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

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

In view of the fact that diazepam has been shown to prevent an increase in catecholamine synthesis and/or turnover rates in stressful situations, and to modify the cerebral metabolic (and circulatory) response to hypoxia and hypercapnia, the influence of the drug on synthesis rates of DOPA and 5-HTP in three regions of the rat brain were studied under normoxic-normocapnic conditions, as well as in hypoxia and hypercapnia. In order to exclude a modifying influence of variations in tissue pO2 during hypercapnia, cerebral venous pO2 was kept at control values by moderate arterial hypoxia. When compared to the control state (paralyzed animals maintained on 70% N2O) normoxic and normocapnic animals given diazepam (in the absence of N2O) showed a slightly enhanced DOPA synthesis in limbic structures and reduced 5-HTP synthesis in limbic structures and striatum. In hypoxia, the drug considerably curtailed DOPA synthesis in limbic structures and striatum but had no effect on synthesis rate in cortex. The drug also appeared to exaggerate the generalized reduction in 5-HTP synthesis observed under 70% N2O. In hypercapnia, diazepam reduced the enhanced rate of DOPA synthesis (observed under 70% N2O) in striatum but left that in the cortex unchanged. The drug prevented the hypercapnia-induced increase in 5-HTP synthesis, observed under 70% N2O. It is concluded that diazepam significantly alters dopamine and serotonin synthesis in hypoxia and hypercapnia. Probably an indirect action, perhaps related to the stress-alleviating effect of diazepam, is involved. The results suggest that the effect of the drug on cerebral metabolic rate and blood flow in hypoxia and hypercapnia is unrelated to changes in noradrenaline synthesis or turnover. Furthermore, although the results demonstrate that diazepam modulates dopamine metabolism in hypoxia and hypercapnia it seems questionable that this influence can explain the metabolic and circulatory effects of diazepam in these conditions.
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PMID:Effect of diazepam on cerebral monoamine synthesis during hypoxia and hypercapnia in the rat. 681 96

The effect of the method of heart catheterization on the measurement of cerebral blood flow (CBF) with radioactive microspheres was evaluated during various experimental procedures in male Sprague-Dawley rats. Catheters were inserted into the left ventricle via the right carotid or right subclavian artery or directly into the left atrium for microsphere injections. CBF was measured in cerebral cortical and subcortical tissues under control anesthetized (70% N2O, 30% O2), hypoxic or hypercapnic test conditions. Under control conditions, CBF was similar in the right vs the left cerebral hemisphere in subclavian artery and atrial catheterized rats but was greater in the left vs the right cortex in carotid catheterized animals (p less than .05). During hypoxia and hypercapnia CBF increased equally in both cerebral hemispheres in atrial catheterized rats. The increase in CBF was significantly attenuated in the cerebral hemisphere ipsilateral to carotid catheterization during hypoxia and hypercapnia, although the percentage increase in flow was similar in both hemispheres. The results indicate the limitations of measuring regional CBF changes under experimental test conditions in rats with a ligated carotid artery and suggest that atrial catheterization is the method of choice when comparable changes in CBF are desired in both cerebral hemispheres.
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PMID:Regional cerebral blood flow measurement in rats with radioactive microspheres. 688 64

The purpose of this study was to measure changes in local cerebral blood flow (1-CBF) during generalized seizures, and to study whether or not formation of prostaglandins or related substances contributes to the increased flow rates. Seizures were induced in ventilated rats maintained on 70% N2O and 30% O2 by the i.v. injection of the GABA receptor blocker bicuculline (1.2 mg . kg-1). Formation of prostaglandins was inhibited by the administration of the fatty acid cyclo-oxygenase inhibitor indomethacin (10 mg . kg-1). Local CBF in 21 defined brain structures was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. After 20 min of continuous seizure activity 1-CBF increased 1.5--5-fold, the smallest increases (less than 200% of control) being observed in frontal and auditory cortex and in the caudoputamen, and the largest (greater than 400% of control) in substantia nigra, thalamus, visual cortex, lateral geniculate and hypothalamus. In general, the largest increases in 1-CBF occurred in sensory and limbic systems (and hypothalamus) while motor systems showed a pronounced variability. In the majority of structures examined indomethacin failed to modify the CBF response during seizures. Although this result suggests that seizures, in contrast to hypercapnia, lead to an increased CBF by other mechanisms than those related to prostaglandin formation, some structures (nucleus ruber, cerebellum, and superior colliculus) showed a clearly reduced 1-CBF in indomethacin-treated animals.
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PMID:Local cerebral blood flow in the brain during bicuculline-induced seizures and the modulating influence of inhibition of prostaglandin synthesis. 728 97

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

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

The nitric oxide synthase (NOS) inhibitors, nitro-L-arginine, its methyl ester, and N-monomethyl-L-arginine, have been shown to attenuate resting CBF and hypercapnia-induced cerebrovasodilation. Those agents nonspecifically inhibit the endothelial and neuronal NOS (eNOS and nNOS). In the present study, we used a novel nNOS inhibitor, 7-nitroindazole (7-NI) to examine the role of nNOS in CBF during normocapnia and hypercapnia in fentanyl/N2O-anesthetized rats. CBF was monitored using laser-Doppler flowmetry. Administration of 7-NI (80 mg kg-1 i.p.) reduced cortical brain NOS activity by 57%, the resting CBF by 19-27%, and the CBF response to hypercapnia by 60%. The 60% reduction was similar in magnitude to the CBF reductions observed in previous studies in which nonspecific NOS inhibitors were used. In the present study, 7-NI did not increase the MABP. Furthermore, the CBF response to oxotremorine, a blood-brain barrier permeant muscarinic agonist that induces cerebrovasodilation via endothelium-derived NO, was unaffected by 7-NI. These results confirmed that 7-NI does not influence eNOS; they also indicated that the effects of 7-NI on the resting CBF and on the CBF response to hypercapnia in this study were solely related to its inhibitory action on nNOS. The results further suggest that the NO synthesized by the action of nNOS participates in regulation of basal CBF and is the major, if not the only, category of NO contributing to the hypercapnic CBF response.
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PMID:The role of neuronal nitric oxide synthase in regulation of cerebral blood flow in normocapnia and hypercapnia in rats. 754 91

The case of a healthy 59-yr-old man who underwent elective laparoscopic extraperitoneal inguinal hernia repair and general anaesthesia is presented. After one hour of surgery, a sudden increase in the FETCO2 from 5.0% to 9.4% in relation to a massive subcutaneous emphysema, but without any haemodynamic instability, was noticed. The acute rise of FETCO2 was the first sign of an abnormal event. Nevertheless, subcutaneous emphysema was diagnosed with chest wall examination and palpation. Subcutaneous emphysema and hypercarbia are potential complications of laparoscopic surgery, but are more likely to occur in extraperitoneal surgery, since insufflated CO2 can diffuse easily into the surrounding tissues. High insufflation pressures will increase chances of this occurring and was the most likely cause of this complication. This case encouraged us to make recommendations for the management of laparoscopic extraperitoneal surgery which included: monitoring of CO2 insufflation pressure, routine examination and palpation of chest wall, use of N2O with caution, adjusting ventilation to physiological FETCO2 and excluding other causes of subcutaneous emphysema and hypercarbia.
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PMID:Laparoscopic extraperitoneal inguinal hernia repair complicated by subcutaneous emphysema. 762 34

The quality, result, and prognosis of neurosurgery relies heavily on the anaesthetic technique. Many different classes of drugs have been used during neurosurgical anaesthesia. This article reviews the use of intravenous (IV) propofol as an alternative to volatile anaesthetic techniques. Anaesthesia requirements for neurosurgical procedures are elaborated upon in the first part of the article. The priority of neuroanaesthesia is to preserve neuronal function by avoiding complications such as hypoxia, hypercarbia, and cardiovascular instability. Thereafter, the chosen anaesthetic technique should minimally interfere with cerebral autoregulation and CO2 responsiveness, while brain relaxation is encouraged by decreasing the cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF). In addition, the anaesthetic technique should be associated with rapid and predictable recovery in the operating theatre in order to allow early evaluation of the surgery. The second part of the article describes IV techniques for neurosurgery as an alternative to volatile anaesthetics, all of which increase CBF, cerebral blood volume, and intracranial pressure (ICP) in a dose-related manner and diminish cerebral autoregulation and interfere with cerebrovascular CO2 reactivity. Nitrous oxide has a stimulant effect on cerebral metabolism and is associated with an increase in CBF. On the other hand, all IV agents except ketamine are associated with decreases in CMRO2 and are cerebral vasoconstrictors. For this reason, it is rational to use them for the induction and maintenance of anaesthesia for neurosurgery as part of a total IV anaesthetic technique. The third part of the article focuses on propofol as the newest representative of IV anaesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Propofol for neuroanesthesia]. 765 91

The effects of continuous infusions of propofol on baroreceptor reflex regulation of cardiac rate and peripheral sympathetic nerve activity were evaluated in seven healthy, normotensive, young (19-26 yr), male volunteers. Heart rate, radial artery pressure, and continuous recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 micrograms) followed 60 s later by phenylephrine (150 micrograms). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 micrograms.kg-1 x min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 micrograms.kg-1 x min-1) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Propofol and autonomic reflex function in humans. 831 Dec 93


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