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

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
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PMID:Acidosis induced by hypercapnia exaggerates ischemic brain damage. 811 21

The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMRO2) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; non-diabetic acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 +/- 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 micrograms/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 +/- 0.3, 14.9 +/- 2.5, 3.3 +/- 0.8, and 13.3 +/- 0.7 mM, respectively, at control. The corresponding baseline CMRO2 levels were 2.8 +/- 0.2, 3.0 +/- 0.2, 4.1 +/- 0.4, and 4.0 +/- 0.3 ml O2.100 g-1 x min,1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 +/- 3, 50 +/- 3, 51 +/- 3 vs. 36 +/- 1 ml x 100 g-1 x min-1) and cerebrovascular resistance was lower (2.24 +/- 0.15, 2.51 +/- 0.14, 2.38 +/- 0.21 vs. 3.35 +/- 0.18 mmHg.ml-1 x 100 g.min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs. 847 84

The present article is concerned with mechanisms which are responsible for the exaggerated brain damage observed in hyperglycemic animals subjected to transient global or forebrain ischemia. Since hyperglycemia enchances the production of lactate plus H+ during ischemia, it seems likely that aggravation of damage is due to exaggerated intra- and extracellular acidosis. This contention is supported by results showing a detrimental effect of extreme hypercapnia in normoglycemic rats subjected to transient ischemia or to hypoglycemic coma. Enhanced acidosis may exaggerate ischemic damage by one of three mechanisms: (i) accelerating free radical production via H(+)-dependent reactions, some of which are catalyzed by iron released from protein bindings by a lowering of pH, (ii) by perturbing the intracellular signal transduction pathway, leading to changes in gene expression or protein synthesis, or (iii) by activating endonucleases which cause DNA fragmentation. While activation of endonucleases must affect the nucleus, the targets of free radical attack are not known. Microvessels are considered likely targets of such attack in sustained ischemia and in trauma; however, enhanced acidosis is not known to aggravate microvascular dysfunction, or to induce inflammatory responses at the endothelial-blood interface. A more likely target is the mitochondrion. Thus, if the ischemia is of long duration (30 min) hyperglycemia triggers rapidly developing mitochondrial failure. It is speculated that this is because free radicals damage components of the respiratory chain, leading to a secondary deterioration of oxidative phosphorylation.
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PMID:Molecular mechanisms of acidosis-mediated damage. 878 Jul 90

The clinical effects of sevoflurane, isoflurane, and halothane anesthesia with or without nitrous oxide, were compared in healthy, premedicated cats breathing spontaneously during 90 minutes of anesthesia. The effect of nitrous oxide in accelerating the induction of and recovery from anesthesia was more evident for halothane than for sevoflurane or isoflurane. The cats recovered more rapidly from sevoflurane-oxygen than from either halothane- or isoflurane-oxygen. Heart rates did not significantly change during anesthesia with any of the anesthetics. Arterial blood pressures during sevoflurane-oxygen anesthesia were somewhat higher than those with either isoflurane- or halothane-oxygen. There were no significant differences in arterial blood pressures among sevoflurane, isoflurane, and halothane anesthesia when combined with nitrous oxide. The respiration rate during sevoflurane-oxygen was similar to that during halothane-oxygen. There were no significant differences in respiration rate among sevoflurane, isoflurane, and halothane anesthesia when combined with nitrous oxide. The degree of hypercapnia and acidosis during sevoflurane anesthesia was similar to that observed during isoflurane anesthesia and less than during halothane anesthesia. The three anesthetic regimens, with or without nitrous oxide, induced a similar degree of hyperglycemia and hemodilution during anesthesia. Serum biochemical examination did not reveal any hepatic or renal injuries after each anesthesia.
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PMID:Comparisons of sevoflurane, isoflurane, and halothane anesthesia in spontaneously breathing cats. 901 9

We investigated the influence of hyperoxia (arterial pO2 446 +/- 43 mmHg) and hyperglycemia (blood glucose 19.4 mmol/l) on somatosensory stimulation (whisker deflection) employing laser Doppler flowmetry (LDF). Our aim was to test the hypothesis that a possible substrate-sensing mechanism for glucose and oxygen contributes to the coupling between cortical activity and regional cerebral blood flow (rCBF) in order to match increased demand with substrates. In addition, we looked at the influence of hyperglycemia (blood glucose 17.9 mmol/l) and hypercapnia (arterial pCO2 62 mmHg) on rCBF (LDF) and regional cerebral blood oxygenation changes (rCBO) in the even stronger metabolic stimulus of cortical spreading depression (CSD). For the latter we employed the new non-invasive technique of near infrared spectroscopy (NIRS). All experiments were done using chloralose/urethane-anesthetized rats. Somatosensory stimulation increased rCBF by about 20% of baseline, in the case of both norm- and hyperoxia as well as both normo- and hyperglycemia. The blood-flow response to CSD consisted of a temporary sharp increase in rCBF to more than 400%. At the same time, the concentration of oxyhemoglobin [HbO2] increased, while deoxyhemoglobin [Hb] decreased, indicating excessive oxygenation. Hyperglycemia altered neither the rCBF nor the rCBO response. Preexisting hypercapnia, however, produced reductions in both hyperperfusion (rCBF) and hyperoxygenation (rCBO) during CSD. We found that, for experimental hyperglycemia, i.v. may be superior to i.p. application of glucose because of the latter's side effects in connection with blood flow. Our findings cannot support the hypothesis of a substrate sensing mechanism in coupling.
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PMID:Excessive oxygen or glucose supply does not alter the blood flow response to somatosensory stimulation or spreading depression in rats. 925 28

Preischemic hyperglycemia or superimposed hypercapnia exaggerates brain damage caused by transient forebrain ischemia. Because high regional levels of brain-derived neurotrophic factor (BDNF) protein correlate with resistance to ischemic damage, we studied the expression of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, hyperglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA in dentate granule cells was attenuated and that in CA3 pyramidal neurons completely prevented in hyperglycemic rats. No ischemia-induced increases of BDNF mRNA levels in the hippocampal formation were detected in hypercapnic animals. Hyperglycemic and hypercapnic rats showed transiently decreased expression of BDNF mRNA levels in the cingulate cortex, which was not observed in normoglycemic animals. The results suggest that suppression of the BDNF gene might contribute to the increased vulnerability of the CA3 region and cingulate cortex in hyperglycemic and hypercapnic animals.
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PMID:Hyperglycemia and hypercapnia suppress BDNF gene expression in vulnerable regions after transient forebrain ischemia in the rat. 939 29

Metabolic complications from overfeeding critically ill patients are serious and sometimes fatal. Nutrition care is best provided through repeated evaluation of patients' responses to feeding. Nutrition support may need to be modified over time to maintain metabolic stability and promote recovery. This article describes the etiology of 10 metabolic complications of overfeeding. Guidelines for recommending macronutrients are discussed, as are factors that could increase the risk of overfeeding. Patients who are very small, very large, or very old are particularly vulnerable to overfeeding. Overfeeding protein has led to azotemia, hypertonic dehydration, and metabolic acidosis. Excessive carbohydrate infusion has resulted in hyperglycemia, hypertriglyceridemia, and hepatic steatosis. High-fat infusions have caused hypertriglyceridemia and fat-overload syndrome. Hypercapnia and refeeding syndrome have also been caused by aggressive overfeeding. Dietitians can prevent or curtail the metabolic complications of overfeeding by identifying patients at risk, providing adequate assessment, coordinating interdisciplinary care plans, and delivering timely and appropriate monitoring and intervention. Dietitians need to document complications, interventions, and the outcomes of their clinical care to evaluate the appropriateness of existing nutrition guidelines.
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PMID:Overfeeding macronutrients to critically ill adults: metabolic complications. 966 22

Some metabolic and endocrine effects of hypercapnia were studied in six ponies during halothane anaesthesia with neuromuscular blockade and controlled ventilation. Each was anaesthetised twice, once with a 40-minute-period of hypercapnia (10 kPa) and once when normocapnia (5.3 kPa) was maintained throughout two hour's anaesthesia. Routine cardiovascular monitoring was performed and blood samples were taken for assay of cortisol, insulin, glucose, lactate, muscle and liver enzymes and total protein. Anaesthesia induced hypotension and lacticacidaemia which were slightly ameliorated during hypercapnia. Hyperglycaemia was more marked during hypercapnia. Plasma cortisol increased in a similar manner in both groups and insulin tended to decrease. There were no major changes in the other variables measured. It was concluded that 40 minutes of hypercapnia during halothane anaesthesia in ponies may have improved perfusion and did not markedly alter the stress response.
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PMID:Effects of hypercapnia on endocrine and metabolic responses to anaesthesia in ponies. 976 71

The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF.
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PMID:Hyperglycemia and focal brain ischemia. 1007 81

Systemic hyperglycemia and hypercapnia severely aggravate ischemic brain damage when instituted prior to cerebral ischemia. An aberrant cell signaling following ischemia has been proposed to be involved in ischemic cell death, affecting protein kinase C (PKC) and the calcium calmodulin kinase II (CaMKII). Using a cardiac arrest model of global brain ischemia of 10 min duration, we investigated the effect of hyperglycemia (20 mM) and hypercapnia (pCO(2) 300 mmHg) on the subcellular redistribution of PKC (alpha, beta, gamma) and CaMKII to synaptic membranes and to the microsomes, as well as the effect on PKC activity. We confirmed the marked translocation of PKC and CaMKII to cell membranes induced by ischemia, concomitantly with a decrease in the PKC activity in both the membrane fraction and cytosol. Hyperglycemia and hypercapnia markedly enhanced the translocation of PKC-gamma to cell membranes while other PKC isoforms were less affected. There was no effect of acidosis on PKC activity, or on translocation of CaMKII to cell membranes. Our data strongly suggest that the enhanced translocation of PKC to cell membranes induced by hyperglycemia and hypercapnia may contribute to the detrimental effect of tissue acidosis on the outcome following ischemia.
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PMID:Acidosis enhances translocation of protein kinase C but not Ca(2+)/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia. 1059 93


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