Effects of extremes of respiratory and metabolic alkalosis on cerebral blood flow in man.

MATERIALS AND METHODSWe studied 12 5-IO-day-old mongrel dogs who weighed 505-855 g. They were anesthetized with 70% nitrous oxide throughout the study and paralyzed with 0.1 mgjkg of pancuronium. Their tracheae were intubated, and their lungs were mechanically ventilated with a Harvard small animal volume ventilator. Their tracheal pressures were continuously recorded from an 18-gauge needle; the needle tip was positioned near the tracheal end of the endotracheal tube. The needle was connected by stiff pressure tubing to a Gould-Statham 823DB pressure transducer. The response time of the needle, catheter, and strain gauge was flat to 15.1 Hz.The right groin and both sides of the neck were infiltrated with 0.5 ml of 1% xylocaine and catheters were inserted into the femoral artery and vein, left ventricle (via left carotid artery), and right ventricle (via right jugular vein). The femoral vein catheter was used to infuse 10% dextrose in 0.2 normal saline (2-4 ml/kg/h), transfuse blood, and administer pancuronium bromide. The femoral artery catheter was used to monitor arterial blood pressure, blood gases, and pH, and to withdraw blood for reference samples during microsphere injections (28). The left ventricular catheter was used to inject radionuclide-labeled microspheres. The right ventricular catheter was used to measure right ventricular pressures, and to withdraw blood for determination of mixed venous blood gases and pH. We were unsuccessful in advancing catheters into the pulmonary arteries of these small animals so we used right ventricular systolic pressure as an index of pulmonary artery pressure.After allowing 30 min for recovery from the surgical manipulations, we measured blood gases and pH. We found them to be normal in all but two animals. These two had a small amount of metabolic acidosis which was corrected with 2 meqJkg of sodium bicarbonate. Two-tenths ml of blood was withdrawn from the femoral artery and from the right ventricle before each microsphere injection. With each sample, we determined pH, Po 2 , PC02, oxygen saturation, and hemoglobin concentration. Blood gases and pH were measured with a Corning 175 blood gas analyzer and corrected for body temperature and pH. Hemoglobin concentration and oxygen saturation were determined with a Radiometer Hemoximeter. Next, microspheres were injected into the left ventricle to determine control (normocarbic) cardiac output and organ blood flow. The microspheres were injected over 20-30 sec and 5 ml of arterial blood ("reference organ sample") were withdrawn over a 2-min period. An equal volume of maternal blood was infused into the femoral vein during the withdrawal to maintain a constant blood volume. We injected 200,000 to 800,000 15-~m radionuclide microspheres during each cardiac output measurement to ensure that there was an adequate number of micropheres present to accurately determine organ blood flows (28). Because injecting the spheres did not affect the arterial blood pressure, we conclude that they did not significantly obstruct the circu...

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“…This study confirms previous observations in adults (8,40,43,49) and neonates (37,43) that cerebral bloOd. flow is reduced by hyperventilation.…”

supporting

confidence: 92%

“…Respiratory alkalosis reduces the cerebral blood flow of neonates and adults (22,23,27,37,49). The relationship between Paco2 and cerebral blood flow is linear when the PaC02 is between 20 and 80 mm Hg (22,37,43).…”

mentioning

confidence: 99%

The Effect of Hypocarbia on the Cardiovascular System of Puppies

et al. 1984

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“…4 ( n = 18): Brain energy metabolism was measured at 4 MAC of sevoflurane (10.4%, end-expired) under normocapnia (Exp. 4a) ( n = 9), and rCBF was also assessed (Exp.…”

Section: Methodsmentioning

confidence: 99%

Erratum

1994

Acta Anaesthesiol Scand

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ErratumIn: FUJIBAYASHI T, SUCIURA Y, YANAGIMOTO M, HARADA J, GOTO Y. Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations. Acta Anaesthesiol Scand 1993: 37: [806][807][808][809][810]. Tables 1-3 were inadvertently omitted and we are therefore reprinting the entire article.Brain energv metabolism and blood flow during The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo-and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (3'P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco, of 2.7 kPa with 2 MAC of sevoflurane (goo/, of the control), and at a Paco, of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when Paco, was $2.7 kPa with 2 MAC of sevoflurane and 54.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco, of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism. Received 28 August 1992, accepted for publication 7 April 1993Key words: Anesthesia, experimental: cat; brain: cerebral blood flow, energy metabolism; hypocapnia; nuclear magnetic resonance spectroscopy; pharmacology: halothane, sevoflurane.High concentrations of halothane exert influences on brain energy metabolism (1) which are different from those caused by isoflurane (2) and thiopental (3). Under normocapnia, no volatile anesthetics at comparatively low concentrations (up to 2 MAC) cause deterioration of brain energy metabolism. In the non-anesthetized state, hypocapnia itself also has 0 Acta Anaesthesiologica Scandinavica 38 (1994) no effect on brain energy metabolism (4) although CBF decreases to some degree. However, it still remains to be clari...

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“…7,8 In addition, hypocapnia induces a further reduction in CBF, eg, resulting in a 43% CBF decrease at a PaCO 2 level of 19 mm Hg. 9 Patients under mechanical ventilation during anesthesia are likely to experience hypocapnic conditions, and deliberate hyperventilation to reduce the intracranial pressure (ICP) is common in neuroanesthesia for patients with a brain tumor or cerebral hemorrhage. Therefore, we hypothesized that such a decrease in PaCO 2 may be critical, especially in the elderly and/or in stroke patients.…”

mentioning

confidence: 99%

Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion

Miyamoto

Tomimoto

Nakao

et al. 2001

Stroke

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Background and Purpose-Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. Methods-Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Klüver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. Results-The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. Conclusions-These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia. (Stroke. 2001;32: 2920-2925.)

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Effects of extremes of respiratory and metabolic alkalosis on cerebral blood flow in man.

Cited by 109 publications

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The Effect of Hypocarbia on the Cardiovascular System of Puppies

The Effect of Hypocarbia on the Cardiovascular System of Puppies

Erratum

Caudoputamen Is Damaged by Hypocapnia During Mechanical Ventilation in a Rat Model of Chronic Cerebral Hypoperfusion

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