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

The infrared CO2 analyzer continuously monitors the CO2 tension in exhaled air at end-tidal expiration. In experimental animals, we found a consistent relationship between PaCO2 and end-tidal CO2 (ET.CO2) in the normal steady state, and in acid-base disturbances (respiratory acidosis and alkalosis, and hypoperfusion acidosis). Paired data analyses of PaCO2 (X) and ET.CO2 (Y) yielded correlation coefficients of r = 0.98 (Y = 0.96X + 4.43) during progressive hypercarbia (PaCO2: 32----110 torr), and r = 0.93 (Y = 0.89X + 0.93) during hyperventilation hypocapnia (PaCO2: 41----14 torr). The relationship between PaCO2 and ET.CO2 was seen during hypovolemic shock if pulmonary perfusion was maintained uniform in all areas of lung. The ability of the ET.CO2 sensor to predict instantaneously the PaCO2 makes it attractive enough to be used in conjunction with the subcutaneous tissue pH(pHe) sensor in the management of acid-base disturbances. After hypercarbia (FiCO2 0.15 X 40 min; PaCO2/ET.CO2: 100/101 torr), when the dogs were returned to room air, abruptly both the ET.CO2 and pHe sensors were sensitive to the changes in Fi.CO2. But the response of the ET.CO2 was swifter. The advent of transcutaneous gas monitors has shown that intermittent blood gas analyses, however frequent, are inadequate for the monitoring of the rapidly altering blood gas status in the acutely ill. The ability of the pHe sensor to identify whole-body acidosis and alkalosis combined with the speed and ease of the ET.CO2 monitor in pinpointing hypercarbic and hypocarbic states makes this two-parameter system suitable for the continuous, noninvasive monitoring of the critically ill.
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PMID:End-tidal CO2 and tissue pH in the monitoring of acid-base changes: a composite technique for continuous, minimally invasive monitoring. 644 Sep 69

Ventilatory regulation of intact, unrestrained lugworms Arenicola marina living in glass-tube artificial burrows was examined for values of inspired seawater PO2, PIO2, from 20 to 700 torr, at constant ambient pH and PCO2 values. The water ventilation rate and the respiratory characteristics of the ventilated seawater were measured. The water convection requirement and the corresponding specific rates of O2 uptake and CO2 production were calculated. The mean ventilatory water flow was a complex function of PIO2: decrease in hyperoxia, increase in hypoxia, decrease in extreme hypoxia. Compared to the normoxic responses, hyperoxia led to a hypercapnia (and acidosis) and moderate hypoxia to a hypocapnia (and alkalosis) in the expired water, variations which presumably reflect blood acid-base balance changes. Thus, as in other water breathers, the regulation of the organism's oxygenation may override the regulation of its acid-base balance. The lugworm's oxygen exchanger is highly efficient. However, below a critical partial pressure, PIO2 ca 120 torr, values of O2 consumption and ventilation decreased. A second critical O2 partial pressure appeared at PIO2 values between 80 and 40 torr; a 'switch-on' of anaerobic metabolism. These phenomena may be viewed as features of an adaptative respiratory strategy selected for in relation with the lugworm's particular peristaltic ventilatory mechanism and its intertidal mode of life.
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PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

We compared vasoactive effects of intravenous nicotine (36 micrograms/kg/min) in regional cerebral circulations under pentobarbital and chloralose anesthesia. Experiments were conducted in three groups of dogs: Group I, pentobarbital anesthesia with fixed ventilation; Group II, chloralose anesthesia with fixed ventilation; Group III, chloralose anesthesia with free breathing. Values for regional cerebral blood flow measured with 15 mu radioactive microspheres were used to compute regional cerebral vascular resistance (rCBR). In Group I, nicotine had no effect on rCVR in cerebral cortex, and it increased significantly rCVR in cerebellum (+17%), pons (+13%), medulla (+23%), and spinal cord (+19%). Using chloralose instead of pentobarbital in dogs with fixed ventilation (Group II), caused a significant reduction in rCVR in the cerebral cortex during nicotine, although it did not alter significantly nicotine-induced changes in rCVR in other regions of the brain. Hypocapnic alkalosis during nicotine-induced hyperventilation (Group III) resulted in significant increases in rCVR in all regions of the brain; however, the increases in rCVR in non-cortical regions more than doubled those in the cerebral cortex. The present results indicate: Nicotine-induced vasodilation in cerebral cortex was blunted by pentobarbital anesthesia. Nicotine-induced vasodilation in cerebral cortex under chloralose anesthesia was sufficient to nullify in part the potent vasoconstrictor effect of hypocapnic alkalosis.
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PMID:Regional blood flow in canine brain during nicotine infusion: pentobarbital vs. chloralose anesthesia. 646 62

For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arterial blood acid-base regulation during exercise in rats. 646 9

Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2, 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and ammonia production expressed per 100 mL of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma potassium concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64 to 0.38 mM during hypocapnia while alpha-ketoglutarate, glutamate, malate, oxaloacetate, and citrate did not change. Lactate concentration rose from 1.1 to 2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. Our data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the hydrogen ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Consequently, renal glutamine extraction and ammonia production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.
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PMID:Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog. 649 24

Glomerular filtration rate (GFR) was altered by varying renal perfusion pressure in volume-expanded, anesthetized dogs infused with ethacrynic acid. Phosphate reabsorption varied linearly with GFR (r greater than 0.9), 0.83 of the increase in filtered load being reabsorbed. Phosphate reabsorption at comparable filtered loads was not significantly changed by raising plasma bicarbonate concentration from 30 to 55 mM and adjusting PCO2 to keep plasma pH constant. Plasma pH was altered by inducing hyper- and hypocapnia or infusing bicarbonate. Plasma phosphate concentration varied with plasma pH before phosphate infusion and was kept constant at 3.4 +/- 0.1 mM in intact and thyroparathyroidectomized dogs; some of which were also examined during hyperchloremic acidosis. At comparable GFR, phosphate and bicarbonate reabsorption correlated (r greater than 0.9), except during acidosis when the filtered load of bicarbonate became inadequate. In all experiments phosphate reabsorption and plasma pH correlated (r greater than 0.85). Compared with control values at plasma pH 7.4, phosphate reabsorption increased by about 40% during acidosis (pH 7.1) and decreased by about 50% during alkalosis (pH 7.8) both in intact and thyroparathyroidectomized dogs. We propose that net hydrogen ion secretion is the common determinant of phosphate and bicarbonate reabsorption.
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PMID:Glomerular filtration rate and plasma pH as determinants of phosphate reabsorption. 650 33

Exercise was found to produce pseudoischemic changes of ST segment in 6% of patients with neurocirculatory dystonia, and T-wave inversion in 15-16%, which may be due to hyperventilation. It was demonstrated that T-wave inversion could not be a reliable indicator of coronary insufficiency, nor could respiratory alkalosis, hypocapnia, tachycardia, increased work of respiratory muscles, hypoxemia be immediate causes of hyperventilation changes. It is suggested that the changes in question are related to disrupted vegetative control of the cardiovascular system.
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PMID:[Pseudo-ischemic changes in the ECG caused by hyperventilation]. 664 70

Radioactive microspheres were used to measure cardiac output and blood flow to most major tissues in sheep at rest and during treadmill exercise (3- to 6-fold increase in metabolic rate for 30 min) in thermoneutral (TN) [dry bulb temperature (Tdb) = 16 degrees C, wet bulb temperature (Twb) = 12 degrees C] and mildly hot (MH) (Tdb = 40 degrees C, Twb = 23 degrees C) environments. During exercise, rectal temperature increased more under MH than under TN conditions; exercise-induced changes in the major central cardiovascular parameters were unaffected by MH. Exercise in TN caused mild hypocapnia, and in MH, severe respiratory alkalosis. Skin blood flow in the torso decreased during exercise in TN and MH. Extremity skin blood flow was increased by heat but not exercise. Exercise-induced increases in flows to respiratory muscles and upper respiratory tract tissues were greatly enhanced in MH. Exercise caused large increases in blood flow to fore- and hindlimb muscles, which were less in MH than in TN. Effects of MH on exercise-induced changes in flow to these and other tissues (e.g., abdominal viscera and adipose tissue) are discussed in terms of the conflicting requirements of energy expenditure and body temperature regulation during exercise in sheep and other species, particularly humans.
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PMID:Influence of heat stress on exercise-induced changes in regional blood flow in sheep. 666 83

Arterial blood gases (pH, pO2, p CO2) were studied in 100 patients with documented pulmonary embolism (Group A), confirmed by pulmonary angiography (n = 51) or scintigraphy ( n = 49). The pO2 ranged from 32 to 97 mm Hg (average 60,5 +/- 13 mm Hg). Hypoxaemia was found in 97 cases and would therefore seem to be a reliable sign of pulmonary embolism. In the three cases in which it was absent, the embolism was small. Hypoxaemia was associated with hypocapnia and alkalosis in 91 cases. However, hypoxaemia was not a specific finding; it was also present in 49 patients with suspected pulmonary embolism (Group B) in whom the diagnosis was excluded by pulmonary angiography or scintigraphy. A previous history of cardiovascular disease was found in 37 patients (76%) in this group: of the 12 remaining patients, 6 were heavy smokers and 4 were significantly obese. No correlation was found between the degree of hypoxaemia and the extent of amputation of the vascular bed on pulmonary angiography or scintigraphy. Nevertheless, a pO2 of under 50 mm Hg was always associated with a severe embolism with amputation of over 40% of the pulmonary vascular bed. A significant correlation was found between the severity of hypoxaemia and the degree of cyanosis (p less than 0,05) and ECG changes (p less than 0,01). The average pO2 was 59 +/- 12 mm Hg in patients with cardiovascular disease ( n = 21) and 55 +/- 11 mm Hg with known pulmonary disease ( n = 6). A higher average pO2 was found when these conditions were absent (61,5 +/- 13 mmHg). The difference was not statistically significant unless previous cardiac and pulmonary disease were associated (pO2 = 51 +/- 14 mm Hg, p less than 0,05).
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PMID:[Arterial blood gas analysis in acute pulmonary embolism]. 678 77

Demyelinating lesions in the trigeminal root were produced by chronic implantation of chromic suture in 12 cats. Two types of abnormal repetitive action potential generation were recorded from demyelinated fibers: reflected spikes and afterdischarge. Both types of abnormal impulse generation were increased by hypocalcemia induced by disodium edetate infusion, hypocapnia produced by hyperventilation, and, to a lesser extent, alkalosis secondary to sodium bicarbonate administration. This hyperexcitability of fibers could be inhibited by hypoventilation with elevation of PaCO2 or by calcium chloride administration. These results may help explain the pathophysiological basis of paroxysmal symptoms in multiple sclerosis and other disorders in which demyelination is a prominent feature.
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PMID:Ectopic impulse generation in demyelinated axons: effects of PaCO2, pH, and disodium edetate. 678 65


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