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

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.
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PMID:Local mechanism of CO2 action of cat pial arterioles. 1 34

The authors report the values of mean hemispheric blood-flow and cerebral arterial consumption they found in 34 neurosurgical comatous cases in acute state. In basal conditions, mean values of mean hemispheric bloodflow and oxygen consumption are lowered. There seems to be a relation between the values found and the comatous stage on one hand, the prognosis on the other hand. The cerebral response to hypercapnia (16 assays) allows to separate 2 groups, one with a noticeable improvement of cerebral bloodflow, the other with only a minimal response. There was no significant variation of cerebral oxygen consumption in both group. Cerebral response to CO2 seems to be clearly related to the stage of coma (low in the most severe cases) but pronostic incidence remained uncertain. A hypertensive test by means of Aramine (18 assays) allows to separate 3 groups : 1 group (8 cases) where the mean hemispheric bloodflow remained stable during hypertension as did the cerebral oxygen consumption -(autoregulation remained unchanged), 1 group (4 cases) where mean hemispheric bloodflow and cerebral oxygen consumption were lowered (excessive autoregulation), 1 group (6 cases) where mean hemispheric bloodflow increases clearly while under Aramine perfusion (loss of autoregulation). Those dynamic tests, either hypercapnic or hypertensive, allow, in comparing oxygen consumption variations with cerebral bloodflow variations, the distinction between : patients where metabolic autoregulation seems maintained (good prognosis) - (10 cases), patients where metabolic regulation is lost with either "luxury perfusion" (14 cases) - poor prognosis, or "insufficient perfusion" (10 cases). The authors are discussing the treatment concerning those last mentioned patients.
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PMID:[Value of cerebral metabolic exploration in post-traumatic coma states in the acute phase]. 1 86

CSF HCO3- increases more than plasma HCO3- in hypercapnia, and there are at least two sources for the CSF HCO3- increase--one derived from the simultaneous increase in plasma HCO3-, and the other, HCO3-formed from hydration of CO2 in the choroid plexus and glia and susceptible to inhibition by acetazolamide (J. Appl. Physiol. 38: 504-512, 1975). It was proposed that the H+ formed in the CNS in CO2 hydration is actively exchanged for plasma Na+ utilizing the Na-K ATPase pump. H+ transport from the CNS was therefore studied in four groups of dogs breathing 5% CO2 at constant VA for 4 h with repeated injections of saline, acetazolamide 5 mg/ml, ouabain 0.1 mg/ml, and acetazolamide and ouabain together into lateral cerebral ventricles. Arterial HCO3-increased 2.5 meq/l at 4 h of hypercapnia in all groups. CSF HCO3-increased 5.8 meq/l in the saline-injected animals, but it increased only about 2 meq/l and equaled plasma HCO3- rise in the other three groups. Therefore CNS HCO3- formation in hypercapnia can be blocked by inhibiting the CO2 hydration reaction with acetazolamide or by blocking H+ removal by inhibiting Na-K ATPase with ouabain. The data support the thesis of active H+ removal from the CNS in exchange for plasma Na+ in hypercapnia.
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PMID:H+ transport from CNS in hypercapnia and regulation of CSF [HCO3-]. 1 62

1. Blood O2 transport and acid-base balance were studied at 20 degrees C in rainbow trout (Salmo gairdneri) which had been kept in water of high CO2 content (15 mmHg) for at least a week. Also the blood gas chemistry of fish rapidly entering or leaving the hypercapnic environment was studied. 2. Fish entering high CO2 water suffered a sharp decrease in blood pH which significantly reduced O2 transport by the blood, but after a few hours considerable compensation was achieved. 3. After at least a week in high CO2 water, trout showed elevated plasma bicarbonate and PCO2 levels, and a decrease in plasma chloride, while pH was about 0 - 1 pH unit below the level for control fish. Oxygen transport by the blood was marginally reduced. 4. Hypercapnic fish rapidly entering fresh water showed a sharp increase in blood pH and a decrease in blood PO2. These parameters regained normal values after a few hours but plasma bicarbonate and chloride levels took much longer to regain control concentrations. 5. Acid-base balance in hypercapnic fish is discussed with particular reference to the role of the branchial ion exchanges.
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PMID:Blood respiratory properties of rainbow trout (Salmo gairdneri) kept in water of high CO2 tension. 1 48

The cooling of rats under conditions of hypercapnia and hypoxia during the first 15 minutes increases the contents of free fatty acids, acetoacetate and beta-oxybutyrate in the tissues of the brain, myocardium, liver, skeletal muscles and blood and decreases them by the end of the effect (120 min later) down to the initial values, in the liver and skeletal muscles tissues the content of the mentioned intermediates falls lower the initial values. In the carbohydrate metabolism the amount of phosphoenolpyruvate 15 and 120 min after the action beginning and the amount of malate in the myocardium and brain at the end of the experiment increase to a different extent; the content of lactate rises only in the brain 30 and 120 min after the beginning of cooling. In the rat venous blood the value of pCO2 increases up to 71.8+/-6.0 mm Hg, the total content of CO2 rises, the values of the standard bicarbonates decrease and the pH value drops sharply down to 6.98+/-0.03. It is suggested that one of the main reasons of such changes in metabolism is development of hypercapnia state and acidosis and the resulted increase in intensity of the carboxylation processes in the tissues.
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PMID:[Changes in lipid and carbohydrate metabolism in rat tissues under combined effect of hypercapnia, hypoxia and cooling]. 1 64

The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
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PMID:Mechanisms of hypercapneic pulmonary hypertension. 2 1

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.
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PMID:Contribution of a net transmembrane HCO3- flux to intracellular acid-base regulation. 2 30

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.
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PMID:The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1. 2 69

Thirteen adult rabbits were exposed to a breathing air mixture containing an increasing amount of CO2 for eight weeks. When the CO2 content reached 9 Vol% the animals became apathic and lost body weight. The EEG showed a reduction of the amplitudes of 1o Hz frequences. Blood gases revealed an increase of bicarbonate but no change of pH. The blood brain barrier which was tested when the animals were killed was not disturbed. Enzyme histochemistry, light and electron microscopy revealed that moderate brain edema had occurred. From these results it is concluded that chronic hypercapnia has a hypnotic effect which in combination with chronic edema may depress vital activities considerably. However, there seem to be no irreversible morphological alterations of the brain.
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PMID:The effect of prolonged experimental hypercapnia on the brain. 2 57

Using a 14C-labeled DMO, 36Cl and 3H method, we have determined the in vivo buffering capacity of lung, kidney, heart, skeletal muscle, and extracellular fluid (ECF) of guinea pigs during hypercapnia (FICO2 = 0.15). After 1 days' exposureto 15% CO2, both the relative CO2 buffer values (delta HCO3/deltapH) and the "%pH regulation" were lung greater than kidney greater than heart greater than ECF greater than skeletal muscle. For lung tissue the intracellular pH was significantly decreased only during acute (8 h) hypercapnia and had completely returned to control values after 7 days with arterial PCO2 congruent to 122 Torr. Kidney and cardiac muscle also showed ca. 100% regulation of pH at 7 days, whereas skeletal muscle and ECF showed only 80 and 70% pH regulation, respectively. The results are discussed with respect to the important (and pH-dependent) metabolic functions of the lung and kidney.
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PMID:Regulation of intracellular pH in lungs and other tissues during hypercapnia. 2 85


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