Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of clinical senile dementia patients underwent a series of cerebrovascular examinations. Some of them were standard examinations (fundus oculi, electroencephalogram, rheoencephalogram, cerebral angiogram and pneumonencephalogram) while the others were studying regional cerebral blood flow (rCBF) and modification of flow under fonctional tests (hypercapnia, hypocapnia and intravenous injection of 50 mg chl. papaverine) using the 133Xe clearance technique. The senile dementia group (III) was compared with 'normal' old patients group (I) and with patients suffering from sequelae of a previous stroke or from minor mental disorders (group II). Elderly subjects regarded as 'normal' often present alterations in usual vascular examinations but reveal a relative integrity of cerebral autoregulation. Some patients considered irreversibly 'sclerotic' still have a good grey matter flow (r1CBF) with real vasomotor possibilities. In each of the three groups of elderly subjects, there seemed to be a lack of correlation between the clinical symptoms and certain specific vascular examination.
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PMID:Cerebral vasoreactivity in senile dementia. 83 Feb 50

The cardiopulmonary effects of mechanical distension of the rumen were studied in nonanesthetized sheep. Results in group I ewes indicated that simply increasing intraruminal pressure by compressed air insufflation did not seriously affect cardiopulmonary hemodynamics. Changes were more serious in group II ewes when water injection was followed by ruminal insufflation with compressed air. Heart rate, total peripheral resistance, and total pulmonary resistance increased, with a concommitant increase in arterial and pulmonary blood pressure and decrease in stroke volume. Infusion of water alone increased heart rate and cardiac output. The blood gas data indicated a definite arterial hypoxemia and hypercapnia, suggesting impaired ventilation during ruminal distension. The increase in total pulmonary resistance was thought to be due to alveolar hypoxia caused by a significant decrease in ventilation.
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PMID:Cardiopulmonary effects of mechanical distension of the rumen in nonanesthetized sheep. 93 5

The concept that reflex control of cerebral vessels is unimportant has been challenged by recent studies which suggest that carotid baroreceptors have an important role in regulation of cerebral blood flow (CBF). In this study we have tested the hypothesis that arterial baroreceptors contribute to regulation of total or regional CBF. CBF was measured in anesthetized dogs with 15 mu microspheres. Stimulation of carotid baroreceptors, by raising carotid sinus pressure, did not alter or redistribute cerebral flow. Responses to baroreceptor stimulation were intact, as manifested by vasodilation in skeletal muscle. CBF decreased during systemic hypocapnia and increased during hypercapnia, which indicates that failure of cerebral flow to change during baroreceptor stimulation was not due to unresponsiveness of cerebral vessels. During hypercapnia, baroreceptor stimulation also failed to alter CBF. In other studies CBF was measured during increases in systemic arterial pressure, before and after denervation of arterial baroreceptors. Increases in arterial pressure did not increase CBF either before or after denervation of baroreceptors. We conclude that baroreceptor stimulation does not alter total or regional CBF and that baroreceptors do not regulate cerebral flow during systemic hypertension.
Stroke
PMID:Total and regional cerebral blood flow during stimulation of carotid baroreceptors. 94 13

One hundred consecutive patients were randomly given hypocarbic (PaCO2 less than 25 torr) or hypercarbic (PaCO2 greater than 60 torr) general anesthesia during carotid endarterectomy to test the effect of the two regimens upon the incidence of postoperative neurological deficit. An indwelling shunt was not used. One patient died, two have permanent neurological deficits and two have temporary neurological deficits. Although hypocarbic patients had fewer neurological complications than hypercarbic patients, the difference was not statistically significant (p less than 0.13). Hypercarbia significantly increased the incidence of intraoperative arrhythmia. Also, no relationship was found between the incidence of postoperative stroke and the internal carotid back pressure or the time of carotid occlusion.
Stroke
PMID:An evaluation of hypocarbia and hypercarbia during carotid endarterectomy. 96 Jan 66

In the present study, the dynamics of the cerebral blood flow (CBF) and ventilatory response to hypercapnia was investigated in a group of patients with a cerebrovascular disease and compared to responses measured in a group of normal volunteers. There was a significant correlation between the rapidity of the transient CBF and ventilatory responses and the severity of the cerebrovascular disease. While the steady state CBF response showed no such correlation, the steady state ventilatory response was reduced in patients with severe cerebrovascular disease. Various explanations for the differences in the dynamic responses of CBF and ventilation in patients with mild or severe cerebrovascular disease compared to normal subjects are considered. Measurement of these circulatory and ventilatory responses may be sensitive means for assessing the changing statls of patients with cerebrovascular disease.
Stroke
PMID:Transient responses of cerebral blood flow and ventilation to changes in PaCO2 in normal subjects and patients with cerebrovascular disease. 100 33

The effect of induced hypercarbia on the cardiovascular system during steady-state halothane-nitrous oxide anaesthesia was investigated in 4 male patients without cardiac disease. Heart rate, cardiac index, systemic and pulmonary blood pressures rose as pCO2 was increased. Stroke volume, systemic and pulmonary vascular resistance remained unchanged. Oxygen consumption decreased and oxygen saturation of mixed venous blood increased. In conclusion the primary effect of hypercarbia was an increased heart rate and a resultant increase of cardiac output. The pressure changes merely reflect the effect on cardiac output. Under these circumstances a regulatory role of mixed venous pO2 on cardiac output is highly unlikely.
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PMID:Cardiovascular effects of induced hypercarbia during halothane-nitrous oxide anaesthesia. 107 49

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).
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PMID:Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia. 109 15

Blood flow and patency rates obtained by lingual to basilar artery anastomosis were compared with those obtained by saphenous vein bypass graft from the carotid to the basilar artey in two groups of ten dogs. Flow was measured by an electromagnetic technique while blood pressure and blood gases were monitored. Graft patency also was determined by angiography and histological examination. The arterial and venous grafts carried more than enough blood to maintain a normal flow (9.5 ml per minute) through the basilar system of dogs. Immediately after anastomosis, average flow through the vein grafts was 15.5 ml per minute (range 10 to 24 ml per minute). Six weeks later, average flow through the vein graft was 11.5 ml per minute and through the arterial graft 13 ml per minute. With induced hypertension, flow increased in the arterial grafts to an average of 26.2 ml per minute and in the vein grafts 24 ml per minute. Hypercarbia increased arterial graft flow to an average of 27.8 ml per minute and vein graft flow to 23.5 ml per minute. By angiography, graft patency was shown in only 80% of the grafts at one week and in 60% at six weeks postoperatively, even though all grafts were patent by flow and histological determinations. This failure of angiography represents a limitation of the radiographical resolution in millimeter-sized vessels.
Stroke
PMID:Comparison of blood flow and patency in arterial and vein grafts to basilar artery. 109 33

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.
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PMID:Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation. 111 85

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
Stroke
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79


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