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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory effects elicited by spinal (C2-C3) stimulation at the level of descending inspiratory axons were studied in paralysed, non-vagotomized and artificially ventilated cats anaesthetized with urethane-chloralose. The activation of inspiratory bulbospinal axons in the ventrolateral quadrant was confirmed by recording the ipsilateral phrenic excitation following a single pulse. Brief stimulus trains delivered at the same locus during expiration elicited short- and long-term phrenic activations. The short-term activation consisted of a tetanic orthodromic response. The long-term activation, of central origin, exhibited the same pattern as a spontaneous inspiration and consisted of an inspiratory resetting which necessitated weak anaesthesia and light hypocapnia. Control experiments (restricted lesions of the medulla and the cervical cord, recording of afferent activity in thalamic sensory nuclei, medullary stimulation) revealed that this inspiratory resetting could not be related to appreciable activation of either non-respiratory efferents or spinal afferent pathways studied but was likely to depend on the activation of the descending inspiratory axons. We conclude that the respiratory resetting obtained by spinal stimulation resulted from mass antidromic activation of the inspiratory bulbospinal neurons which thus appear to be involved in the generation of the respiratory rhythm.
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PMID:Respiratory resetting induced by activation of inspiratory bulbo-spinal neurons. 376 20

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumors. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anesthesia was induced with thiopental 5-7 mg X kg-1, fentanyl 0.2 mg, and pancuronium, and maintained with 0.75% inspired isoflurane concentration in 67% nitrous oxide, and moderate hypocapnia. In one group of patients (n = 7), the inspired isoflurane concentration was maintained at 0.75% throughout anesthesia. One hour after induction of anesthesia, CBF and CMRO2 averaged 31 +/- 3 ml X 100 g-1 X min-1 and 2.1 +/- 0.2 ml O2 X 100 g-1 X min-1 (X +/- SEM), respectively. During repeat studies 1 h later, CBF and CMRO2 were unchanged. In a second group of patients (n = 7), an increase in the inspired isoflurane concentration from 0.75% to 1.5% was associated with a significant decrease in CMRO2 from 2.4 +/- 0.1 to 1.9 +/- 0.1 ml O2 X 100 g-1 X min-1, and no change in CBF. It is concluded that this anesthetic regimen is safe to use in patients with small supratentorial tumors in whom only a small midline shift has occurred.
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PMID:The effect of isoflurane on cerebral blood flow and metabolism in humans during craniotomy for small supratentorial cerebral tumors. 382 91

The reduction in cerebral blood flow (CBF) caused by hypocapnia is an important element of neuroanesthetic techniques. While it has been demonstrated previously that the CO2 response of the cerebral circulation (CO2 X R) is enhanced (i.e., greater delta CBF/delta PaCO2) during halothane administration, the effect of isoflurane on CO2 X R has not been evaluated completely. Accordingly, the authors examined CO2 X R in cats during anesthesia with 1.0 MAC isoflurane (with 75% N2O) and compared it with CO2 X R during anesthesia with 1.0 MAC halothane (with 75% N2O) and with CO2 X R during the administration of 75% N2O alone. CO2 X R during anesthesia with isoflurane-N2O was enhanced relative to that observed during administration of both halothane-N2O (P less than 0.025) and N2O alone (P less than .001). CO2 X R during anesthesia with halothane-N2O was, in turn, greater than that observed during the administration of N2O alone (P less than 0.025). Furthermore, at similar levels of hypocapnia (PaCO2 18-20 mmHg), CBF was significantly lower (P less than 0.01) during administration of isoflurane-N2O (29.0 +/- 4.5 ml X 100 g-1 X min-1) than during administration of either N2O (40.6 +/- 5.5 ml X 100 g-1 X min-1) or halothane-N2O (39.6 +/- 7.8 ml X 100 g-1 X min-1). CBF values during administration of the N2O alone and halothane-N2O were not different during hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide. 391 14

A case of Moya-moya disease requiring anaesthesia for both investigation and attempted surgical correction is presented. The influence of the anaesthetic technique on the abnormal cerebral vasculature, with particular reference to induced hypocapnia, is discussed. Guidelines for a safe method of anaesthesia in this group of patients are suggested.
Anaesthesia 1985 Dec
PMID:Anaesthetic management in Moya-moya disease. 408 49

Regional cerebral blood flow was measured by injection of (133)Xenon into the internal carotid artery in 11 patients with cerebrovascular disease. All patients were studied under general anaesthesia, first at normocapnia and then at hypocapnia. The 15 minute isotope clearance curves were analysed by computer by two-compartmental analysis and regional changes in flow and the proportions of fast and slow clearing tissue obtained at two levels of arterial CO(2) tension. Hypocapnia caused a fall in blood flow which was consistently accompanied by a decrease in the proportion of fast clearing tissue. Regional changes were not significantly different from the hemisphere mean changes. There was no correlation between changes in blood flow through grey matter and the proportion of fast clearing tissue on a hemisphere mean basis, but on regional analysis the data from 10 out of the 11 patients showed that in areas where blood flow through grey matter changed most the proportion of fast clearing tissue changed least and vice versa. A hypothesis has been proposed to explain this phenomenon.
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PMID:Effect of changes in cerebral blood flow on proportion of high and low flow tissue in the brain. 484 31

1. The circulatory effects of artificial hyperventilation with air and low oxygen mixtures were studied in rabbits anaesthetized with chloralose-urethane and given decamethonium iodide. The role of vagal afferents in the response to hypoxia was also assessed in spontaneously breathing unanaesthetized and anaesthetized animals.2. In the anaesthetized rabbit artificial hyperventilation inhibited all the changes in autonomic activity to the heart and peripheral circulation resulting from stimulation of the arterial chemoreceptors, and also reduced vagal efferent tone. In animals with section of the carotid sinus and aortic nerves the changes in autonomic activity observed during hypoxia and hyperventilation were much smaller than in normal animals and affected only cardiac autonomic activity.3. The effects of hyperventilation during hypoxia were mediated chiefly through vagal afferents rather than through the effects of hypocapnia. In the absence of changes in autonomic activity (e.g. during artificial hyperventilation with air) the circulatory effects were small and less clearly related to afferent vagal activity.4. In the spontaneously breathing anaesthetized and unanaesthetized rabbit vagal afferent activity resulting from the respiratory response to hypoxia inhibits sympatho-adrenal activity in the same way as during hypoxia with artificial hyperventilation.5. The importance of the vagal afferent input in the rabbit is discussed in relation to the qualitative differences in circulatory response with increasing severity of hypoxia, and in relation to the effects of anaesthesia.
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PMID:Effects of hyperventilation on the circulatory response of the rabbit to arterial hypoxia. 572 12

Many factors influence the outcome after surgery of the bowel. However, care in anaesthetic and postoperative management may help to reduce the frequency of complications. Such care can be directed at maintenance of or improvement in oxygen delivery to the bowel by the avoidance of hypoxia, hypocapnia and hypovolaemia, and by careful selection of drugs and techniques used during anaesthesia. Tension on anastomoses can be reduced by care in the administration of neostigmine, and possibly by the use of pethidine rather than morphine for analgesia during and after operation. Postoperative ileus may be affected by sedative and analgesic therapy.
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PMID:Anaesthesia and bowel surgery. 614 Sep 34

Organ blood flow and distribution of cardiac output (CO) were determined in 9 awake (control) and ketamine-anesthesized swine (4 mg/kg bolus followed by continuous infusion of 0.3 mg/kg/min, IV), using 15 micron diameter radionuclide-labeled microspheres. Absolute values of blood flow (per 100 g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 55.83 +/- 5.13% of the CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.10%, 2.67%, 19.84%, 11.81%, and 16.84%, respectively. During ketamine anesthesia, the fraction of CO perfusing the kidneys and liver (hepatic artery) increased from control and values for brain, heart, and splanchnic organs remained unchanged. Blood flow (per unit weight) of brain, cardiac, and splanchnic organs decreased; kidney and skeletal muscle blood flow was unaltered; and hepatic arterial blood flow increased from the awake (control) values. The hyperdynamic state often associated with ketamine anesthesia was not evident in these pigs during intermittent positive-pressure ventilation resulting in hypocapnia.
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PMID:Organ blood flow and distribution of cardiac output in hypocapnic ketamine-anesthetized swine. 641 46

The ventilation and carbon dioxide elimination of each lung, and pulmonary arterial pressure, were studied in 17 patients during the early phases of anaesthesia for pulmonary surgery. The patients were ventilated mechanically to moderate hypocapnia. Expired tidal volume and carbon dioxide elimination rate of the lung to be operated on, and of the other lung, were similar in the supine position. There was a significant (P less than 0.01) increase in ventilation and a decrease in end-tidal PCO2 of the upper lung after turning the patient on to the side. Simultaneously, the physiological deadspace fraction of tidal volume (VD/VT) increased from 42 to 45% (P less than 0.05). Mean pulmonary arterial pressure (MPAP) increased slightly as surgery on the chest wall commenced. A concomitant increase of carbon dioxide elimination from the upper lung occurred also, although the distribution of ventilation, between the lungs, was unchanged in comparison with the conditions during undisturbed anaesthesia. Individual changes in MPAP (delta MPAP) and corresponding changes in VD/VT (delta (VD/VT)) were negatively correlated (r = -0.68, P less than 0.01). The regression equation was delta (VD/VT) (%) = 0.7 - 0.83 X delta MPAP (mmHg). It was concluded that variations in pulmonary arterial pressure during surgical stimulation may significantly affect the pattern of carbon dioxide elimination in the lungs. However, there was no evidence that these effects were important clinically.
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PMID:Carbon dioxide elimination from each lung during endobronchial anaesthesia. Effects of posture and pulmonary arterial pressure. 643 15

We compared vasoactive effects of intravenous nicotine (36 micrograms/kg/min) in regional cerebral circulations under pentobarbital and chloralose anesthesia. Experiments were conducted in three groups of dogs: Group I, pentobarbital anesthesia with fixed ventilation; Group II, chloralose anesthesia with fixed ventilation; Group III, chloralose anesthesia with free breathing. Values for regional cerebral blood flow measured with 15 mu radioactive microspheres were used to compute regional cerebral vascular resistance (rCBR). In Group I, nicotine had no effect on rCVR in cerebral cortex, and it increased significantly rCVR in cerebellum (+17%), pons (+13%), medulla (+23%), and spinal cord (+19%). Using chloralose instead of pentobarbital in dogs with fixed ventilation (Group II), caused a significant reduction in rCVR in the cerebral cortex during nicotine, although it did not alter significantly nicotine-induced changes in rCVR in other regions of the brain. Hypocapnic alkalosis during nicotine-induced hyperventilation (Group III) resulted in significant increases in rCVR in all regions of the brain; however, the increases in rCVR in non-cortical regions more than doubled those in the cerebral cortex. The present results indicate: Nicotine-induced vasodilation in cerebral cortex was blunted by pentobarbital anesthesia. Nicotine-induced vasodilation in cerebral cortex under chloralose anesthesia was sufficient to nullify in part the potent vasoconstrictor effect of hypocapnic alkalosis.
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PMID:Regional blood flow in canine brain during nicotine infusion: pentobarbital vs. chloralose anesthesia. 646 62


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