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

Guinea pigs and rats exposed to 15% CO2 for 7 days showed a parallel time course of changes in pH, body temperature (TB), and oxygen consumption (VO2). Between 1 and 6 h of exposure the maximal drop in actual pH occurred in guinea pigs simultaneously with the maximal fall in TB and VO2. During the subsequent period pH TB, VO2 rose again. Skin blood content (heat loss) also exhibited a biphasic pH-dependent time course. Animals showing no partial compensation of respiratory acidosis during 3 days exposure also failed in raising their TB back to normal in this time. The behavior of TB was found to be a good indicator of the acid-base status and adaptive potential of the animals to hypercapnia. Similar results were obtained in rats. Thermo-regulatory processes in the hypothalamus were affected during exposure to 15% CO2. Both guinea pigs and rats showed a decrease in norepinephrine content of the hypothalamus during the first part of exposure reaching a maximal fall at the end of 24 h. The serotonin content increased slightly during this period. During prolonged exposure to 3% CO2 for 7 days, TB showed a transient rise, and VO2 was slightly elevated.
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PMID:Effect of chronic hypercapnia on body temperature regulation. 23 76

The effects on hemoglobin oxygen transport of acute respiratory acidosis have been studied in dogs inhaling a gaseous mixture with 12% CO2 (O2 21%) for two to five hours. In a first series of experiments, it was shown that the shape of the oxyhemoglobin dissociation curve (ODC) was not modified by severe acidosis (pH congruent to 7) lasting for two and a half hours. The Hill number (N equals 2.6) did not change significantly. The aim of the second experimental series was to stuey the Bohr effect and the hemoglobin oxygen affinity (P50). The control value for the respiratory Bohr coefficient (B) was --0.54; neither after two hours (--0.52), nor after five hours of hypercapnia (--0.55) was it significantly modified. The P50 expressed at arterial pH was much increased in acidosis (congruent to 45 torr); when expressed at standard p/ 7.4, it was slightly but significantly decreased (congruent to 1 torr) at the fifth hour. At the same time there was a decrease (p smaller than 0.05) in the erythrocyte 2,3-DPG approaching 15 p. cent; on the other hand the ATP concentration did not change significantly. No significant individual correlation was found between P50(7.4), 2,3-DPG and mean hemoglobin corpuscular concentration. These results suggest that during severe respiratory acidosis neither a change in the shape of ODC, nor a change in Bohr effect do affect the hemoglobin oxygen transport. The main characteristic remains the decrease in oxygen affinity of hemoglobin, due to the erythrocyte [H+] increase induced by hypercapnia ; this phenomenon is observed as long as the 2,3-DPG decrease stays moderate.
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PMID:[Hemoglobin oxygen transport during experimental acute hypercapnia (author's transl)]. 23 80

During acute hypercapnia (5% carbon dioxide) in resting conscious dogs, ventilation (Ve) attained a new level above control within 5 min, but rectal temperature decreased gradually to reach a steady state lower than control after 40-60 min. At 2 days of breathing 5% carbon dioxide, Ve remained elevated, as in acute hypercapnia, but Paco2 increased and the threshold of the ventilatory response shifted to a higher Paco2. By 2 days of hypercapnia, rectal temperature (Tr) had returned to normal, reflecting an alteration of hypothalamic temperature control that might be expected to result in enhanced respiratory drive. Surprisingly, despite blood acid-base compensation between 2 and 14 days of hypercapnia, Ve did not decrease, whereas Paco2 decreased to the level observed during acute hypercapnia, and the threshold of the ventilatory response returned to normal. Therefore, at 14 days of respiratory acidosis, acid-based compensation resulting from increase in bicarbonate was not associated with reduced respiratory drive. This result could not be accounted for on the basis of a temperature mechanism because temperature adaptation occurred earlier.
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PMID:Body temperature and ventilatory responses to CO2 during chronic respiratory acidosis. 43 17

Direct assessment of tracheal circumference, which permits evaluation of constriction and dilatation in vivo, was made continuously in intact, pentobarbital-anesthetized, spontaneously breathing dogs. Immediate response to induction of hypercapnia included tracheal constriction and cessation of normal, vagus-dependent rhythmicity of airway tone. The characteristic constrictor response to acetylcholine was exaggerated significantly during hypercapnic acidosis and returned to normal when arterial pH, but not CSF pH, was corrected by NaHCO3 infusion. Epinephrine produced significant tracheal dilatation (infrequently followed by constriction) and isoproterenol produced only dilatation at normal pH. The catecholamine-induced dilatation was decreased significantly during hypercapnic acidosis, but improved after NaHCO3 infusion. Responses to acetylcholine and epinephrine were the the same as control during alkalemia, whereas the response to isoproterenol was unexplainedly diminished. Thus alkalemia may inhibit the action of isoproterenol; acidemia enhances parasympathomimetic constriction and reduces sympathomimetic dilatation; and correction of arterial pH returns these responses to normal, even if hypercapnia and CSF acidosis persist.
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PMID:Arterial pH, airway caliber and response to acetylcholine and catecholamines in vivo. 50 32

Net base and mineral balances were evaluated in a group of male 350 g Wistar rats exposed to 10% carbon dioxide in air for 10 days with a view to identifying the source of net base subject to retention during renal compensation of sustained respiratory acidosis. In response to hypercapnia, the rate of renal net acid excretion rose but insignificantly. However, a rise in whole body net base concentration from about 215 mmol/kg to about 250 mmol/kg came about by ongoing gastrointestinal absorption in the weight-losing animal, absorbed net base being distributed to extracellular and non-extracellular compartments of the body, presumably including bone. During an 8-day recovery period, a small decrement in whole body net base concentration was observed.
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PMID:Balance of net base in the rat: adaptation to and recovery from sustained hypercapnia. 53 94

A retrospective analysis of 811 patients admitted to the hospital for status asthmaticus over a nine-year period was performed. Eight patients died, and 19 required mechanical ventilation. All persons who died of status asthmaticus were in the group that required mechanical ventilation. In 12 of the patients who received ventilation, no definite cause for the acute exacerbation could be identified, although initial arterial blood gas analyses showed profound hypoxemia, hypercapnia, and acute respiratory acidosis. Seventy-eight major complications occurred during mechanical ventilation. Pneumothorax, endotracheal tube malfunction, alveolar hypoventilation on the ventilator, and pneumonia were associated with decreased survival. Mucous plugging of the airways was found in all autopsied patients. Mechanical ventilation in status asthmaticus is a life-support system associated with substantial morbidity and should be instituted only when it becomes evident that maximal medical therapy will not be efficacious.
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PMID:Status asthmaticus. A nine-year experience. 57 61

24 subjects with chronic obstructive pulmonary disease were investigated in the course of acute respiratory failure defined by hypoxaemia, hypercapnia and respiratory acidosis. Haemodynamic data of right heart catheterization and coagulation tests were particularly studied. 12 of these subjects had right heart failure defined by a rise of right ventricular end-diastolic pressure above 10 Torr. Coagulation tests brought evidence of consumption coagulopathy in 8 patients, 7 of whom had right heart failure. Data suggest a significant correlation between right heart failure and coagulation disorders in patients with acute exacerbation of chronic obstructive pulmonary disease. These disturbances, accompanied by reduction of pulmonary vascular area, could be in part related to the presence of microthrombi in pulmonary arterial vessels.
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PMID:[Haemodynamic data, blood gas measurements and coagulation disorders in acute respiratory failure of patients with chronic lung disease (author's transl)]. 67 57

An electron microscope study of the left ventricular myocardium from rat acclimatized to chronic hypercapnia was done in order to complete the preceding work concerning general effects of respiratory acidosis. After 15 and 30 days of the acclimatation to 8% CO2 no lesions of the myocardium could be found. The results of the morphometric analysis indicated, however, discrete modifications of heart ultrastructure similar to those found before in hypoxic and failing hearts: namely a decrease of mitochondrial mean diameter and a non significant decrease of mitochondrial fractional volume. The latter was accompanied by a significant decrease of myofibrillar mass. The presence of cellular oedema seems to be suggested by an increase of fractional volume of the cytosol. The mechanism of these changes is not easy to explain. Further work will be necessary to make a choice between two possibilities: (1) depressed contractility related to some direct effect of high pCO2 and (2) tissue hypoxia secondary to local effects of the former.
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PMID:[The rat ventricular myocardium in chronic hypercapnia. Electron microscopic study]. 77 46

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7


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