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

In order to test the relationship between changes in plasma potassium concentration and pH changes of respiratory origin, we produced hypercapnia (mean PaCO2 71 mmHg = 9.5 kPa) in a group of 17 patients and hypocapnia (mean PaCO2 21 mmHg = 2.8 kPa) in another 20 patients during neurolept analgesia and intraabdominal operations. A control group of 19 patients was studied under normocapnia but otherwise identical conditions. During hypercapnia, serum potassium rose, deltaK/deltapH amounting to -0.82, -1.05 and -1.34 after 30, 60 and 90 min, respectively. During hypocapnia, serum potassium decreased, deltaK/deltapH being a little more negative than during hypercapnia (mean values -1.62, -2.44 and -1.60). Red cell potassium concentration decreased in all three groups to a similar extent. Blood lactate levels during hypercapnia decreased to 75% of control and during hypocapnia rose to a maximum of 186% of control. In order to obtain reasonable values for base excess in primarily respiratory acid-base disorders, it is necessary to use nomograms based on in vivo ECF-CO2-titration curves. With this premise, hypercapnia or hypocapnia in our patients was not associated with significant changes in base excess.
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PMID:Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia. 3 56

Continuous tissue pH and intermittent central arterial pH were measured in six rabbits during 10-min exposures to a mixture of 10% CO2 and 90% O2. In control and recovery situations tissue pH was more acidic than arterial pH by a mean value of 0.07 pH units. During periods of rapidly increasing pCO2, the steady state relationship was inverted with tissue pH being more alkaline than arterial pH. After a second exposure to CO2, mean tissue pH values did not recover to baseline. It is concluded that in the rabbit during acute hypercarbia, the relationship of tissue to central pH is variable. The possible implications of these results in human fetuses during labor are discussed.
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PMID:The relationship between tissue and arterial pH in hypercarbic rabbits. 3 19

In 29 cats, the extent and time-course of the pial arterial reactions to hypo- and hypercapnia were studied by means of the skull-window technique. The typical, well-known dilatations and constrictions during hyper- and hypocapnia were seen. The latent period for dilatation after the beginning of CO2-inhalation was ca. 20 sec. There was no stable relation observable between vessel diameter and arterial carbon dioxide tension (paCO2). Diameter changes lagged behind CO2-changes, indicating that CO2 acts via metabolic regulation, probably extracellular pH.
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PMID:Pial arterial reactions to hyper- and hypocapnia: a dynamic experimental study in cats. 3 9

The effects of different dosages of methadone on respiration were determined by evaluating arterial blood pCO2, pO2 and pH in naive and opioid-addicted animals. Male Sprague-Dawley rats were treated (i.p.), acutely or chronically, with either 2.5, 5.0 or 7.5 mg/kg of dl-methadone hydrochloride; appropriate saline controls were utilized. Blood was sampled from the tail artery before injection and 15, 30, 60, 120, 180 and 240 min postinjection. Animals exposed to methadone in acute experiments exhibited a respiratory depression that involved hypoxemia, hypercapnia and/or acidosis. In addition, the magnitude of this respiratory depressant action was dose-dependent and reached a maximal point 15 to 30 min after drug administration. Rats receiving chronic methadone exposure showed few alterations from control blood gas concentrations and pH. This study demonstrates that acute methadone administration is associated with respiratory depression, with the extent of reductions in pCO2, pO2 and pH related to drug dosage. In addition, chronic methadone treatment confers a substantial tolerance to the respiratory depressant action of methadone.
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PMID:Acute and chronic methadone exposure in adult rats: studies on arterial blood gas concentrations and pH. 3 7

Intramuscular tissue pO2, pCO2, and pH were monitored distal to a pneumatic tourniquet in a dog hindleg preparation. A severe state of tissue hypoxia, hypercarbia, and acidosis was quantitated. The recovery time for tissue gases following release increased with increasing tourniquet time. Elevated c.p.k. and lactic acid values were noted at 2 hours of ischemia, reflecting the muscle changes at that time. Histologic sections revealed early signs of degeneration by 1 hour which progressively increased with increased tourniquet ischemia. On the basis of this study, we conclude that ischemia should not exceed 1 to 1 1/2 hours if significant pathophysiologic tissue changes are to be avoided. If longer time is required, intermittent release of the tourniquet for 10 minutes at the end of each hour of inflation will avoid complications.
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PMID:Pathophysiologic effects distal to a tourniquet in the dog. 3 19

Thirty monkeys were exposed to controlled systemic hypotension of different magnitudes and duration to determine factors leading to brain injury or cardiovascular failure. Fourteen monkeys developed brain injury. Of these, 6 survived indifinitely and 8 were sacrificed or died within 12-62 hours due to neurologic deterioration accompanied by respiratory failure. Sixteen animals did not develop brain injury, but 9 of these died within 24 hours from documented cardiovascular failure with the remaining 7 survived indefinitely. A highly reproducible threshold for the development of brain injury was found at a mean arterial blood pressure (MABP) of 25 mm Hg. Maintenance MABP was less than or equal to 25 mm Hg in 13 of 14 lesioned monkeys and greater than 25 mm Hg in 15 of 16 non-lesioned monkeys. Maintenance MABP averaged 20.1 +/- 1.1 mm /g in lesioned and 32.1 +/- 1.7 mm Hg in non-lesioned animals (p less than 0.001). Among the non-lesioned animals, death from delayed cardiovascular failure ensued when MABP was maintained between 27 and 35 mm Hg for 90 min or longer. Animals exposed to this range of hypotension for less than 90 min or to MABP exceeding 35 mm Hg for as long as 3 h survived intact. EEG changes occurring during hypotension most accurately predicted neurologic outcome. The threshold MABP required to produce cerebral electric silence was 21-22 mm Hg. Monkeys developing marked brain injury had greater than 25 minutes of EEG flattening, while slightly injured animals had it for 5-15 minutes and those without injury for less than 5 min. Changes in acid-base state, common carotid artery blood flow, and cerebral uptake of glucose and oxygen during hypotension also correlated with neurologic and cardiovascular outcome. Hypoxemia and hypercarbia were not contributory factors in the production of brain injury in this study.
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PMID:Neurologic and cardiovascular effects of hypotension in the monkey. 3 62

The cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) in the rat during normocapnia and hypercapnia were investigated by means of the intraarterial 133Xenon injection technique; measurements were performed during normocapnia and hypercapnia and the effect of propranolol upon CBF and CMRO2 was studied. The CBF technique applied to rat yield reliable results even in high flow situations. A steady state period of only 10--15 s is all that is necessary to obtain the initial slope of the 133Xenon clearance curve from which CBF is calculated and measurements may be repeated within minutes. Hypercapnia caused an increase in CMRO2 of 35% which confirms the findings of other investigators. The beta-adrenergic receptor blocker propranolol (2 mg per kg i.v.) prevented this increase and could eliminate an increase in CMRO2 already induced; this indicates that CO2 affects adrenergic mechanisms. Although propranolol eliminated the CMRO2 response to hypercapnia, it only reduced the CBF response; this dissociation of CBF and CMRO2 response occurred probably because the beta-receptor blockage only eliminated a CBF increase mediated through an increased CMRO2 (cellular response) whereas a direct CO2 effect upon the arterioles (vascular response) persisted.
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PMID:The effect of propranolol on cerebral oxygen consumption and blood flow in the rat: measurements during normocapnia and hypercapnia. 3 22

We studied 129 patients during acute, severe asthmatic attacks. Electrocardiograms showed P pulmonale in 49% of patients who had an arterial carbon dioxide tension (PaCo2) greater than or equal to 45 mm Hg and an arterial pH less than or equal to 7.37, whereas P pulmonale was present in only 2.5% of asthmatics who had a PaCO2 less than or equal to 44 mm Hg and a pH greater than or equal to 7.38 (p less than 0.001). P wave and QRS axes were 79 +/- 8 degrees and 80 +/- 20 degrees, respectively, in the presence of P pulmonale. When P pulmonale disappeared, the P wave and QRS axes shifted significantly to the left (p less than 0.001). Electrocardiographic P pulmonale persisted 12 to 60 hr after correction of hypoxemia, hypercapnia, and acidosis. In 7 patients with P pulmonale and respiratory acidosis, cardiac catheterization demonstrated normal artery pressures (PAPs) measured relative to atmospheric pressure. In 12 of these peak inspiratory pulmonary artery transmural pressures (PATPs) were increased. Since increased right heart transumural pressures could result in chamber distention, these data are consistent with the hypothesis that reversible P pulmonale in status asthmaticus is explainable on the basis of markedly negative tidal pleural pressures and increased right heart transmural pressures.
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PMID:P pulmonale in status asthmaticus. 3 21

The effect of a changed atmosphere, hypoxia, hypercapnia, their combinations and different motor activities on the adrenocortical function was studied in 36 test subjects kept in an 8 m3 altitude chamber. Human adaptation to the environmental changes developed with an active involvement of the adrenal cortex. The level and direction of the changes depended on both the force of the influences and on the initial state of the test subjects.
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PMID:[Effect of sealed chamber conditions on the functional state of the human adrenal cortex (based on data from a study of the 11-hydroxycortico-steroid content in the blood plasma)]. 3 70

An electromagnetic flow meter was used to assess the changes in coronary blood flow in response to four levels of increased PaCO2 in six dogs. Mean, diastolic and systolic flow all increased during hypercapnia, the increase being maximal at mean PaCO2 11.3 KPa. Mean and diastolic coronary vascular resistances decreased progressively as PaCO2 increased, but systolic resistance, although decreasing with the lower levels of hypercapnia, returned to control at the greatest PaCO2. Although the oxygen available to the myocardium was increased markedly during hypercapnia, coronary sinus PO2 increased also, reflecting a reduction in myocardial oxygen extraction; thus myocardial oxygen consumption was unchanged. Cardiac output was increased significantly only at the greatest PaCO2. Total body oxygen handling was not altered significantly.
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PMID:Response of mean and phasic coronary arterial blood flow to graded hypercapnia in dogs. 3 65


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