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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Four human subjects exercised in hypoxia (end-tidal partial pressure of O2 (P(ET),O2) ca 55 Torr; heart rate ca 100-130 beats min-1), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus. 2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3.5 Torr (at nearly constant P(ET),O2) and PO2 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-P(ET),CO2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method. 3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72% of the total gain following steps of P(ET),CO2 during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise. 4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3.5 and 9 s respectively) and to the central chemoreflex pathways (ca 9.5 and 47 s respectively) are some of the shortest reported. 5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other. 6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.
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PMID:Dynamics of the ventilatory response in man to step changes of end-tidal carbon dioxide and of hypoxia during exercise. 129 45

We tested the hypothesis that differential sympathetic innervation explains the attenuated cerebral blood flow (CBF) response to hypercapnia (hyper) in fore-brain (fb) compared with brain stem in 1- to 2-wk-old piglets. In pentobarbital sodium-anesthetized piglets, CBF (microspheres) was measured during hypocapnia, normocapnia (normo), and hypercapnia [arterial CO2 partial pressure (PaCO2) of 25, 40, and 65 mmHg, respectively] in random sequence. After pretreatment values were obtained, piglets were randomized to undergo sham treatment (n = 5), high cervical spinal cord transection (n = 6), or pharmacological alpha-adrenergic blockade (prazosin 1 mg/kg + yohimbine 1 mg/kg, n = 6). After each experimental treatment, CO2 reactivity was again measured. Before experimental manipulation, hypercapnic reactivity [(CBFhyper - CBFnormo)/(PaCO2hyper - PaCO2normo)] in brain stem was approximately three times greater than in forebrain (e.g., sham; 3.6 +/- 0.8 vs. 1.2 +/- 0.3 ml.min-1.100 g-1.mmHg-1). Hypercapnic reactivity in forebrain was not increased by cord transection (1.4 +/- 0.3 vs. 1.1 +/- 0.2 ml.min-1.100 g-1.mmHg-1) or alpha-blockade (1.6 +/- 0.6 vs. 1.2 +/- 0.4 ml.min-1.100 g-1.mmHg-1). Likewise, hypercapnic cerebral vascular resistance (CVR) was unchanged by experimental treatment (e.g., CVRfb; cord transection 1.1 +/- 0.1 vs. 1.0 +/- 0.1; alpha-blockade 1.1 +/- 0.2 vs. 1.0 +/- 0.1 mmHg.ml-1.min-1.100 g-1). Hypocapnic vasoconstriction, however, was attenuated by both cord transection and alpha-blockade in forebrain and brain stem. We conclude that physiological stimulation of the noradrenergic component of the sympathetic nervous system does not explain regional differences in CBF reactivity during hypercapnia in 1- to 2-wk-old piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercapnic blood flow reactivity not increased by alpha-blockade or cordotomy in piglets. 135 31

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

In order to estimate the role of peripheral chemosensitivity in dyspnea sensation, we performed BH experiment under the acute or chronic hypoxic condition. The former was simulated by a given rate (0-3.2 mg/kg/hr) of doxapram infusion. The latter experiment was carried out during sojourn in Lhasa (3700 m), China. Subjects conducted BH by inhaling 7% CO2 in O2 and assessed dyspnea sensation by visual analog scale (VAS) while repeatedly measuring PCO2 at breaking point (BP). Lowering of resting PETCO2 by augmented ventilation was derived by doxapram infusion and during acclimatization at high altitude. The effect of PCO2 on VAS was enhanced by doxapram. However, altitude acclimatization resulted in attenuated effect of PCO2 on VAS despite of further development of hypocapnia. The rate of PCO2 elevation during doxapram infusion was reduced and it might be attributed to decreased body storage of CO2. On the other hand, its rate was tended to recover to sea level value after acclimatization at high altitude and it may have cancelled the mitigated dyspnea sensation. Thus, BHT almost comparable period in both acute hypoxia and during altitude acclimatization. These results suggest that CO2 storage in the body contributes to modify dyspnea sensation as well as augmented peripheral chemosensitivity.
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PMID:[Dyspnea sensation and chemical control of breathing]. 140 63

Ketanserin, a 5HT2- and alpha 1-receptor antagonist, decreases blood pressure by decreasing systemic vascular resistance without causing reflex cardiac stimulation, while cardiac output remains unchanged. To date, little is known about the effects of ketanserin on cerebral haemodynamics and cerebral metabolism. According to a recently published study, ketanserin seems not to impair cerebral blood flow autoregulation in man. The present study was designed to investigate the influence of ketanserin on cerebral circulation and metabolism, and the cerebrovascular response to CO2 in man. METHODS. Twenty male patients between 44 and 67 years of age who were scheduled for coronary artery bypass surgery were randomly allocated to one of two groups. In group 1 measurements were performed after induction of anaesthesia during normocapnia (p(a) CO2 approximately 40 mm Hg) and hypocapnia (p(a) CO2 approximately 30 mm Hg). Then, ketanserin was given at a bolus dose of 0.3 mg.kg-1 followed by an infusion of 0.06 mg.kg-1.h-1 and measurements were repeated under hypocapnic and normocapnic conditions. Patients of group 2 were hyperventilated at first, then normoventilated. Afterwards, ketanserin was administered at the above-mentioned dose and measurements were again performed during normocapnia and hypocapnia. Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral perfusion pressure (CPP) was calculated by subtracting jugular bulb pressure from mean arterial pressure and cerebral vascular resistance (CVR) by dividing CPP by CBF. Cerebral metabolic rates of oxygen, glucose, and lactate were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. RESULTS AND DISCUSSION. Ketanserin decreased CPP by 16% to about 60 mm Hg. Cerebral blood flow remained unchanged as a result of an insignificant decline in CVR. Hyperventilation increased CVR by 32%, while CBF decreased by 27% to the same value that had been obtained during hypocapnia without ketanserin. The percentage changes in CBF per mm Hg change in CO2 were 1.45%/mm Hg (group 1 and 2.91%/mm Hg (group 2), respectively, without ketanserin and 1.98%/mm Hg and 2.22%/mm Hg with ketanserin. As CO2-responsiveness with ketanserin was higher in group 1 but lower in group 2 than without ketanserin, the direction in which ventilation was changed rather than ketanserin was responsible for these changes in CO2-responsiveness. Neither during normocapnia nor during hypocapnia did ketanserin have any effects on cerebral metabolic activity. Thus, it can be concluded that ketanserin does not impair CBF regulation and metabolism and that cerebral vascular responsiveness to hypocapnia is preserved.
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PMID:[Cerebral effects of ketanserin. The influence on hemodynamics and brain metabolism]. 144 11

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. 144 39

The oxygen-binding properties of Hb molecule are unchanged in the third trimester of normal pregnancy and in pregnancy complicated by slight iron-deficiency anemia. Hb affinity to oxygen in whole blood is formed under the effect of the three main ligands H+, CO2, and 2,3-DPH. The development of hypocapnia in pregnant women results in elevation of pH values, reduction of pCO2, increase of intraerythrocytic 2,3-DPH concentration by 15-18%. Variously directed effects of H+, CO2, and 2,3-DPH on Hb affinity to O2 result in normal P50 values and therefore the Hb-O2 dissociation curve is not shifted to the right. Thus, in pregnant women with alkalosis 2,3-DPH effect on Hb affinity to oxygen completely eliminates H+ and CO2 effects but not compensates for Hb deficiency in the blood.
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PMID:[Status of the oxygen transport system of hemoglobin in physiological pregnancy and pregnancy complicated by iron deficiency anemia]. 147 17

Forty adult patients with acute severe asthma were assessed for arterial blood gases and acid-base changes at presentation at the Casualty Unit, Kenyatta National Hospital, Nairobi, Kenya. Marked degrees of hypoxaemia (mean P(a)O2 of 8.02 kP(a)), hypocapnia (mean P(a)CO2 of 4.62kP(a)) with apparently normal pH (mean 7.384) were documented in the majority of these patients. Based on these findings, a significant number of the patients (68.5%) were either candidates (5.3%) or potential candidates (63.2%) for artificial ventilation. Records at this hospital suggest an increasing trend in asthma admissions and mortality. Additionally, Intensive Care Unit (ICU) admissions for asthma are associated with high mortality (54.4%). Pulsus paradoxicus emerged as the most significant (p = 0.002) clinical correlate to asthma severity. Central cyanosis was detected in none of the study patients suggesting that it is an unusual finding in the common presentation of acute severe asthma at this hospital. Its clinical detection would therefore imply an ominous clinical state. It is recommended that clinicians should take every opportunity to adequately assess their asthma patients before prescribing medications. They are also encouraged to more frequently request for blood gas studies in acute asthma. Those in charge of clinical teaching should direct appropriate efforts towards improved understanding of the pathophysiology and interpretation of acid-base disorders.
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PMID:Arterial blood gases and acid-base status of adult patients presenting with acute severe asthma at Kenyatta National Hospital, Nairobi. 150 18

Very low arterial CO2 tension (PaCO2) experienced by birds during high-altitude flight may result in cerebral vasoconstriction and reduced cerebral O2 delivery. To examine this possibility, we measured regional cerebral blood flow (CBF) and tissue PO2 in pentobarbital-anesthetized geese (Anser domesticus). Twenty-five-micrometer Teflon-coated platinum electrodes for H2-clearance measurements of local blood flow or tissue PO2 were implanted in the cerebral cortex in 11 geese. Tissue H2 and O2 were measured by voltage clamping the electrodes at +0.30 and -0.5 V, respectively. Washout kinetics of H2 gas administered via unidirectional lung ventilation was used to calculate local blood flow for those electrodes exhibiting one- or two-compartment washout kinetics of H2 (128 of 296 washouts in 31 electrodes). PaCO2 was controlled between 8 and 55 mmHg by altering pulmonary gas flow or by adjusting inspired PCO2. CBF decreased as PaCO2 fell from 50 to 20 mmHg but did not decrease further as PaCO2 was reduced below 20 mmHg. CBF was uniformly distributed in different regions of the cortex. Despite the plateau in CBF during severe hypocapnia, tissue PO2 continued to decline as PaCO2 fell below 20 mmHg. Severe alkalosis may limit cerebral O2 delivery in birds during high-altitude flight.
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PMID:Regional cerebral blood flow and tissue oxygenation during hypocarbia in geese. 151 Jan 62

Carbon dioxide (CO2) has been well documented to act as a potent vasodilator of coronary vessels under normal conditions. But there is little data available on the effect of CO2 on the collateral perfusion of patients with coronary insufficiency. We studied the effects of CO2 on the myocardial tissue PO2 in anesthetized dogs with critical coronary stenosis. Twelve mongrel dogs were anesthetized with pentobarbital and ventilated with 100% O2 to maintain normocapnia. Electromagnetic blood flow (BF) probe was applied on the left anterior descending artery (LAD). Regional myocardial PO2 was measured at two different sites using two pairs of monopolar polarographic needle electrodes; one inserted in the epicardial (EPI) layer, and the other in the endocardial (ENDO) layer. These were placed in the regions supplied by LAD and circumflex. Following the baseline recording, critical stenosis of LAD was produced by adjusting a copper-wire clamp occluder until LADBF was reduced by 50%. After a stable normocapnic ventilation, hypocapnia was produced by hyperventilation. To induce hypercapnia, exogenous CO2 was added to the inspired gas stepwise until end-tidal CO2 fraction reached 10%. Hypocapnia resulted in a significant reduction in myocardial PO2 in both EPI and ENDO non-stenotic areas, while hypercapnia increased these PO2 values dose-dependently. After coronary stenosis, hypocapnia resulted in a small but significant reduction of PO2 in endocardial ischemic area. Hypercapnia did not induce any sign of reduced regional myocardial PO2 or evidence of regional or intramural "steal" phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of carbon dioxide (hypocapnia and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary stenosis]. 155 62


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