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

Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing 133Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 +/- 19 mm Hg, and a mean arterial PCO2 of 36.2 +/- 2.9 mm Hg, mean CBF was 103 +/- 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial PCO2. CBF was measured during steady state levels of hypo- and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg. CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.
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PMID:Cerebral blood flow autoregulation in the rat. 64 8

Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were measured in rats under nitrous oxide anaesthesia, using a 133Xenon modification of the Kety and Schmidt inert gas technique with sampling of cerebral venous blood from the retroglenoid vein. Extracerebral contamination of the venous blood sampled was studied by comparing the rates at which the activity of 133Xenon decreased in blood and tissues. Contamination was avoided by gentle compression of the contralateral retroglenoid vein during sampling. CBF and CMRo2 of the rat brain were 80+/-2 and 7.6+/-0.2 ml-(100g)-1-min-1, respectively. These values are about 25% lower than those previously obtained for cerebral cortical tissue under similar conditions. Induced hypercapnia (Paco2 about 70 mm Hg) or hypocapnia (Paco2 15-20 mm Hg) gave rise to expected changes in CBF but did not alter CMRo2. The CMRo2 of the rat brain is at least twice that of the human brain. This species difference, which is similar to that previously reported for the oxygen uptake of cerebral tissue in vitro, probably reflects on inverse relationship between brain weight and neuronal packing density.
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PMID:A method for determining blood flow and oxygen consumption in the rat brain. 125 48

We propose a simple method that can be used to measure cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral glucose consumption (CMRglu) in the conscious, freely moving rat. The method is based on the classical Kety-Schmidt approach, and uses a chronic cannula in the confluens sinuum. We tested the method by investigating the response of CBF, CMRO2, and CMRglu to hypercapnia and used the approach to investigate the effects of acute alcohol administration. Severe hypercapnia (PaCO2 approximately 80 mmHg) increased the CBF by a factor of 3.5, decreased the CMRO2 by 30%, and had no significant effect on the CMRglu. Under normocapnic conditions moderate blood alcohol levels (100-200 mg%) caused no significant effects on CBF, CMRO2, or CMRglu, but high blood alcohol levels (250-400 mg%) decreased all three parameters by approximately 25%. Under hypercapnic conditions high blood alcohol levels had no effect on CBF, CMRO2, and CMRglu.
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PMID:Cerebral blood flow and metabolic rate in the conscious, freely moving rat: the effects of hypercapnia, and acute ethanol administration. 175 6

The effect of lesions of the locus coeruleus neuron system on cerebral metabolic rate for oxygen (CMRO2) and blood flow (CBF) was evaluated in paralyzed and mechanically ventilated rats, using a 133xenon modification of the Kety-Schmidt inert gas technique. Bilateral electrothermic lesions of its ascending bundle caused no significant change in CBF or CMRO2. The 6-hydroxydopamine lesions did not influence the CBF and CMRO2 responses to hypercapnia and hypoxia. It is concluded that the locus coeruleus does not exert any resting tone on CBF and CMRO2 and that no influence on the CBF and CMRO2 responses to hypercapnia and hypoxia is mediated via its ascending projections.
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PMID:Cerebral blood flow and oxygen consumption in the rat brain after lesions of the noradrenergic locus coeruleus system. 678 64

The present study explores the possibility that the central dopaminergic and serotoninergic neuron systems influence CBF under normocapnic and hypercapnic conditions. In the first part of the study the effect of unilateral 6-hydroxydopamine lesion of the nigrostriatal dopamine pathway on local cerebral blood flow (1-CBF) was measured autoradiographically with [14C]iodoantipyrine as the diffusible tracer. The lesion caused no major effect on CBF under normocapnic or hypercapnic conditions. However, the circulatory response to hypercapnia was slightly enhanced (about 10%) in the denervated caudate-putamen. It is suggested that under hypercapnic conditions the pronounced increase in blood flow in the caudate-putamen is normally modulated by a slight vasoconstriction caused by dopamine release from the nigrostriatal system. In the second part of the study the effect of intraventricular 5,7-dihydroxytryptamine on cerebral metabolic rate for oxygen (CMRO2) and CBF was evaluated using a 133xenon modification of the Kety-Schmidt inert gas technique. The lesion, which removed about 90% of cortical 5-hydroxytryptamine, had no effect on the circulatory response to hypercapnia, not did it alter CMRO2. Under normocapnic conditions, though, the lesion seemed to induced a minor increase in CMRO2, which indicates that the serotoninergic system exerts a depressant resting tone on metabolic rate in the brain.
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PMID:Cerebral circulatory response to hypercapnia: effects of lesions of central dopaminergic and serotoninergic neuron systems. 679 77

The objective of the present study was to explore whether the systemic consequences of sympathoadrenal activation influence the cerebral circulatory and metabolic effects of hypercapnia in the rat. To that end, a bilateral blockade of the sympathetic chain was performed at the low thoracic level by paravertebral injection of local anaesthetic. The injection was followed by a reduction in blood pressure and, in comparison to animals injected with local anaesthetic intramuscularly, those with paravertebral blockade showed lower blood and tissue concentrations of glucose and lactate. Overall ("cortical") CBF and CMRO2 were measured with a 133xenon modification of the Kety-Schmidt technique, and local CBF was estimated autoradiographically with 14C-iodoantipyrine as the diffusible tracer. Paravertebral blockade failed to modify the circulatory response to hypercapnia, nor did it prevent the increase in CMRO2d previously noted in this preparation. In animals maintained ventilated on 70% N2O, paravertebral blockade reduced overall CBF by 30% and local CBF by 30-40%, with a suggested but statistically nonsignificant reduction in CMRO2. In unparalysed, awake animals the blockade failed to affect local CBF. It is concluded, therefore, that blockade of the sympathetic chain causes a reduction of CBF only in the stressful conditions prevailing in paralysed and ventilated animals.
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PMID:Cerebral blood flow and oxygen consumption in normocapnia and hypercapnia: modulating influence of paravertebral sympathetic blockade at the low thoracic level. 681 Jun 41

Although results obtained in baboons and rats have demonstrated that the fatty acid cyclo-oxygenase inhibitor indomethacin reduces cerebral blood flow (CBF) under control conditions and markedly attenuates the CBF response to hypercapnia, nonconfirmatory results have been obtained in rabbits and cats. Since these latter studies were carried out under barbiturate anesthesia, we tested the effect of indomethacin (10 mg kg-1) on CBF and cerebral oxygen consumption in rats anesthetized with 150 mg kg-1 of phenobarbital. At normocapnia the barbiturate reduced CBF, measured with a 133Xe modification of the Kety-Schmidt technique, to about 50% of nitrous oxide control values as previously determined with a similar technique. At this CBF level, indomethacin induced a small, albeit highly significant decrease in CBF. We suggest that a reduction of this magnitude will escape detection with some CBF techniques in current use. Indomethacin induced a highly significant decrease in CBF during hypercapnia, demonstrating that the barbiturate does not eliminate the effect of indomethacin on CO2 responsiveness. The magnitude of the reduction in CO2 response was so large that is should be detected with most methods for measuring CBF. A comparison with previous data on animals under 70% N2O demonstrated that phenobarbital reduced the CO2 responsiveness. defined as the ratio deltaCBF/deltaPCO2, to 39% of that observed under nitrous oxide analgesia. With both types of anesthesia, indomethacin curtailed the CO2 responsiveness 4- to 5-fold.
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PMID:Effects of indomethacin on cerebral blood flow and oxygen consumption in barbiturate-anesthetized Normocapnic and hypercapnic rats. 732 33

The effect of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (PaCO2 approximately 60 mm Hg and PaCO2 approximately 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety-Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect on either CMRO2 or CBF under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.
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PMID:Role of nitric oxide in regulating cerebrocortical oxygen consumption and blood flow during hypercapnia. 816 93

We investigated the cerebral haemodynamic effects of 1 MAC desflurane anaesthesia in nine male patients scheduled for elective coronary bypass grafting. For the measurement of cerebral blood flow (CBF) a modified Kety-Schmidt saturation technique with argon as inert tracer gas was used. Measurements of CBF were made before induction of anaesthesia and 30 min after induction under normocapnic, hypocapnic and hypercapnic conditions in sequence. Changes in mean arterial pressure after induction of anaesthesia and during the course of the study were minimized using norepinephrine infusion. In comparison with the awake state under normocapnic conditions, desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51% and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly, CBF was significantly reduced by 22%; jugular venous oxygen saturation (SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22% decrease and a 178% increase in CBF, respectively. These findings may be interpreted as the result of two opposing mechanisms: cerebral vasoconstriction induced by a reduction of cerebral metabolism and a direct vasodilator effect of desflurane. CBF alterations under variation of PaCO2 indicate that cerebrovascular carbon dioxide reactivity is not impaired by application of 1 MAC desflurane.
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PMID:Effects of 1 MAC desflurane on cerebral metabolism, blood flow and carbon dioxide reactivity in humans. 981 15

1. The present study compares the indirect Fick nitrous oxide equilibration method of Kety and Schmidt for cerebral blood flow (CBF) estimation with a direct ultrasonic Doppler index of venous outflow. 2. Cerebral blood flow was determined simultaneously by the direct measurement of sagittal sinus blood velocity and the indirect Kety and Schmidt method in five anaesthetized sheep during high and low steady states of CBF. High- and low-flow states were achieved by altering ventilation to produce hypercarbia and hypocarbia, respectively. 3. Four different sets of calculations were used to make the Kety and Schmidt estimations: arterial-venous nitrous oxide concentration differences during uptake or elution of the indicator and with or without extrapolation of arterial-venous differences to infinity. 4. During 15 min nitrous oxide administration, apparent blood:tissue equilibration of nitrous oxide was rapid in some data sets and slow in others. 5. There were no significant differences in CBF estimates between any of the four Kety and Schmidt calculations or the direct ultrasonic Doppler venous outflow method; however, CBF estimates based on nitrous oxide uptake correlated more strongly with the direct method than estimates based on nitrous oxide elution. 6. In the high-flow state, CBF estimates based on nitrous oxide uptake, but not those based on elution, distinguished between rapid and slow blood:tissue equilibration of nitrous oxide. 7. This provides validation of the Doppler sheep brain venous outflow method against the widely used Kety and Schmidt method.
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PMID:Agreement between ultrasonic Doppler venous outflow and Kety and Schmidt estimates of cerebral blood flow. 1049 64


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