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

The effect of oxygen saturation and PCO2 on brain uptake of glucose analogues was studied in rabbits. Using a modified Oldendorf technique, 14C-labeled glucose analogues with a 3H2O reference standard were introduced into the cerebral circulation via the common carotid artery, and the radioactivity of the ipsilateral cerebral cortex was counted and expressed in terms of a brain uptake index (BUI). Severe hypoxia (oxygen saturation less than or equal to 18%) resulted in approximately a 40% decrease in the BUI of 2-deoxy-D-glucose and a 45% decrease in the BUI of 3-0-methyl-D-glucose. Severe hypercapnia (PCO2 = 100 mm Hg) caused a 45% decrease in the BUI of both of these glucose analogues. Hypercapnia superimposed on severe hypoxia had no additional effect. Hypocapnia (PCO2 = 15 mm Hg) increased the BUI of 3-0-methyl-D-glucose by 35% of the control value, and this increase was extremely sensitive to competitive inhibition. When BUI values were plotted against pH rather than PCO2 for the same experiments, there was a good correlation with the calculated linear regression. These results are compared with previous findings on pathologically induced changes in brain uptake of glucose analogues, and the possible role of blood flow is considered in detail.
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PMID:Effects of oxygen saturation and pCO2 on brain uptake of glucose analogues in rabbits. 0 Aug 21

This study was designed to determine the effect of methylprednisolone on the profile of hepatic oxygen supply and selected blood parameters in fasted, male rats administered an LD85 dosage of E coli endotoxin intraperitoneally. Mortality rates within 24 hours were 85% in rats receiving endotoxin only, 9% in rats receiving a 30 mg/kg dosage of methylprednisolone intraarterially one hour subsequent to endotoxin insult, and 0% in methylprednisolone controls. Beginning with the fourth hour, untreated endotoxin rats had significantly higher heart rates and lower plasma glucose; by the sixth or eighth hour there was significantly greater hypocapnia, lower blood pH, and higher plasma lactate levels in comparison to endotoxic rats receiving methylprednisolone. In addition, mean hepatic pO2 between the sixth and seventh hours was 2.6 mm Hg in endotoxic rats, 10.6 mm Hg in endotoxic methylprednisolone rats, and 17.7 mm Hg in methylprednisolone controls. Methylprednisolone controls showed a steady increase of plasma glucose levels through eight hours but were otherwise stable. Maintenance of hepatic circulation is cited as the probable basis for differences of morbidity and mortality between treated and glucocorticoid-treated endotoxic rats.
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PMID:The effect of methylprednisolone on hepatic oxygen supply and plasma lactate and glucose in endotoxemia. 4 Jul 7

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.
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PMID:Effect of hyperventilation on dynamics of cerebral energy metabolism. 23 2

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95

Total cerebral blood flow and oxidative cerebral metabolism were measured at normal pCO2, hypocapnia and hypercapnia in 15 unconscious patients in the acute phase after head trauma. In the basal position (normal CO2) measurements were within normal limits and did not correspond to the severity of the clinical picture. But on altering arterial pCO2 there were market changes in oxidative cerebral metabolism, which suggests an abnormal cerebral regulatory mechanism. Measurement of the same functions 14 days later indicated, on the one hand, persistence of changes, but, on the other, a return to normal of previously markedly elevated cerebral glucose uptake. Comparing cerebral blood flow and metabolism between patients who survived and those who died in the acute phase after brain damage, there were no significant differences.
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PMID:[Changes in cerebral blood flow and oxidative cerebral metabolism after extensive acute head trauma (author's transl)]. 112 47

Ketanserin, a 5HT2- and alpha 1-receptor antagonist, decreases blood pressure by decreasing systemic vascular resistance without causing reflex cardiac stimulation, while cardiac output remains unchanged. To date, little is known about the effects of ketanserin on cerebral haemodynamics and cerebral metabolism. According to a recently published study, ketanserin seems not to impair cerebral blood flow autoregulation in man. The present study was designed to investigate the influence of ketanserin on cerebral circulation and metabolism, and the cerebrovascular response to CO2 in man. METHODS. Twenty male patients between 44 and 67 years of age who were scheduled for coronary artery bypass surgery were randomly allocated to one of two groups. In group 1 measurements were performed after induction of anaesthesia during normocapnia (p(a) CO2 approximately 40 mm Hg) and hypocapnia (p(a) CO2 approximately 30 mm Hg). Then, ketanserin was given at a bolus dose of 0.3 mg.kg-1 followed by an infusion of 0.06 mg.kg-1.h-1 and measurements were repeated under hypocapnic and normocapnic conditions. Patients of group 2 were hyperventilated at first, then normoventilated. Afterwards, ketanserin was administered at the above-mentioned dose and measurements were again performed during normocapnia and hypocapnia. Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral perfusion pressure (CPP) was calculated by subtracting jugular bulb pressure from mean arterial pressure and cerebral vascular resistance (CVR) by dividing CPP by CBF. Cerebral metabolic rates of oxygen, glucose, and lactate were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. RESULTS AND DISCUSSION. Ketanserin decreased CPP by 16% to about 60 mm Hg. Cerebral blood flow remained unchanged as a result of an insignificant decline in CVR. Hyperventilation increased CVR by 32%, while CBF decreased by 27% to the same value that had been obtained during hypocapnia without ketanserin. The percentage changes in CBF per mm Hg change in CO2 were 1.45%/mm Hg (group 1 and 2.91%/mm Hg (group 2), respectively, without ketanserin and 1.98%/mm Hg and 2.22%/mm Hg with ketanserin. As CO2-responsiveness with ketanserin was higher in group 1 but lower in group 2 than without ketanserin, the direction in which ventilation was changed rather than ketanserin was responsible for these changes in CO2-responsiveness. Neither during normocapnia nor during hypocapnia did ketanserin have any effects on cerebral metabolic activity. Thus, it can be concluded that ketanserin does not impair CBF regulation and metabolism and that cerebral vascular responsiveness to hypocapnia is preserved.
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PMID:[Cerebral effects of ketanserin. The influence on hemodynamics and brain metabolism]. 144 11

With a level of hypoglycemia (1-1.5 mM) that does not alter cerebral O2 uptake and glucose uptake in dogs, induction of hypocapnia may cause severe electroencephalographic (EEG) abnormalities. The aim of this study was to determine the effect of hypoglycemia (blood glucose = 1.1 +/- 0.1 mM) and hypocapnia (arterial PCO2 = 15 +/- 1 mmHg) on cerebral ATP, phosphocreatine, and intracellular pH (pHi; 31P magnetic resonance spectroscopy), cerebral blood flow (CBF; radiolabeled microspheres), global O2 uptake, and glucose uptake in anesthetized dogs. Neither hypoglycemia nor hypocapnia alone altered brain high-energy phosphates, pHi, O2 or glucose uptake or caused major EEG abnormalities. Hypocapnia alone decreased CBF to 62 +/- 4% of control. The combination of hypoglycemia and hypocapnia did not decrease CBF (85 +/- 6% of control), and O2 and glucose uptake were unchanged. During hypocapnic hypoglycemia, isoelectric EEG was seen in 40% of animals, ATP and phosphocreatine decreased to 38 +/- 12 and 43 +/- 12% of control, respectively, while pHi increased from 7.13 +/- 0.05 to 7.43 +/- 0.09. The increase in pHi was related reciprocally to the decrease in venous PCO2, indicating little change in intracellular bicarbonate concentration ([HCO3-]i). With normoglycemic hypocapnia, in contrast, estimated [HCO3-]i decreased 57 +/- 1%. These data suggest that active regulation of pHi during normoglycemic hypocapnia is impaired during hypoglycemic hypocapnia associated with decreased ATP.
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PMID:Hypocapnic-hypoglycemic interactions on cerebral high-energy phosphates and pH in dogs. 148 10

Sufentanil, a synthetic opioid that is 5-10 times as potent as fentanyl, has been suggested for use during neurosurgical procedures because it maintains cardiovascular stability and produces hypnosis without the use of additional anesthetic agents. Doses as low as 2.5 micrograms.kg-1 are reported to create deep levels of anesthesia as demonstrated by EEG changes to high-amplitude delta-waves. However, there are no reports concerning the effects of sufentanil on blood flow and metabolism in the human brain. The present study was designed to investigate the influence of high-dose sufentanil-O2 anesthesia on the cerebral circulation, metabolism, and the cerebrovascular response to CO2 in man. METHODS. Nine male and 2 female patients between 41 and 60 years of age who were scheduled for coronary artery bypass surgery were studied. Premedication consisted of flunitrazepam 2 mg orally and piritramide 15 mg and promethazine 50 mg i.m. 1 h before arrival in the induction room. Measurements were performed with the patients awake (I), after sufentanil 10 micrograms.kg-1 as an induction dose followed by 0.15 micrograms.kg-1.min-1 as an infusion with normocapnia (pa CO2 42.1 +/- 2 mmHg) (II), during hypercapnia (pa CO2 53.7 +/- 3.5 mmHg) (III), and during hypocapnia (pa CO2 31.7 +/- 2 mmHg) (IV). Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral metabolic rates of oxygen (CMRO2) glucose (Mgluc) lactate (CMlac) were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. The Anaerobic Index was calculated from the equation avD lactate x 100/2 x avD glucose = ANI (%) Cerebral electrical activity was recorded by aperiodic analysis of the EEG (Lifescan). RESULTS AND DISCUSSION. In the EEG sufentanil anesthesia was characterized by a decrease in the number of high-frequency waves and an increase in the number and amplitude of delta-waves, a pattern that did not change throughout the study period. Concomitantly, under normocapnic conditions high-dose sufentanil led to the significant decrease in CBF by 29% accompanied by an 18% increase in cerebral vascular resistance (CVR). CMRO2 decreased by 22% while CMRgluc and CMRlac changed only insignificantly such that the ANI, which represents the percentage of anaerobically metabolized glucose, essentially remained unchanged. Mean perfusion pressure declined by 18% but stayed within the range of autoregulation. Hypoventilation (III) was followed by an 82% increase in CBF as a result of a 55% reduction in CVR, whereas cerebral metabolic parameters did not show important changes when compared to measurement II. Hyperventilation (IV), on the other hand, produced a distinct fall in CBF by 56% to a value that was 21% below the one obtained under normocapnia. This was due to an increase in CVR of the same magnitude. There was a 31% rise in CMRO2, resulting in a decrease in cerebral venous oxygen tension, but in no case did it fall below the critical value of 20 mmHg at which tissue hypoxia becomes severe. Although CMRlac increased and CMRgluc did not significantly change, the ANI remained essentially unchanged, which suggests a predominantly aerobic metabolism. The increase in metabolic activity with sufentanil during hypocapnia might be caused by an alkalosis-induced stimulation of glycolysis. It might also be related to a reduction in the depth of anesthesia, although neither the EEG nor the hemodynamic parameters indicated this. This study shows that the coupling between CBF and metabolism is well maintained and that the cerebrovascular response to CO2 is unimpaired during high-dose sufentanil anesthesia.
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PMID:[The effect of sufentanil on cerebral blood flow, cerebral metabolism and the CO2 reactivity of the cerebral vessels in man]. 182 62

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
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PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37

Hypocapnia and induced hypotension have been claimed by some to cause cerebral hypoxia because of insufficient perfusion. Regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCMRglc) were measured simultaneously in the same animal subjected to hypocapnia or hypocapnia combined with induced arterial hypotension. The rCMRglc was measured with (3H) deoxyglucose and the rCBF with (14C) iodoantipyrine with the use of tissue biopsy methods and scintillation counting. Nineteen male Wistar rats were anesthetized with halothane and artificially ventilated. Anesthesia was maintained with nitrous oxide/oxygen (70:30) and succinylcholine. Six rats were maintained at normocapnia, six rats were ventilated to a PaCO2 of 20 mmHg, and seven animals were ventilated to PaCO2 20 mmHg combined with arterial hypotension of 50 mmHg (mean blood pressure) induced by infusion of adenosine. Although hypocapnia alone did not cause a statistically significant decrease of rCBF except in hippocampus, hypocapnia combined with hypotension resulted in a significant reduction of rCBF in four of seven regions when compared with hypocapnia alone; rCMRglc values were unchanged during hypocapnia. However, the addition of hypotension induced by adenosine led to a significant decline of glucose utilization in five of seven brain regions. In the present study the authors observed no increase of regional glucose utilization and hence no signs of cerebral ischemia during hypocapnia alone or combined with hypotension induced by adenosine.
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PMID:Regional cerebral blood flow and glucose utilization during hypocapnia and adenosine-induced hypotension in the rat. 249 11


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