use of tissue biopsy methods and scintillation counting. Nineteen male Wistar rats were anesthetized with halothane and artificially ventilated. Anesthesia was maintained with nitrous oxide/oxygen (70:30) and succinylcholine. Six rats were maintained at normocapnia, six rats were ventilated to a PaCO2 of 20 mmHg, and seven animals were ventilated to PaCO2 20 mmHg combined with arterial hypotension of 50 mmHg (mean blood pressure) induced by infusion of adenosine. Although hypocapnia alone did not cause a statistically significant decrease of rCBF except in hippocampus, hypocapnia combined with hypotension resulted in a significant reduction of rCBF in four of seven regions when compared with hypocapnia alone; rCMRglc values were unchanged during hypocapnia. However, the addition of hypotension induced by adenosine led to a significant decline of glucose utilization in five of seven brain regions. In the present study the authors observed no increase of regional glucose utilization and hence no signs of cerebral ischemia during hypocapnia alone or combined with hypotension induced by adenosine.
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PMID:Regional cerebral blood flow and glucose utilization during hypocapnia and adenosine-induced hypotension in the rat. 249 11

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.
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PMID:Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity. 249 46

The effect of hypocapnia on regional cerebral glucose utilization (L-CMRg) was studied in 14 Sprague Dawley rats. After cannulation of femoral vessels, halothane was discontinued and anesthesia was maintained with 70% N2O in oxygen. The animals' lungs were mechanically ventilated to achieve normocapnia (PaCO2 = 40 +/- 2 mmHg) in group A or hypocapnia (PaCO2 = 25 +/- 2 mmHg) in group B. L-CMRg was measured by the 14C-2-deoxyglucose autoradiographic method. Twenty-six anatomically discrete structures representing cortical, subcortical, limbic, and brainstem areas were studied. In hypocapnic animals, mean values for L-CMRg were higher in 25 out of 26 structures studied. The increase in L-CMRg was heterogenous. The structures that had higher L-CMRg during normocapnia showed the greatest increase in L-CMRg. When the two groups were compared using a profile analysis, in six regions (lateral and ventral thalamus, inferior colliculus, lateral habenulla, medial geniculate body, and auditory cortex), a value of P less than 0.05 was obtained.
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PMID:Effect of hypocapnia on local cerebral glucose utilization in rats. 249 55

We evaluated the cognitive effects of hypoxemia independent of hypocapnia in 20 right-handed male subjects using a battery of brief neuropsychological tests. Results of a profile analysis indicated that performance during hypoxia was reliably different for Digit Symbol and Finger Tapping tests. Trend analysis demonstrated a significant linear pattern for Finger Tapping results, such that lower levels of oxygen were associated with slower rates of tapping. No significant trends were observed for Digit Symbol results. The observation of hypoxic effects on Digit Symbol and Finger Tapping tests is consistent with previous findings of neuropsychological changes secondary to hypoxia. The negative results observed for the remaining tests are inconsistent with past literature. It is likely that methodological differences contributed to these discrepancies, including previous reliance on inspired air to index hypoxemia rather than monitoring arterial oxygen saturation directly and failure to control for differences in CO2 levels during induced hypoxia. These variables should be controlled in future research.
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PMID:Isocapnic hypoxemia and neuropsychological functioning. 249 22

Magnetic resonance imaging was used to measure the effect of inhalation of 7% CO2 and hyperventilation with 60% O2 on human cranial cerebrospinal fluid volume. During CO2 inhalation there was a reduction in the cranial CSF volume ranging from 0.7-23.7 ml (mean 9.36 ml). The degree of reduction in cranial CSF volume was independent of the individual subject's increase in end-expiratory pCO2 or mean arterial blood pressure, in response to hypercapnia. During hyperventilation with high concentration oxygen the cranial CSF volume increased in all subjects (range 0.7-26.7 ml, mean 12.7 ml). The mean changes in cranial CSF volume, induced by hypercapnia and hypocapnia, were very similar to the expected reciprocal changes in cerebral blood volume.
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PMID:Changes in cranial CSF volume during hypercapnia and hypocapnia. 249 39

We studied the effects of prolonged (6 hours) hypocapnia and the abrupt termination thereof on cerebral blood flow and metabolism in six paralyzed, sedated (but not anesthetized) newborn lambs. Thirty minutes after institution of hyperventilation to an arterial carbon dioxide pressure of 15 +/- 2 torr, hyperventilation, cerebral blood flow had returned to baseline. Abrupt termination of hyperventilation after 6 hours resulted in a 110 +/- 71% increase in cerebral blood flow over baseline after 30 minutes of normocapnia. This cerebral hyperemia persisted for at least 90 minutes after hyperventilation was discontinued. Cerebral oxygen consumption did not change throughout the study. The posthypocapnia hyperemia noted in these animals after abrupt normalization of arterial carbon dioxide pressure may contribute to the increased risk of intracranial hemorrhage in newborn infants who are treated similarly in the management of pulmonary hypertension.
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PMID:Cerebral blood flow and metabolism during and after prolonged hypocapnia in newborn lambs. 250 13

To investigate the effects of carbon dioxide on the local blood flow during hemorrhagic shock, the tissue surface PO2 of liver, kidney and femoral muscle was measured during normocapnia, hypocapnia and hypercapnia. Eight adult mongrel dogs were anesthetized with pentobarbital, intubated and ventilated mechanically with 100% oxygen to maintain normocapnia. After laparotomy, miniature clark-type polarographic oxygen electrodes were placed on the surface of the liver, kidney and femoral muscle. The animals were hemorrhaged via arterial catheter to a mean arterial blood pressure of 50mmHg. The hypocapnia was produced by increasing respiratory rate and the hypercapnia was induced by adding the exogenous carbon dioxide. Hypocapnia decreased the liver and kidney surface PO2, and increased the muscle surface PO2. On the contrary, hypercapnia increased the liver and kidney surface PO2 and decreased the muscle surface PO2. So, it is possible that hypocapnia may compromise the oxygenation of the liver and kidney in the hemorrhagic shock.
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PMID:[The effects of hypocapnia and hypercapnia on tissue surface PO2 in hemorrhaged dogs]. 251 54

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

To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation.
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PMID:The cost to the central nervous system of climbing to extremely high altitude. 251 83


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