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

The effects of enflurane anesthesia on the cerebral cortical energy state and glycolytic metabolism were studied in rats. Twenty-four rats were divided into four groups with increasing concentrations of enflurane in the arterial blood, i.e. control (1.9 +/- 0.3 mg/dl, means +/- s.e.mean), level I (16.1 +/- 1.1 mg/dl), level II (26.0 +/- 1.6 mg/dl), and level III (32.9 +/- 0.9 mg/dl). At level I, high voltage 1-3 Hz slow waves superimposed on low voltage 10-12 Hz waves were predominant, and at levels II and III, spiking activity and burst suppression were recorded in the EEG. The duration of suppression at level III was significantly longer than that at level II. During enflurane anesthesia, there were no significant differences compared with the control group in the cerebral energy state or energy charge. Glycolytic metabolism remained unchanged except for an increase in glucose at levels II and III. Effects of hypocapnia and hypercapnia were examined in an additional 12 rats with an enflurane concentration in the blood similar to that at level II. Irrespective of PaCO2 levels, there were no significant changes in cerebral energy charge and glycolytic metabolites except for a decrease in glucose and an increase in lactate at hypocapnia. It was concluded that there was neither evidence of derangement of energy state nor increased anaerobic metabolism in the cerebral cortex during enflurane anesthesia.
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PMID:Cerebral energy state and glycolytic metabolism during enflurane anesthesia in the rat. 673 Aug 86

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
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PMID:A study of profound hypothermia by surface cooling. 677 40

This study is based on the same group of neurosurgical patients as our previous publication. All, except one, had suffered from head injury. We made a first measurement of rCBF under N2O anesthesia, a second under N2O + 1% enflurane anesthesia, both at a PaCO2 of 40 Torr. A third measurement was performed under N2O + 1% enflurane but at a PaCO2 of 30 Torr. The method we used consists of the intracarotid injection of 133Xe and recording of the radioactivity by a gammacamera. Mean arterial pressure was maintained constant by an intravenous phenylephrine drip. For each measurement of each patient, a map was drawn, representing the distribution of the regional cerebral blood flows (rCBF), compared to the mean value of the hemisphere. We have studied rCBF in one case of normal hemisphere, and in cases of traumtic lesions in acute and chronic states, taking into account that the normal brain exhibits areas with higher flow in the frontoparietal and insular regions. In the normal brain, introduction of 1% enflurane decreases uniformally mean CBF, rCBF repartition not being changed. Hyperventilation to 30 Torr shows that regions with previously higher flow react more to hypocapnia by a slightly more decreased flow. In severe brain trauma, mean CBF is generally low, and it is difficult to visualize the lesions under N2O and N2O + 1% enflurane anesthesia. Neither mean CBF, nor rCBF repartition are significantly modified. On the other hand, in the acute phase, hypocapnia causes a more decreased flow in the previously well irrigated areas, and shows a lack of vascular reactivity in the damaged region. Passing to the chronic state, the patient clinically recovering, the rCBF repartition is normalized and the contused area becomes agains vasoactive. Severe losses of neuronal tissue are characterized by definitive low flows without reactivity by hyperventilation.
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PMID:Influence of 1% enflurane (Ethrane) anesthesia on regional cerebral blood flow repartition under normo-and hyperventilation. 677 96

We have measured the CBF in ten neurosurgical patients. A first measurment was made during anesthesia with nitrous oxide 70% and a second with nitrous oxide 70% + 1% enflurane, both at a PaCO2 of 40 Torr. A third measurement was performed also with nitrous oxide + 1% enflurane, but at a PaCO2 of 30 Torr. We used the method of intracarotid 133Xe injection, with a gammacamera recording. In order to avoid any decrease of cerebral perfusion pressure, which might influence the CBF, an infusion of phenylephrine was used, if needed. At a constant PaCO2 of 40 Torr, there was no statistically significant difference in CBF with nitrous oxide + 1% enflurane compared to nitrous oxide alone. No change in cerebral vascular resistance was observed. When PaCO2 was lowered to 30 Torr, under 70% nitrous oxide + 1% enflurane, there was a 43% decrease in CBF (from a mean of 42 ml/100 G/min. to a mean of 24 ml/100 g/min.). Cerebral vascular resistance had an increase of 79%. In some instances, the decrease in CBF reached values around 20 ml/100 g/min. and in one case, even less. That level is generally considered to be the lowest acceptable limit in the conscious man, though not necessarily in the anesthetised one. Under hypocapnia, the cerebral arterio-venous oxygen difference increased, but the CMRO2 did not change. There were little differences in lactate and pyruvate cerebral metabolic rates, all values remaining within normal ranges. In conclusion, we believe that enflurane is a favorable anesthetic agent for neurosurgical operations at the concentration of 1%, CMRO2 is reduced, there is no significant effect on cerebral blood vessels, CBF and CVR do not change. However, a complementary use of hypocapnia may reduce CBF to dangerously low levels, if at the start, it shows already a pathological decrease and if hyperventilation is applied at a marked degree.
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PMID:Effect of 1% enflurane (Ethrane) anesthesia on cerebral blood flow and metabolism in neurosurgical patients during normo- and hyperventilation. 677 97

Epileptogenic foci were created by topical application of penicillin to the cerebral cortex in 40 paralyzed and artificially ventilated cats receiving halothane anesthesia. The animals were divided into two equal groups to compare primary and secondary foci. The following variables were recorded at normocapnia, hypocapnia, and hypercapnia prior to and during seizure activity: cerebral blood flow (CBF), determined by clearance of xenon 133; cortical redox states, measured by the fluorescence of reduced pyridine nucleotides (PN); brain pH, measured using a lipid-soluble, pH-sensitive fluorescent indicator; and electroencephalograms (EEG). Mean arterial blood pressure, arterial pH, arterial carbon dioxide tension (PaCO2), and arterial oxygen tension (PaO2) were monitored in each animal. All animals had a normal PaCO2-CBF response prior to the creation of a seizure focus, assuring the presence of autoregulation and normal metabolic function. CBF increased equally with seizures in the primary and secondary hemispheres. The relative increase was related to the PaCO2 but approximated 68% at normocapnia. There was an alteration in the PaCO2-CBF response with seizures, but the ability of the cerebral vasculature to constrict and dilate with hypocapnia and hypercapnia was retained. There was no significant difference in the reduced PN signal with variations in PaCO2 prior to seizures, but there was an apparent 10 to 15% fall with seizures. The "equivalent" intracellular pH fell to 6.94 at normocapnia in the primary focus but remained essentially unchanged from the control value of 7.10 in the secondary focus. These differences in pH were consistent with the greater degree of seizure activity observed in the primary focus. We conclude that a nonhypoxic acidosis existed in the primary focus and that changes in CBF were not related to it because the CBF changed equally in both hemispheres.
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PMID:Correlation of intracellular redox states and pH with blood flow in primary and secondary seizure foci. 678 36

A description is given of the effect of hypercapnic acidaemia and hypocapnic alkalaemia on scalp tissue PO2 as measured with a subcutaneous needle-electrode and a transcutaneous electrode in 6 fetal lambs. The experiments were carried out under general anaesthesia with the fetus kept in utero. Hypocapnia was induced by hyperventilating the ewe and hypercapnia was achieved by administering extra CO2 to the ewe. Fetal carotid arterial, subcutaneous and transcutaneous PO2 were continuously recorded, and fetal and maternal arterial pH and arterial PCO2 were determined from blood samples taken at short intervals. In each experiment the H+ Bohr factor of fetal and maternal blood was measured. During hypocapnic alkalaemia, there was a fall in all fetal PO2 levels, whereas a marked rise was observed during hypercapnic acidaemia. The variations in fetal PO2 observed in vivo even exceeded the variations due to the H+ Bohr effect (measured in vitro). This was due to small variations in fetal carotid arterial oxygen saturation, which tended to fall during hypocapnic alkalaemia and to rise during hypercapnic acidaemia. The results of these findings strongly suggest that tissue PO2, as measured with the subcutaneous and transcutaneous electrodes, is dependent on the H+ Bohr effect. This adds to the uncertainty as to the value of subcutaneous and transcutaneous PO2 monitoring during labour as an early warning system for impending fetal asphyxia.
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PMID:Influence of variations in pH and PCO2 on scalp tissue oxygen tension and carotid arterial oxygen tension in the fetal lamb. 679 86

Concern has often been expressed that hypocapnia produced by controlled hyperventilation might further reduce cerebral perfusion during drug-induced hypotension. In the present studies, hypotension was induced in cats with either practolol/trimetaphan (five experiments) or practolol/nitroprusside (five experiments) together with controlled haemorrhage. Arterial PCO2 was altered between 17 and 51 mm Hg by varying inspired CO2 during constant-volume ventilation, first during control conditions of light halothane/nitrous oxide anaesthesia and then during hypotension to mean blood pressure of 36-37 mm Hg. Cerebral cortical perfusion was measured by the krypton clearance technique and pial artery diameter by the image-splitting method. Cerebral cortical blood flow did not alter with PaCO2 changes during trimetaphan hypotension, but some responsiveness to CO2 persisted during nitroprusside hypotension, though at less than half control levels. No changes in pial artery diameter were seen with CO2 during hypotension under either technique. It is postulated that CO2 responsiveness persisted with nitroprusside because cerebral blood flow (CBF) values were higher when hypotension was produced with this drug, as compared with trimetaphan. It would appear that hypocapnia does not further reduce CBF during trimetaphan hypotension but does do so with nitroprusside. However, the combination of hypocapnia and nitroprusside hypotension did not in any instance lower CBF below the values found during trimetaphan hypotension.
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PMID:CO2 responses of the cerebral circulation during drug-induced hypotension in the cat. 679 28

The authors use the Bain Circuit with spontaneous breathing during head surgery (neurosurgery and ophthalmological procedures). Suitable for both adult and pediatric use, it seems to be, due to its unique characteristics, the choice circuit for all anaesthesia procedures in which the physician does not have direct control over the patient's head. Comparative analysis of blood gas levels is effected, on the one hand in children connected to a Digby-Leigh system and Bain Circuit, and on the other hand in adults, some of whom are connected to a two-way system and the other under a filter circuit; all of the patients are then connected to the Bain Circuit. In children the analysis of results shows that for an identical protocol of anaesthesia the quality of spontaneous breathing obtained using the Bain Circuit is the same as that obtained using the Digby-Leigh. In adults anaesthetized using fluothane and with spontaneous breathing, the average level of hypercapnia under filter circuit and Bain Circuit is identical. Also, the same level of alveolar hypoventilation is obtained under spontaneous breathing with the two-way and Bain Circuit systems when there are properly provisioned. Thus this work confirms other studies by showing that the Bain Circuit is particularly well adapted to head surgery because of its low weight and easy manageability. On the other hand, when using spontaneous breathing the level of alveolar hypoventilation, and thus the degree of hypercapnia, is directly related to the level of anaesthesia and independent of the circuit chosen. Only the setting up of controlled breathing would allow the physician to work under the desired level of normo or hypocapnia.
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PMID:[Blood gas levels using spontaneous breathing and the Bain circuit. Our experience during head surgery (author's transl)]. 680 Feb 85

The haemodynamic effects of nitroprusside (SNP) were studied in six patients undergoing surgery for intracranial aneurysm under controlled hypotension in endotracheal anaesthesia with halothane-nitrous oxide during hypocapnia. Mean arterial pressure was reduced with SNP from mean 12.25 kPa to mean 8.29 kPa (32%). There were concomitant statistically significant decreases in systemic vascular resistance (-21%), cardiac index (-17%), stroke index (-23%), pulmonary arterial mean pressure (-27%) and pulmonary capillary wedge pressure (-27%). Heart rate, central venous pressure and pulmonary vascular resistance did not change significantly. After the infusion of SNP was discontinued all parameters, except cardiac index and heart rate, returned to values not significantly different from the control values. The hypotension induced by SNP resulted from reductions in cardiac index and systemic vascular resistance. The reduction in cardiac index did not reach a critical level in any of the patients.
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PMID:Haemodynamic changes during sodium nitroprusside induced hypotension and halothane/nitrous oxide anaesthesia. 683 56

Six children who remained in deep coma after immersion accidents in fresh water received therapy to maintain normal intracranial pressure (ICP). This involved controlled ventilation to ensure hypocapnia and hyperoxaemia, maintenance of low normothermia, fluid restriction, dexamethasone (1-1.5 mg/kg initially, 1-1.5 mg/kg/day as maintenance) and barbiturates (phenobarbitone and thiopentone). The latter were given in a wide range of dosage. Increased ICP was common to all patients, but could always be kept at acceptable levels. All patients suffered from pulmonary oedema; three developed broncho-pneumonia and two developed adult respiratory distress syndrome. All children survived with good recovery, two needed active rehabilitation for several months.
Anaesthesia 1982 Dec
PMID:Intensive care after fresh water immersion accidents in children. 718 Oct 62


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