Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the possibility that changes of cerebral extracellular pH (PH e) or adenosine concentration may provide coupling mechanisms of a general nautre, adjusting cerebral blood flow (CBF) to metabolic demands. Although there is considerable indirect evidence that CBF varies inversely with pHe, results obtained during the last few years indicate that large increases in flow may occur in the absence of a fall in pHe. Thus, induction of hypoxia or epileptic seizures leads to maximal increase in CBF before pHe falls or even when there is initial alkalosis due to concomitant hypocapnia. Furthermore, CBF increases in hypoglycaemia and after administration of amphetamine, two conditions unassociated with tissue acidosis. The possibility that adenosine may be a coupling factor was examined in hypoxia and during epileptic seizures in rats. In both conditions a four- to fivefold increase in CBF occurs in spite of the fact that tissue adenosine concentrations remain at or below 1 mumolkg-u. It is concluded that adenosine accumulates first when there is a perturbation of cerebral energy state with a rise in AMP concentration. It seems unlikely that adenosine, formed by breakdown of AMP, acts as a general coupling factor.
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PMID:Coupling of cerebral metabolism and blood flow in epileptic seizures, hypoxia and hypoglycaemia. 2 37

This article attempts correlating changes in cellular energy metabolism, acid-base alterations, and ion homeostasis in ischemia and other conditions. It is emphasized that loss of ion homeostasis, with thermodynamically downhill fluxes of K+, Ca2+, Na+, Cl-, and H+, occurs because energy production fails and (or) ion conductances are increased. In ischemia, energy failure is the leading event but, in hypoglycemia, activation of ion conductances is what precipitates energy failure. The initial event is a rise in K+ e, at least in part caused by activation of K+ conductances modulated by Ca2+ or ATP/ADP ratio. Secondarily, this leads to release of excitatory amino acids and massive activation of unspecific cation (and anion) conductances. Production of H+ occurs in states characterized by energy failure (ischemia and hypoxia) or by alkalosis (hypocapnia and ammonia accumulation). H+ equilibrates between intra- and extra-cellular fluid via nonionic diffusion of lactic acid, and transmembrane fluxes of H+ or HCO3- via ion channels. Since the relationship between lactate and either pHi or pHe is linear, there are no abrupt pH shifts explaining why hyperglycemia worsens ischemic damage. The reversible insults seem to induce a sustained stimulation of H+ extrusion from cells giving rise to intracellular alkalosis and extracellular acidosis.
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PMID:Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. 128 29

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

Epileptogenic complications after supratentorial intracranial surgery are, strictly defined, the events which promote a further complication, i.e. seizures in any form, partial, simple or complex, or generalized. The most common epileptogenic complications are, therefore, electrolyte imbalance, hypoxia, hypoglycemia, hypocapnia, and intracerebral or extradural hematoma. However, also inadequate anticonvulsant prophylaxis and use of convulsant drugs can yield to the onset of post-operative seizures. Anesthetic drugs have been each time defined pro or anti-convulsant: however, data from the literature show that it is not possible to certainly define the role of general anesthetics in the genesis of post-operative seizures.
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PMID:[Epileptogenic complications of neurosurgical interventions]. 162 Apr 64

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.
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PMID:Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity. 249 46

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

We investigated the in vivo changes in cerebral energy metabolism and pHi in newborn mice noninvasively during 8 h of hypoxia with FiO2 = 5%, using phosphorus magnetic resonance spectroscopy continuously. The intracellular brain pH (pHi) increased from 7.20 +/- 0.03 to 7.36 +/- 0.03 (P < 0.05) at 1 h of hypoxia and then decreased gradually. On the other hand, the mixed arterial and venous blood pH decreased gradually during hypoxia, reaching a minimum value of 7.16 +/- 0.01 at the end of the hypoxia. There was no significant difference in PCO2 between control (47.4 +/- 0.8 mm Hg) and 1-h hypoxic (49.0 +/- 1.1 mm Hg) mice. The blood glucose concentration was significantly increased at 1 h of hypoxia. These results indicate that the alkaline shift in pHi during hypoxia was caused neither by systemic alkalosis due to hypocapnia nor hypoglycemia.
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PMID:Intracellular alkalosis during hypoxia in newborn mouse brain in the presence of systemic acidosis: a phosphorus magnetic resonance spectroscopic study. 750 87

Moderate hypoglycemia (MH) may be associated with blunting of cerebral hypocapnic vasoconstriction. Coincident with this change, electroencephalogram (EEG) flattening occurs. Previous reports show that brain extracellular potassium activity ([K+]o) increases in association with the onset of isoelectricity during severe hypoglycemia and that K+ increases cause pial vessel vasodilation. Using a model of MH, we tested the hypothesis that increases in [K+]o (approximately 15 mM) correlate with blunting of cerebral hypocapnic vasoconstriction. Cerebral blood flow (CBF), [K+]o, and EEG were measured during normocapnia [arterial Pco2 (Paco2) = 35 Torr)] and hypocapnia (PaCO2 = 15 Torr) in MH (< 2 mM) and normoglycemic dogs. During MH, increases in [K+]o occurred in association with EEG flattening (from 4.2 +/- 0.5 to 13.8 +/- 3.8 mM). During normoglycemia and MH without [K+]o elevations, hypocapnic vasoconstriction occurred. [K+]o elevations with MH were associated with increased CBF and decreased vascular resistance (146 +/- 5 and 42 +/- 2% of control, respectively) during normocapnia, and blunting of cerebral hypocapnic vasoconstriction (93 +/- 16% normocapnic control) when [K+]o increased during hypocapnia. This study shows that increases in [K+]o during MH are necessary for both normocapnic increases in CBF and blunting of cerebral hypocapnic vasoconstriction. Increases in [K+]o may represent a mechanism for decreases in cerebral vascular resistance during MH.
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PMID:Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs. 832 5

We tested the hypothesis that severe insulin-induced hypoglycemia would depress cerebrovascular reactivity to CO2 via a mechanism that could be prevented by administration of the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 in infant piglets. Cerebral blood flow (CBF) was measured (microspheres) in 2- to 3-wk-old pentobarbital-anesthetized piglets during hypocapnia, normocapnia, and hypercapnia. Repeat CBF measurements were made either 1 (n = 5) or 2 h (n = 6) after insulin (200 U/kg iv) to elicit the time course of altered reactivity to CO2. Repeat CBF measurements were made in a third group (n = 5) 2 h after treatment with insulin and MK-801 (1.5 mg/kg iv bolus, 0.15 mg.kg-1.h-1 iv infusion) to determine whether any alteration in reactivity to CO2 was due to a mechanism involving the NMDA receptor. Cerebrovascular resistance and cerebral O2 consumption (CMRO2) were calculated with each measurement of CBF. Cerebrovascular response to CO2 (change in cerebrovascular resistance/change in arterial CO2 tension) was ablated in the group of piglets exposed to 1 or 2 h of hypoglycemia (preinsulin 1-h group, 0.038 +/- 0.007; preinsulin 2-h group, 0.023 +/- 0.004 mmHg.ml-1.min.100 g.mmHg CO2(-1)). Treatment with MK-801 did not alter normoglycemic CO2 reactivity (preinsulin, 0.032 +/- 0.005 mmHg.ml-1.min.100 g.mmHg CO2(-1)) and did not prevent ablation of cerebrovascular CO2 reactivity during hypoglycemia. CMRO2 was not affected by hypoglycemia in any group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:MK-801 does not prevent impaired cerebrovascular reactivity to CO2 during hypoglycemia in piglets. 832 42


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