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

Five healthy males took part in two separate studies. In one study subjects breathed air (control, C) and in the other 5% CO2 in 21% O2 (respiratory acidosis, RA). Measurements were made at rest, during exercise at 30 and 60% maximal O2 uptake (VO2 max), (20 min each) and in recovery. RA was associated with higher arterial CO2 partial pressure (PCO2) and bicarbonate and lower pH than C. The increase with exercise in plasma lactate (mmol . l-1) was less in RA than C from 1.0 +/- 0.15 (SE) (C = 1.1 +/- 0.17) at rest to 5.3 +/- 1.25 (C = 6.8 +/- 0.98) at 60% VO2 max (P less than 0.10). Plasma pyruvate, alanine, and glycerol concentrations increased with exercise; free fatty acids did not change. There were no significant differences between RA and C in any of these metabolites. Norepinephrine concentrations were similar at rest but increased to a greater extent during exercise in RA than C (P less than 0.02). Epinephrine levels were also higher in RA than C at 60% VO2 max (NS); the two subjects in whom lactate was not lower with RA showed the greatest increase in epinephrine. Exercise in RA was associated with higher heart rates (P less than 0.05), blood pressures (NS), and ventilation (P less than 0.01). In hypercapnia the metabolic effects of acidosis are modified by increased levels of circulating catecholamines.
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PMID:Effect of respiratory acidosis on metabolism in exercise. 681 26

In anesthetized cats, under perfusion and with constant volume of the hemodynamically isolated brain, hypercapnia and hypoxia led to a decrease of cerebral vessels resistance and to a reduction of the brain blood flow, whereas a decrease in the PCO2 and an increase in the PO2 in the blood exerted on opposite effect. The different responses of the vessels had some similar features in respect to threshold changes of the PCO2 and PO2, to potentiation of effects of both parts of the brain vascular system on increased shifts of the blood gas tension, to greater sensitivity of both parts to PCO2 changes, to effect of the blood gas tension on reactivity of both parts to noradrenaline. The authors suggest a possibility of alterations of the filter-absorption interrelationships in the brain due to different responses of arterial and venous vessels to changes of the blood gas tension.
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PMID:[Conjunct changes in the resistance and engorgement of the cerebral vessels in shifts in the blood gas composition]. 681 50

In view of the fact that diazepam has been shown to prevent an increase in catecholamine synthesis and/or turnover rates in stressful situations, and to modify the cerebral metabolic (and circulatory) response to hypoxia and hypercapnia, the influence of the drug on synthesis rates of DOPA and 5-HTP in three regions of the rat brain were studied under normoxic-normocapnic conditions, as well as in hypoxia and hypercapnia. In order to exclude a modifying influence of variations in tissue pO2 during hypercapnia, cerebral venous pO2 was kept at control values by moderate arterial hypoxia. When compared to the control state (paralyzed animals maintained on 70% N2O) normoxic and normocapnic animals given diazepam (in the absence of N2O) showed a slightly enhanced DOPA synthesis in limbic structures and reduced 5-HTP synthesis in limbic structures and striatum. In hypoxia, the drug considerably curtailed DOPA synthesis in limbic structures and striatum but had no effect on synthesis rate in cortex. The drug also appeared to exaggerate the generalized reduction in 5-HTP synthesis observed under 70% N2O. In hypercapnia, diazepam reduced the enhanced rate of DOPA synthesis (observed under 70% N2O) in striatum but left that in the cortex unchanged. The drug prevented the hypercapnia-induced increase in 5-HTP synthesis, observed under 70% N2O. It is concluded that diazepam significantly alters dopamine and serotonin synthesis in hypoxia and hypercapnia. Probably an indirect action, perhaps related to the stress-alleviating effect of diazepam, is involved. The results suggest that the effect of the drug on cerebral metabolic rate and blood flow in hypoxia and hypercapnia is unrelated to changes in noradrenaline synthesis or turnover. Furthermore, although the results demonstrate that diazepam modulates dopamine metabolism in hypoxia and hypercapnia it seems questionable that this influence can explain the metabolic and circulatory effects of diazepam in these conditions.
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PMID:Effect of diazepam on cerebral monoamine synthesis during hypoxia and hypercapnia in the rat. 681 96

Pial arterial vessels were inspected in hypercapnia (PaCO2 97 +/- 9 (S.E.) mmHg) and in acute hypertension induced by 5 microgram kg-1 noradrenaline i.v. (mean arterial pressure 210 +/- 5 mmHg) by means of a cranial window. The diameter of arterial vessels with a resting diameter of 10 to 150 micrometer was measured either from photographs or by aid of an image splitting eyepiece. Arterioles with a resting diameter less than or equal to 30 micrometer exhibited the highest degree of dilatation both in hypercapnia and acute hypertension. The mean dilatation was higher in hypertension than in hypercapnia in vessels of all sizes, the difference being statistically significant in arterioles up to 50 micrometer resting diameter.
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PMID:Dilatation of pial arterial vessels in hypercapnia and in acute hypertension. 744 69

Hypercapnia induces initial constriction and prolonged relaxation of rat small mesenteric arteries. The mechanism of the relaxation is unknown, but has been attributed to lowering of pHi in the vascular smooth muscle. In this study we have investigated the response to raised PCO2 at constant pHo, in mesenteric small arteries precontracted with noradrenaline. 10% CO2 led to a fall in pHi associated with acute potentiation of tension, and subsequent relaxation. The relaxation did not occur in arteries in which the endothelium had been removed, nor in arteries pretreated with the nitric oxide synthase inhibitor, L-NAME (10(-4)M, NG-nitro-L-arginine methyl ester). The D-enantiomer, D-NAME, was without effect. We conclude that hypercapnic-induced vasodilatation in this circulation occurs via endothelium derived nitric oxide production.
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PMID:Carbon dioxide induced vasorelaxation in rat mesenteric small arteries precontracted with noradrenaline is endothelium dependent and mediated by nitric oxide. 768 47

Dopamine (DA) and noradrenaline (NA) were measured in the rabbit carotid body (CB) in vitro bv HPLC-ED under the following experimental conditions: 1h superfusion in normoxic, hypoxic (10% O2 in N2) or hypercapnic (8% CO2, 20% O2, 72% N2) medium, 5h superfusion in normoxia or hypoxia. The contents of DA and NA were decreased by hypoxia and hypercapnia after 1 h and 5h indicating a possible DA and NA secretion. Under the same experimental conditions synthesis of DA and NA and catabolism of DA were studied with enzymatic inhibition of tyrosine hydroxylase and monoamine oxidase (MAO) respectively. In hypoxia (1 h and 5h) the rate constant of DA synthesis was the same as in normoxia; however NA synthesis was decreased after 1 h hypoxia. On the contrary, hypercapnia, appeared to be a very effective stimulus of DA and NA synthesis.
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PMID:Dopamine metabolism in the rabbit carotid body in vitro: effect of hypoxia and hypercapnia. 810

1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2-5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12-0.94) nmol/l and of adrenaline was 0.15 (0.05-0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2-3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12-0.86) nmol/l] or that of adrenaline [0.16 (0.05-0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6-13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79-2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20-2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.
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PMID:Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man. 838 37

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.
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PMID:Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse. 852 55

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.
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PMID:Recent insights into the regulation of cerebral circulation. 880 May 65

The purpose of the present study was to determine the effect of various types of acidosis on vessel diameter, intracellular pH (pHi), and calcium concentration ([Ca2+]i) in a cannulated preparation of the mesenteric arteriole of the rabbit. The effect of acidosis on vessel contraction was also studied in the wire-mounted preparation. In the cannulated preparation, pre-contracted by noradrenaline, hypercapnia caused vasoconstriction and increases in [Ca2+]i. In the wire-mounted preparation pre-contracted by either noradrenaline or high KCl, hypercapnia caused a transient vasoconstriction. In contrast, in the cannulated preparation pre-contracted by high KCl, hypercapnia caused a transient vasorelaxation and decreases in [Ca2+]i. Intracellular acidosis, induced by a NH4Cl prepulse, caused vasoconstriction and increases in [Ca2+]i even in the cannulated preparation pre-contracted by high KCl. The decrease in pHi during hypercapnia was similar to that observed after NH4Cl withdrawal. These data suggest that: (1) the effect of acidosis on vascular tone and [Ca2+]i is different depending upon the type of preparation and the mode of pre-activation, and (2) [Ca2+]i may, at least partly, regulate vascular contraction and relaxation during acidosis.
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PMID:Effect of acidosis on contraction, intracellular pH and calcium in the rabbit mesenteric small artery. 887 81


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