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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman with chronic respiratory failure (status after tuberculosis) was given an infusion of doxapram hydrochloride (1 to 2 mg/kg of body weight per hour) for four episodes of acute exacerbation of her condition. Treatment with the drug prevented worsening of hypercapnia in the four episodes, when administration of 24 percent oxygen had occasioned rises in the arterial carbon dioxide tension of 23, 10, 9, and 7 mm Hg.
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PMID:Doxapram hydrochloride in the treatment of acute exacerbation of chronic respiratory failure. A patient with four episodes treated without use of a respirator. 2 44

Thirty monkeys were exposed to controlled systemic hypotension of different magnitudes and duration to determine factors leading to brain injury or cardiovascular failure. Fourteen monkeys developed brain injury. Of these, 6 survived indifinitely and 8 were sacrificed or died within 12-62 hours due to neurologic deterioration accompanied by respiratory failure. Sixteen animals did not develop brain injury, but 9 of these died within 24 hours from documented cardiovascular failure with the remaining 7 survived indefinitely. A highly reproducible threshold for the development of brain injury was found at a mean arterial blood pressure (MABP) of 25 mm Hg. Maintenance MABP was less than or equal to 25 mm Hg in 13 of 14 lesioned monkeys and greater than 25 mm Hg in 15 of 16 non-lesioned monkeys. Maintenance MABP averaged 20.1 +/- 1.1 mm /g in lesioned and 32.1 +/- 1.7 mm Hg in non-lesioned animals (p less than 0.001). Among the non-lesioned animals, death from delayed cardiovascular failure ensued when MABP was maintained between 27 and 35 mm Hg for 90 min or longer. Animals exposed to this range of hypotension for less than 90 min or to MABP exceeding 35 mm Hg for as long as 3 h survived intact. EEG changes occurring during hypotension most accurately predicted neurologic outcome. The threshold MABP required to produce cerebral electric silence was 21-22 mm Hg. Monkeys developing marked brain injury had greater than 25 minutes of EEG flattening, while slightly injured animals had it for 5-15 minutes and those without injury for less than 5 min. Changes in acid-base state, common carotid artery blood flow, and cerebral uptake of glucose and oxygen during hypotension also correlated with neurologic and cardiovascular outcome. Hypoxemia and hypercarbia were not contributory factors in the production of brain injury in this study.
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PMID:Neurologic and cardiovascular effects of hypotension in the monkey. 3 62

The cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) in the rat during normocapnia and hypercapnia were investigated by means of the intraarterial 133Xenon injection technique; measurements were performed during normocapnia and hypercapnia and the effect of propranolol upon CBF and CMRO2 was studied. The CBF technique applied to rat yield reliable results even in high flow situations. A steady state period of only 10--15 s is all that is necessary to obtain the initial slope of the 133Xenon clearance curve from which CBF is calculated and measurements may be repeated within minutes. Hypercapnia caused an increase in CMRO2 of 35% which confirms the findings of other investigators. The beta-adrenergic receptor blocker propranolol (2 mg per kg i.v.) prevented this increase and could eliminate an increase in CMRO2 already induced; this indicates that CO2 affects adrenergic mechanisms. Although propranolol eliminated the CMRO2 response to hypercapnia, it only reduced the CBF response; this dissociation of CBF and CMRO2 response occurred probably because the beta-receptor blockage only eliminated a CBF increase mediated through an increased CMRO2 (cellular response) whereas a direct CO2 effect upon the arterioles (vascular response) persisted.
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PMID:The effect of propranolol on cerebral oxygen consumption and blood flow in the rat: measurements during normocapnia and hypercapnia. 3 22

An electromagnetic flow meter was used to assess the changes in coronary blood flow in response to four levels of increased PaCO2 in six dogs. Mean, diastolic and systolic flow all increased during hypercapnia, the increase being maximal at mean PaCO2 11.3 KPa. Mean and diastolic coronary vascular resistances decreased progressively as PaCO2 increased, but systolic resistance, although decreasing with the lower levels of hypercapnia, returned to control at the greatest PaCO2. Although the oxygen available to the myocardium was increased markedly during hypercapnia, coronary sinus PO2 increased also, reflecting a reduction in myocardial oxygen extraction; thus myocardial oxygen consumption was unchanged. Cardiac output was increased significantly only at the greatest PaCO2. Total body oxygen handling was not altered significantly.
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PMID:Response of mean and phasic coronary arterial blood flow to graded hypercapnia in dogs. 3 65

Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were measured during acute and long-term ethanol intoxication in the rat. The purpose was to investigate whether the adaptive changes (development of tolerance) occurring in the CNS during ethanol intoxication were associated with changes in CBF and/or CMRO2. Consistent with other studies we found that acute severe ethanol intoxication (median blood alcohol concentration (BAC = 5.4 mg/ml)) caused a significant decrease in CBF and CMRO2. After 3-4 days of severe intoxication (BAC of 6.6 mg/ml) these physiological variables were less affected indicating that functional tolerance had developed: CMRO2 and CBF during acute ethanol intoxication were 9.3 ml/100 g/min and 60 ml/100 g/min respectively; after the long term intoxication period these variables reached 11.2 ml/100 g/min and 78 ml/100 g/min respectively, i.e. values not significantly lower than those of the control group. After induction of hypercapnia (PaCO2 about 80 mmHg) CBF increased by 360% in the control group; in the acutely intoxicated group CBF increased by only 127% and in the long term intoxicated group by 203% indicating that the cerebrovascular CO2-reactivity had also adapted to the ethanol intoxication. It is concluded that adaptive changes of the CNS to chronic ethanol intoxication comprise alterations in CMRO2, CBF and cerebrovascular reactivity.
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PMID:Adaptive changes in cerebral blood flow and oxygen consumption during ethanol intoxication in the rat.. 4 9

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10-15 Torr) to normocapnia and moderate hypercapnia (30-50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10-40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.
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PMID:Aortic body chemoreceptor responses to changes in PCO2 and PO2 in the cat. 4 29

To investigate the influence of variations in arterial oxygen tensions (PaO2), arterial carbon dioxide tensions (PaCO2), and arterial pH on long bone medullary pressures, seven anaesthetized dogs were investigated. Comparing the control medullary pressures, i.e. the mean medullary pressures obtained at the normal range of PaO2 (75--110 mmHg) with the mean medullary pressures corresponding to the range of PaO2 of less than 75 mmHg, statistically significant (P less than 0.05) decreases were seen in both epiphyseal, metaphyseal and diaphyseal medullary pressures, from 27.6 +/- 5.0 to 15.5 +/- 3.6 mmHg, from 23.5 +/- 2.9 to 13.9 +/- 2.3 mmHg and from 27.7 +/- 3.9 to 18.3 +/- 2.5 mmHg (all mean values +/- s.e. mean), respectively. Hyperoxia, hypocapnia, hypercapnia or metabolic acidosis had no effect on medullary pressures in any of the regions studied.
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PMID:Observations on long bone medullary pressures in relation to arterial PO2, PCO2 and pH in the anaesthetized dog. 4 59

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catherized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals.
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PMID:Haemodynamic changes in the cerebral circulation of the cat during occlusion of the middle cerebral artery. 10 Oct 24

Thirteen years' experience with home oxygen for patients with advanced chronic obstructive pulmonary disease are reviewed. Home oxygen is safe and relieves pulmonary hypertension and elevated RBC mass in some, but not all patients. Marked clinical improvement is the most important result of long-term home oxygen use, including reduced hospitalizations and return to gainful employment for a few patients. Chronic compensated carbon dioxide retention is well tolerated and adaptive in cases of severe chronic airflow obstruction. New oxygen concentrators are effective in correcting hypoxemia and may make home oxygen administration more convenient and less expensive.
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PMID:Outpatient oxygen therapy in chronic obstructive pulmonary disease. A review of 13 years' experience and an evaluation of modes of therapy. 10 79

A technique is described for the production of subarachnoid haemorrhage in baboons and their subsequent recovery for chronic study of cerebrovascular reactivity. The baboons make complete neurological recoveries but the response of their cerebral circulation to hypercapnia is impaired one week later. Baseline values of cerebral blood flow and of cerebral oxygen consumption are unaffected at this time. There is no evidence of hypoxic brain damage.
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PMID:Delayed effects of subarachnoid haemorrhage on cerebral metabolism and the cerebrovascular response to hypercapnia in the primate. 11 80


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