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

In 7 baboons and 5 macaques the effects of hypercapnia, hypocapnia, hypertension, and combinations of hypertension plus hypocapnia and of hypertension plus hypercapnia on the regional perfusion pressure (rPP) in the brain area rendered ischaemic by occlusion of the middle cerebral artery (MCA) were studied. A new technique for recording the pressure in the occluded MCA was used. The regional tissure pressure (rTP) was recorded with the so called wick type pressure transducers. Hypercapnia produced a marked decrease in rPP in the ischaemic brain area. Hypertension, especially in combination with hypocapnia, produced a very pronounced increase in rPP in the ischaemic brain area. The clinical implications of these findings are discussed. Occlusion of the homolateral common carotid artery (CCA) was followed by a very slight and transient drop in the occluded MCA pressure. Occlusion of the occluded MCA pressure.
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PMID:The influence of changes in arterial CO2 and blood pressure on the collateral circulation and the regional perfusion pressure in monkeys with occlusion of the middle cerebral artery. 81 1

In 7 baboons and 5 macaques the effects of hypercapnia, hypocapnia, hypertension, and combinations of hypertension plus hypocapnia and of hypertension plus hypercapnia on the regional perfusion pressure (rPP) in the brain area rendered ischaemic by occlusion of the middle cerebral artery (MCA) were studied. A new technique for recording the pressure in the occluded MCA was used. The regional tissue pressure (rTP) was recorded with the so called wick type pressure transducers. Hypercapnia produced a marked decrease in rPP in the ischaemic brain area. Hypertension, especially in combination with hypocapnia, produced a very pronounced increase in rPP in the ischaemic brain area. The clinical implications of these findings are discussed. Occlusion of the homolateral common carotid artery (CCA) was followed by a very slight and transient drop in the occluded MCA pressure. Occlusion of the contralateral CCA was followed by a marked and persistent drop in the occluded MCA pressure.
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PMID:The influence of changes in arterial CO2 and blood pressure on the collateral circulation and the regional perfusion pressure in monkeys with occlusion of the middle cerebral artery. 81 73

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

Increased body temperature stimulates hyperventilation in man but little is known about its effects on ventilatory responsiveness to hypoxia. Hence this study examined the effects of hyperthermia on hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR), and oxygen consumption (VO2). Six fasting subjects had these variables measured under basal conditions and at two levels of hyperthermia. Hypoxic ventilatory response was measured as the shape paramater A of the VE/PAO2 curves. Since hyperthermia produces hyperventilation and, therefore, hypocapnia, HVR was measured at the hyperthermic (hypocapnic alveolar CO2 tension (PACO2) and at the basal (normothermic) PACO2. Hypoxic ventilatory response (A) increased when measured at basal PACO2 levels, from 113 +/- 8.8 (S.E.M.) to 189 +/- 21.8 at 0.7 degrees C. and 240 +/- 34.0 at + 1.40 degrees C. (P less than 0.005). HVR measured during hyperthermic hypocapnia also increased at each temperature level but did not reach statistical significance (P = 0.1). Hypercapnic ventilatory response, as measured by the slope S of VE/PACO2 lines, increased significantly at each temperature elevation (P less than 0.025). We conclude that raising body temperature causes a significant augmentation of ventilatory responses to hypoxia (during normothermic PACO2 conditions) and to hypercapnia.
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PMID:Effects of hyperthermia on hypoxic ventilatory response in normal man. 83 15

The purpose of this study was to determine the effect of arterial PCO2 on blood flow to the avian brain. Cerebral blood flow was measured on curarized, artificially ventilated Pekin ducks by the rate at which intra-arterially injected xenon-133 was cleared from the duck's brain. A two-component clearance curve resulted: the blood flow calculated from the fast and slow components was similar to the blood flow to mammalian grey and white matter, respectively. Hypercapnia markedly increased the fast component of blood flow, whereas hypocapnia had no effect on this component. These effects were not due to changes in blood pressure, which was independent of arterial PCO2. Blood flow calculated from the slow component was independent of arterial PCO2. We conclude that the lack of response to hypocapnia may contribute to the exceptional tolerance of birds to high altitude by maintaining normal cerebral blood flow.
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PMID:Effect of arterial carbon dioxide on cerebral blood flow in ducks. 87 98

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.
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PMID:Total and regional cerebral blood flow during stimulation of carotid baroreceptors. 94 13

The effects of hypercapnia and hypocapnia on haemodynamics, coronary blood flow, and lactate metabolism were evaluated in anaesthetized closed chest dogs. Coronary flow increased with increased pCO2 and oxygen consumption and left ventricular performance were well maintained. Hypocapnia reduced coronary flow, oxygen consumption, and left ventricular functional performance.
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PMID:Effect of hypercapnia and hypocapnia on myocardial blood flow and performance in anaesthetized dogs. 95 18

Changes in cerebrospinal fluid formation rate (VF) with hypocapnia were measured by the ventriculocisternal perfusion technique in 24 rhesus monkeys anesthetized with nitrous oxide. In addition cerebral blood flow (CBF) was measured by the hydrogen clearence methods, Vf in control animals declined at a mean rate of 2.3 mul/min each hour during the last 4.5 h of a 7-h perfusion although variables known to effect Vf remained stable. Three hours after perfusion began, Vf of normocapnic controls was 41.4 mul/min +/- 5.4; CBF, 59P ML/100 G PER MIN. When Pco(2) was reduced to half of control, Vf fell to 35.6 mul/min +/- 6.3 and CBF fell by 27%. When Pco(2) was doubled, Vf fell to 33.1 mul/min +/- 5.3 and CBF increased threefold. The difference in Vf id significant only for the hypercapnic group (p=0.01). When animals were used as their own controls, three were no significant differences in Vf with hypercapnia compared to normocapnia. These results indicated that in the monkey variations of Pco(2) within broad physiologic limits, which are sufficient to cause large changes in CBF, have little effect of Vf.
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PMID:PCO(2) and rate of formation of cerebrospinal fluid in the monkey. 96 50

The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial PCO2 was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. Each PCO2 change was made at a constant coronary flow, and CVR was calculated from the ratio of perfusion pressure to flow. Coronary sinus (CS) PCO2 and PO2 were recorded continuously from blood withdrawn through a CS catheter. Normocapnia (PCO2 = 42.3 +/- 2.8 mm Hg) was obtained with a membrane oxygenator gas composition of 95% O2-5% CO2, and hypocapnia was produced with 100% O2-0% CO2. In addition to physiology normal coronary flow (determined by a CS PO2 of 20-30 mm Hg) relatively high and low flow states were studied. At a normal control CS PO2, a decrease in coronary arterial PCO2 from 42.3 +/- 2.8 to 23.8 +/- 1.3 mm Hg caused CVR to increase by 84.2%, from 1.27 +/- 0.06 to 2.30 +/- 0.04 units. Since pH was inversely related to PCO2, the effect on CVR may have been mediated through a pH change. CS PCO2 decreased from 65.2 +/- 1.9 to 39.4 +/- 1.3 mm Hg. myocardial oxygen consumption was unchanged. Increases in CVR of 74.5, 119.5, and 69.3% occurred during hypocapnia in three additional experiments in which control arterial PO2 was maintained at 52-90 mm Hg. When CS PO2 was greater than 30 mm Hg, the normocapnic CVR was high, and was only minimally increased by hypocapnia. When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial PCO2 can have an important effect on CVR independent of changes in O2 consumption. Myocardial PCO2, derived from metabolically produced CO2 and contributed to by arterial CO2, may be a major factor in normal control of coronary flow.
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PMID:The response of canine coronary vascular resistance to local alterations in coronary arterial P CO2. 96 40

This study was designed to determine blood flow to the liver during hypercapnia and combined hypercapnia-hypoxia with the portal vein and hepatic artery intact except for placement of an electromagnetic flow probe around these vessels. Twenty mongrel dogs weighing 30-45 kg were anesthetized with pentobarbital and flow probes and occluders were surgically implanted. Ten of these dogs were subjected to hypercapnia alone. During inspiration of 6% CO2 in room air, portal vein flow increased from 588 +/- 73 ml/min to 731 +/- 113 ml/min (p less than .05), while hepatic artery flow did not change significantly from its control mean of 221 +/- 38 ml/min. In the remaining dogs, inhalation of 6% O2 resulted in a reduction of portal blood flow within 30 min from 527 +/- 55 ml/min to 381 +/- 41 ml/min (p less than .01). Again, mean hepatic artery flow did not increase significantly above its control of 273 +/- 43 ml/min. Subsequent inhalation of 6% CO2 plus 6% O2 (combined hypercapniahypoxia) for 30 min in these same animals resulted in a significant increase of portal vein blood flow from 514 +/- 46 ml/min to 716 +/- 116 ml/min (p less than .05). Thus, hypercapnia alone increases total liver blood flow, primarily by an increase in portal vein flow. Hypoxia results in a decrease in portal vein flow. The superimposition of hypercapnia on hypoxia restores blood flow to a level close to that found with hypercapnia alone. Hypercapnia in the range of 63 +/- 4 mmHg PCO2 overwhelms the tendency toward a reduction of portal vein blood flow induced by an arterial PO2 of 42 +/- 5 mmHg in the presence of mild hypocapnia (PCO2 : 30.2 +/- 1 mmHg).
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PMID:Carbon dioxide and liver blood flow. 101 83


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