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

The normal ventilatory response to the sudden imposition of sustained hypoxia is characterized by an acute increase followed by a modest decline in ventilation. Since subanesthetic concentrations of potent inhalational anesthetics greatly attenuate the acute response, we hypothesized that ventilation might decrease to less than normoxic levels when hypoxia is sustained. We therefore measured the ventilatory response to 20 min of sustained hypoxia (PETO2 45 mmHg) at two levels of strict isocapnia--normocapnia (PETCO2 1-2 mmHg above resting) and hypercapnia (PETCO2 49 mmHg)--in eight healthy male subjects during inhalation of 0.1 MAC isoflurane or carrier gas (control). An abrupt end-tidal step from normoxia to isocapnic hypoxia was induced using a dynamic end-tidal forcing system. Isoflurane and control experiments were performed on separate days; the order of isoflurane and control days and the order of normocapnia and hypercapnia within days were randomized. Subjects were studied while fasted, always at the same time of day, and were required to watch a documentary videotape to minimize differences in level of consciousness. With normocapnia, there was no difference in ventilation at any time between isoflurane and control (prehypoxic 9.6 +/- 1.5 vs. 9.5 +/- 2.6 1/min, peak hypoxic 24.7 +/- 10.4 vs. 26.2 +/- 10.4 1/min, final hypoxic 15.0 +/- 4.4 vs. 15.9 +/- 3.5 1/min; mean +/- SD). With hypercapnia, prehypoxic ventilation increased to the same level for isoflurane and control (24.8 +/- 6.7 vs. 24.8 +/- 9.6 1/min). Although peak hypoxic ventilation was slightly less in isoflurane than in control hypercapnic experiments, this was not significant (49.6 +/- 16.3 vs. 56.5 +/- 24.3 1/min; P = .22).(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesiology 1992 Dec
PMID:Does a subanesthetic concentration of isoflurane blunt the ventilatory response to hypoxia? 146 64

Variation of PCO2 with concomitant changes in extracellular pH (pHo) may modulate cerebrovascular resistance, but the direct actions of carbon dioxide and pHo on human cerebral arteries are unknown. In this study, we have evaluated the effects of different carbon dioxide tensions (2.7, 4.2 and 7.2 kPa) with either fixed (pHo = 7.44) or concomitant changes in pHo, on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated human pial arteries. Isolated changes in PCO2 had no significant effect on either potency (unchanged EC50 value) or the maximum response (Emax) in potassium-contracted arteries. Hypercapnia with uncompensated pHo significantly decreased both EC50 and Emax values, whereas uncompensated hypocapnia significantly increased the EC50 value without any effect on Emax. Concentration-response curves induced by prostaglandin (PG) F2 alpha were shifted significantly to the right (increased EC50 = decreased potency) during both hypo- and hypercapnia, independent of changes in pHo. The maximal responses were enhanced significantly during hypocapnia (Emax = 110 (SEM 2)%), but this enhancement was converted into a slight attenuation when pHo was compensated (Emax = 92 (4)%). Hypercapnia, with or without compensation of pHo, decreased the Emax values to 69 (16)% and 73 (9)%, respectively. We conclude that hypocapnia increases contractility in human pial arteries--an effect which is reversed by compensation of pHo. In contrast, the hypercapnic decrease of PGF2 alpha-induced contractions appears to be independent of pHo. The results confirm a relationship between contractility and pHo, but do not exclude a direct action of carbon dioxide in receptor-stimulated arteries.
Br J Anaesth 1992 Dec
PMID:Modulation by carbon dioxide and pH of the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 146 6

Charts of all children with severe acute asthma admitted to the Pediatric Intensive Care unit (PICU) of this hospital between January 1987 and December 1990 were reviewed retrospectively. There were 47 admissions for life threatening asthma to the PICU over this period, representing about 2% of all acute asthma admissions to our hospital. The mean duration of symptoms in these patients before admission was 54 hours. Only 55% of the PICU admissions had received bronchodilators before coming to our hospital emergency room from where they were admitted. From arterial blood gas analysis, 57% of the patients had hypercapnia (PaCO2 > 45 mmHg). All the patients received nebulized salbutamol frequently as well as intravenous aminophylline and hydrocortisone. Mechanical ventilation was used in only 8.5% of the patients. Only two patients developed pneumothorax, neither of whom had been mechanically ventilated, but they did not require surgical intervention for drainage. There was only one death in a patient who was known to have sickle cell anemia and developed sagittal sinus thrombosis. We conclude from our series that the mortality for children with life threatening asthma admitted to PICU is very low if bronchodilators and steroids are used optimally in their management, along with judicious selection of those requiring mechanical ventilation.
Ann Allergy 1992 Dec
PMID:Four-year experience with bronchial asthma in a pediatric intensive care unit. 147 85

In clinical practice, bronchospasm could be facilitated by hypoxia and by hypercapnia. In this study we assessed the influence of breathing a hypoxic (FIO2 = 0.10) or a hypercapnic (FICO2 = 0.08) gas mixture on the response to nebulized histamine (2% solution for 5 min) in anesthetized, tracheotomized, paralyzed and mechanically ventilated rabbits. Total respiratory resistance (Rrs) and elastance (Ers) were derived by least-square analysis from the relationship between tracheal pressure and flow. Control values of Rrs were larger during hypoxia and hypercapnia than in air while the values of Ers were similar. The absolute change in Rrs after histamine was similar in air and hypoxia, and larger in hypercapnia. The relative change, however, was smaller in hypoxia than in the two other conditions. Ers was also substantially increased by histamine and, contrary to Rrs, remained high 60 min after the aerosol. The results suggest: (1) that both hypoxia and hypercapnia increase airway resistance but do not change tissue properties; (2) that the response to histamine is depressed by hypoxia; (3) that a substantial part of the immediate response, and most, if not all, of the residual response after 60 min is due to changes in lung tissue viscoelastic properties.
Respir Physiol 1992 Dec
PMID:Changes in inspired gas composition and experimental bronchospasm in the rabbit. 148 Aug 38

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.
Am J Physiol 1992 Dec
PMID:Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits. 148 7

One injection of estradiol benzoate (EB) (100 micrograms) or vehicle was administered to male rat pups 5 days after birth. Two months later ventilation, ventilatory responses to 7% carbon dioxide, and to 580 mg/kg aspartic acid (an agent used as a marker of sexually dimorphism in the control of ventilation) were evaluated and body weight, testes weight, and nose-anus length were measured in animals in each group. The EB-treated rats had similar tidal volumes, frequency of breathing, and minute ventilation as did control male rats. The ventilatory responses of EB-treated rats to hypercapnia were markedly less than those of control animals. Aspartic acid administration depressed ventilation in control animals, but had no effect on ventilation in EB-treated males. Body and testes weights, as well as nose-anus length, were less in EB-treated compared with control rats. However, when body weight was normalized by nose-anus length and testes weight was normalized by body weight, the values were comparable between the two groups. Thus, perinatal EB treatment of male rat pups results in small, hypogonadal adult animals whose ventilation in response to hypercapnia was diminished and whose response to aspartic acid was female-like relative to those of control rats.
Physiol Behav 1992 Dec
PMID:Perinatal estradiol benzoate administration affects control of ventilation in adult male rats. 148 68

In the present study, changes in frequency and amplitude of the rhythmic variations (vasomotion) in blood flow in the intact cerebral circulation of the rat were investigated using laser-Doppler flowmetry (LDF) during stepwise decrease in mean arterial blood pressure (MABP) and hyper- and hypocapnia. Experiments were performed on 12 adult Sprague-Dawley rats of either sex, anesthetized with alpha-chloralose. The rat's head was fixed on a stereotaxic frame and a small hole was made in the parietal bone but the dura and a thin inner bone layer were kept intact. The microvascular blood flow of the parietal cortex on the right or on both sides was continuously recorded by the laser-Doppler flowmeter (Periflux PF2B, Perimed, Stockholm, Sweden). The cerebral circulation of the rat exhibited vasomotion in control conditions with a frequency of 8-10 cycles per minute (cpm) and an amplitude of 5-10% of the cerebral blood flow (CBF). No significant changes in CBF could be detected when the MABP was above 60 mmHg, but it decreased significantly when MABP was reduced below 50 mmHg. However, during stepwise pressure reduction the vasomotion frequency decreased progressively while its amplitude showed a reversed U-shaped curve with a peak at 60-80 mmHg. During hypercapnia, the rhythmical oscillations showed a decrease in both frequency and amplitude, whereas during hypocapnia their frequency did not change but their amplitude increased. These results support the hypothesis that the vasomotion frequency might be dependent of the wall tension and cellular pH while its amplitude could be related to decreased tissue oxygenation.
Acta Physiol Scand 1992 Dec
PMID:Vasomotion in the rat cerebral microcirculation recorded by laser-Doppler flowmetry. 149 61

Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.
Brain Res 1991 Dec 24
PMID:Carotid body chemoreception in the absence and presence of CO2-HCO3-. 166 17

Circulating catecholamines increase by three orders of magnitude in forced submerged ducks; their role in promoting vascular resistance was studied using vascular perfusion of hindlimbs. Perfusion pressure and blood flow were recorded simultaneously in hindlimbs of ducks during forced submergence. One leg was perfused with blood mixtures devoid of catecholamines (test leg) and compared with the other autoperfused leg. Perfusion pressures in test legs perfused with hyperoxic and hypocapnic blood or with hypoxic and hypocapnic blood were not significantly different from those in the matching autoperfused legs. However, when test legs were perfused with hypercapnic blood, regardless of whether blood was hypoxic or hyperoxic, perfusion pressures were significantly lower than in autoperfused legs. Adding catecholamines to test legs perfused with hypoxic and hypercapnic blood, after 3 min submergence, significantly enhanced vasoconstriction. Hypercapnia acts directly on the peripheral vascular beds and impairs the neurally mediated vasoconstriction during submergence, while circulating catecholamines restore peripheral vasoconstriction. Thus circulating catecholamines are needed to compensate for the depressant action of hypercapnia on neurally mediated vasoconstriction.
Am J Physiol 1991 Dec
PMID:Neural and humoral effects on hindlimb vascular resistance of ducks during forced submergence. 175 May 82

At present surgery is accepted as the most effective mode of therapy for carcinoma of the lung. Because the lack of respiratory reserve is the major determinant of postoperative function, it is useful to identify the patient, who is at significant risk. Eighteen patients with lung cancer (mean age = 56 +/- 6.5 years) were studied preoperatively (preop) and postoperative (postop) (three to four months after lung resection) by spirometry, measurement of arterial blood gases, and quantitative lung scanning (99mTc). A predicted postoperative value of some variables was calculated by the formula: postop value = preop value x % function of regions of lung not resected. The correlation coefficient between the predicted (pred) and postoperatively observed (observ) values VC = vital capacity, FEV1 = forced expiratory volume in 1 second) is: VC pred/VC observ r = 0.83 p less than 0.001 FEV1 pred/FEV1 observ r = 0.82 p less than 0.001. The authors' results agree with earlier reports and show that the method used can accurately predict the postoperative respiratory function in patients undergoing lung resection (pneumonectomy or lobectomy). A predicted FEV1 of 0.8 L does not permit a surgical program, because, below this level, carbon dioxide retention becomes more frequent and exercise intolerance is increasingly severe (poor quality of life). The method proposed to predict the postoperative respiratory function is simple and routinely useful. The authors choose a perfusion instead of ventilation scan, because the former provides similar predicted postoperative data, and can be done routinely.
Angiology 1991 Dec
PMID:Prediction of postoperative pulmonary function following thoracic surgery for bronchial carcinoma. 176 32


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