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

A hypothesis was established that, during emergence of inhalational anesthesia, hyperventilation and accompanying hypocapnia beyond a certain limit may actually disturb rather than enhance the washout of inhalational anesthetics from the brain because of a decreased cerebral blood flow. Two mathematical models were constructed and the washout of nitrous oxide, halothane and methoxyflurane were studied. In model I, the whole body consisted of a single compartment, and blood flow to this compartment was assumed to change proprotionally with the PaCO2. In model 2, the body was divided into two compartments, brain and the rest of the body. It was assumed that the blood flow to the brain compartment varies proportionally with the PaCO2, while that to the rest of the body remains constant. The analysis indicated that there indeed existed the PaCO2 values at which the washout of anesthetics from the brain can be maximally achieved. In model 1, they were 49.0, 22.1 and 9.7 mmHg for nitrous oxide, halothane, and methoxyflurane, respectively. In model 2, these PaCO2 values varied with time. While the hypothesis was proven to be valid, we conclude that it is of limited clinical significance. For halothane and methoxyflurane, these theoretically optimum PaCO2 values are sufficiently low. For nitrous oxide, the variation of PaCO2 makes little difference clinically, because its washout is fast enough regardless of PaCO2.
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PMID:PaCO2 for optimum washout of inhalational anesthetics from the brain. A model study. 52 55

1. Extracellular micro-electrodes were used to measure the responses of expiratory bulbospinal neurones to CO2 in anaesthetized, paralyzed cats, ventilated with O2. Simultaneous measurements were made of phrenic nerve and intercostal nerve filament discharges. 2. Hypocapnia produced tonic activity in some of the expiratory neurones and in expiratory filaments but rendered the phrenic and inspiratory filaments silent. 3. A graded excitatory effect of CO2 on tonic activity of both the neurones and the filaments was seen which progressed smoothly and continuously to rhythmic activity as CO2 was increased and to zero as CO2 was decreased. 4. Increases in blood pressure produced effects which were opposite to those produced by CO2, and which had a faster time course. 5. The CO2 response curves of those units showing tonic activity were indistinguishable from the CO2 response curves of those which did not. 6. A mid line lesion in the medulla interrupted inspiratory activity, converting activity of expiratory bulbospinal neurones from periodic to ionic firing patterns. 7. Following such lesions the CO2 threshold for rhythmic excitation of medullary neurones was elevated and the slopes of their CO2 response curves were reduced. 8. These findings fully confirm the hypothesis put forward by Bainton, Kirkwood & Sears (1978b) that bulbospinal respiratory neurones convey both tonic and rhythmic excitation to spinal respiratory motoneurones and that the rhythmic excitation of expiratory muscles derives from a period inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.
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PMID:The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones. 52 96

Recent studies have indicated that the breathing frequency responses to inspired CO2 in part result from changes in pulmonary stretch receptor activity. Pulmonary CO2 may alter frequency by direct inhibition of stretch receptor discharge, or secondarily, by changes in airway mechanics. The vascularly isolated left lower lobe (LLL) of the canine lung was used to determine the effect of hypocapnic airway constriction on the pulmonary CO2 reflex. The upper and middle lobes of the left lung were removed and the right vagus nerve sectioned. Blood was recirculated through the LLL. Diaphragm electromyogram was used as an index of respiratory center activity and to trigger ventilation of the left lower lobe. Lobar hypocapnia increased peak airway pressure and reduced respiratory rate. However, infusion of isoproterenol or the use of a mechanical overflow system to block the airway pressure response prevented the frequency changes associated with CO2. Although both the direct and mechanical effects of CO2 on stretch receptors may contribute to the reflex, in the LLL preparation the mechanical effects predominate.
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PMID:Breathing frequency responses to pulmonary CO2 in an isolated lobe of the canine lung. 53 90

Changes in myocardial performance after administration of gallamine 1.5 mg kg-1 and pancuronium 0.1 mg kg-1 were investigated in hypercapnic (PaCO2 = 7.08 kPa) and hypocapnic (PaCO2 = 2.74 kPa) dogs anaesthetized with thiopentone, nitrous oxide and halothane. Administration of pancuronium during hypocapnia caused a decrease of 25% in dP/dt max (corrected for changes in preload, afterload and heart rate). This change was not seen during hypercapnia, probably because of the associated sympathetic stimulation. By contrast, gallamine was without effect on dP/dt max in both groups. The increase in heart rate and cardiac output caused by the atropine-like action of both groups. The increase in heart rate and cardiac output caused by the atropine-like action of these relaxant drugs differed in the hypercapnic and hypocapnic group of dogs, with the more pronounced response in the latter group. The duration of the chronotropic changes was the same in both groups.
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PMID:Changes in myocardial performance induced by pancuronium and gallamine in hypercapnic and hypocapnic dogs. 58 99

The influence of the prevailing PaCO2 on the water-retaining effects of sustained elevations in ADH was assessed by administering vasopressin (5 U in oil, twice daily) and a fixed water intake to dogs with eucapnia (n, 7), chronic hypercapnia (n, 6), and chronic hypocapnia (n, 8). Although water excretion initially fell to a similar extent in all three groups, cumulative water retention by day 4 of vasopressin administration was 77 mg/kg in the hypocapnic group, 46 ml/kg in the eucapnic group, and only 14 ml/kg in the hypercapnic group. These differences were reflected in a marked disparity in the degree of hyposmolality of body fluids, plasma osmolality falling by day 4 to an average value of 223, 237, and 268 mosmol/kg in the hypocapnic, eucapnic, and hypercapnic animals, respectively. In a separate group of dogs, water deprivation and water loading studies revealed that sustained hypercapnia does not affect the maximal concentrating or diluting ability of the kidney. We conclude, therefore, that the striking influence of the prevailing PaCO2 on the water-retaining effects of administered vasopressin cannot be ascribed to an altered responsiveness of the nephron per se, but that this influence reflects an alteration in the ease with which the kidney can escape from the antidiuretic effects of this substance.
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PMID:Influence of steady-state PaCO2 on escape from ADH-induced water retention in the dog. 64 65

The responses of cerebral precapillary vessels to changes in arterial blood pressure were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation of the parietal cortex. Vessel responses were found to be size dependent. Between mean arterial pressures of 110 and 160 mmHg autoregulatory adjustments in caliber, e.g., constriction when the pressure rose and dilation when the pressure decreased, occurred only in vessels larger than 200 micron in diameter. Small arterioles, less than 100 micron in diameter, dilated only at pressures equal to or less than 90 mmHg; below 70 mmHg their dilation exceeded that of the larger vessels. When pressure rose to 170- 200 mmHg, small vessels dilated while the larger vessels remained constricted. At very high pressures (greater than 200 mmHg) forced dilation was frequently irreversible and was accompanied by loss of responsiveness to hypocapnia. Measurement of the pressure differences across various segments of the cerebral vascular bed showed that the larger surface cerebral vessels, extending from the circle of Willis to pial arteries 200 micron in diameter, were primarily responsible for the adjustments in flow over most of the pressure range.
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PMID:Responses of cerebral arteries and arterioles to acute hypotension and hypertension. 64 75

Oxygen uptake (VO2), expired volume (VE), and arterial blood gases were studied in awake, unrestrained rats over 14 days of hypobaric hypoxia (4,300 m altitude) and upon return to acute normoxia. Control data (at 250 m) showed (mean +/- 95% confidence limits (CL)) arterial oxygen pressure (Pao2) = 85.5 +/- 1.1; arterial carbon dioxide pressure (PaCO2) = 39.8 +/- 0.5; arterial pH pHa) = 7.430 +/- 0.009; VE = 78 +/- 3; VO2 = 2.36 +/- 0.09 ml.min-1.100 g-1; and dead space volumetidal volume ratio (VD/VT) = 0.37 +/- 0.04. During 14 days at 4.300 m the rat showed: a) a constant PaO2 (50-52 Torr); b) a time-dependent hyperventilation (e.g., PaCO2 = 30.2 +/- 1.1 at 1 h of hypoxia, 24.7 +/- 1.3 at day and 21.9 +/- 1.0 at 14 days); c) an increase in VE (85% of control) due to both frequency (33%) and VT (40%); d) a continued but reduced hyperventilation upon acute return to normoxia after 5 h to 14 days at 4,300 m; e) a 24% fall in VO2 after 1 h of hypoxia which returned to control by 4 days at 4,300 m; and f) a rise in pHa to 7.52 after 5 h of hypoxia, which fell to 7.45 by 14-day hypoxia. The rat's marked ventilatory response and changing VO2 during acute hypoxia clearly differs from the human response to sojourn at 4,300 m. However, the progressive and sustained hypocapnia during hypoxic exposure and the continued hyperventilation with acute normoxia in the rat provided essential, perhaps unique characteristics for an animal model of human ventilatory acclimatization.
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PMID:Rat as a model for humanlike ventilatory adaptation to chronic hypoxia. 64 77

As angiography with the usual X-ray tubes only permitted the demonstration of vessels of up to 600-800 micron, more efficient X-ray tubes have been developed permitting vascular demonstrations of up to 100 micron. Since the possibility of demonstrating small and very small vessels under hypocapnia is improved by hyperventilation and a slight increase in arterial blood pressure by ephedrine (30 mg I.A.), 46 patients were examined by employing this combination. Normal vessels contract, tumour vessels remain large. In this way, size and extent of the tumour are better demonstrated, the boundaries become clearer, differential diagnosis safer. Also the venous outflow can be seen earlier and clearer. Insults can be better differentiated. The risk is diminished by an increase in the resistance of the cerebral vessels. The information obtained by this method is a true improvement for diagnostics, indication, and surgical intervention.
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PMID:[Cerebral macroangiography under hypocapnia and moderate arterial hypertension in the diagnosis of intracerebral tumors]. 66 95

The effects of respiratory gas mass-transfer by high-efficiency hemodialyzers with regard to respiratory status and acid-base balance were studied in three groups of patients. Patients dialyzed with acetate dialysate and a single pass delivery system (group I) and those dialyzed with the same dialysate and a recirculating single pass system (group II) had significant intradialytic decreases in PCO2 (p is less than 0.05), while patients hemodialyzed aginst a carbon dioxide/bicarbonate dialysate (group III) had no significant alterations in arterial PCO2. The massfransfer rate of carbon dioxide was 0.3 mM/min in group I and 0.2 mM/min in group II. The hypocapnia caused by dialyzer mass-transfer of carbon dioxide was associated with a significant drop in minute ventilation volume and a decrease in PO2 which was significant in group I (p is less than 0.05). Although bicarbonate mass-transfer reduced serum bicarbonate levels, the loss of carbon dioxide to the dialysate resulted in an increased arterial pH during dialysis.
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PMID:Respiratory gas exchange by high-efficiency hemodialyzers. 67 97

A double-blind crossover trial was conducted in 10 asthmatic patients for comparison of fenoterol with salbutamol, in 12 other asthmatic patients for comparison of reproterol with salbutamol, and in 15 other asthmatic patients for comparison of terbutaline with salbutamol. The following doses were given: 1.25 mg fenoterol, 2.5 mg reproterol, 2.5 mg terbutaline and 1.25 mg salbutamol. 5 drops of each of the inhalation solutions (in 2 ml of saline) were aerosolized by a powered machine and inhaled for 15 min. FEV1 was measured before, and 15 and 45 min after inhalation. Immediately before FEV1 the following parameters for side effects were also determined: 1. heartbeats per min, systolic and diastolic blood pressure; 2. minute ventilation, arterial PCO2 and oxygen consumption; 3. arterial SO2, PO2 and the alveolar-arterial O2-gradient (AaDO2). To estimate the selectivity of each of the 3 betastimulators the ratio (formula: see text) was established for each parameter and compared to that obtained with salbutamol. In further steps the ratio of all parameters for side effects was shown, then only that of the 3 most important side effects tachycardia, hypocapnia (PaCO2) and hypoxemia (PaO2). The following order of selectivity was found: 1. salbutamol, 2. fenoterol, 3. terbutaline, 4. reproterol.
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PMID:[The bronchospasmolytics salbutamol, fenoterol, terbutaline and reproterol. Their effects and side effects in asthmatics after inhalation with an electric nebulizer]. 67 13


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