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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)
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PMID:Does a subanesthetic concentration of isoflurane blunt the ventilatory response to hypoxia? 146 64

Qualitatively different responses of ADP levels have previously been observed in the brain during hypercarbia. One investigation has found that cerebral ADP stayed constant during hypercarbia in rats that were anesthetized with halothane, while another observed that ADP decreased during supercarbia in rats that received no supplemental anesthesia. This article reports an in vivo 31P nuclear magnetic resonance study to test the hypothesis that halothane anesthesia accounts for the discrepant observations. Isoflurane anesthesia was also studied in a second group of rats to see if a different general anesthetic agent would cause the same effects that halothane causes. The two groups of five rats underwent dual episodes of hypercarbia that were separated by a 45-min recovery period. General anesthesia, either 0.5% halothane or 1.0% isoflurane, was administered during the first episode but not during the second. Hypercarbia during halothane anesthesia caused the measured phosphocreatine (PCr) to decrease by 40%, while the calculated change in ADP was 10%, in agreement with the former investigation. In contrast, hypercarbia during either isoflurane anesthesia or no anesthesia caused a decrease of only 10% in PCr, which meant that the calculated decrease in ADP was 60%, in agreement with the results of the second investigation. We conclude that during hypercarbia, clinical concentrations of halothane, unlike clinical concentrations of isoflurane, interfere with the regulation of ATP metabolism.
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PMID:Cerebral intracellular ADP concentrations during hypercarbia: an in vivo 31P nuclear magnetic resonance study in rats. 371 Nov 64

Circulatory and respiratory effects of alveolar concentrations of 1.31, 1.97, and 2.62 vol% of isoflurane in oxygen were studied in eight young, healthy horses during spontaneous and controlled ventilation. These isoflurane concentrations were equivalent, respectively, to 1.0, 1.5, and 2.0 times the minimal alveolar concentration of isoflurane, which prevents movement in horses in response to a standard pain stimulus. Results of the isoflurane studies were compared with similarly derived findings in these same horses during equipotent halothane in oxygen anesthesia. Isoflurane, similar to halothane, produced a dose-related depression of cardiovascular function which was less severe during spontaneous ventilation and associated hypercapnia. The two anesthetic agents produced similar circulatory effects during controlled ventilation and constant arterial carbon dioxide tension except for a significantly (P less than 0.05) less depressed cardiac output/kg of body weight and stroke volume that occurred with minimal alveolar concentration 1.5 and 2.0 isoflurane. Total peripheral resistance was greatest when these horses were anesthetized with halothane regardless of the alveolar dose. In horses, isoflurane was, in general, no more depressing than was halothane to circulatory and respiratory function.
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PMID:Comparison of circulatory and respiratory effects of isoflurane and halothane anesthesia in horses. 740 5

Isoflurane-anesthetized newborn pigs were used to test the hypothesis that nitric oxide mediates autoregulatory dilations of retinal arterioles. Fundus images were monitored by videomicroscopy at x310, and stimulus-induced changes in retinal arteriolar diameter were measured by on-line image analysis. Dilatative responses to systemic hypoxia (arterial O2 tension 20-30 mmHg), hypotension (mean arterial blood pressure 40 mmHg), or hypercapnia (arterial CO2 tension 70-85 mmHg) were assessed after intravitreal microsuffusion of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) over the observed arterioles. Twenty-five nanomoles L-NMMA constricted arterioles by 24 +/- 2% (P < 0.01; n = 17 pigs); a significant constriction (14 +/- 2%) was still observed 80 min after drug administration (n = 5). Complete nitric oxide synthase inhibition at this dose was indicated by the findings that co-administration of 2.5 mumol L-arginine reversed this constriction within 17 +/- 2 min (n = 3), that L-NMMA, but not D-NMMA, completely inhibited the 20 +/- 3% P < 0.01) arteriolar dilation induced by intravitreal acetylcholine (7.5 nmol; n = 4), and that no additional constriction was evidenced after administration of a 10-fold greater concentration of L-NMMA (n = 8). However, despite the prominent arteriolar constriction induced by L-NMMA under baseline conditions, increases in retinal arteriolar diameter still occurred in response to hypoxia (n = 5), hypotension (n = 4), or hypercapnia (n = 5) in animals pretreated with 50 nmol L-NMMA; these responses did not differ significantly from arteriolar dilations observed in untreated control animals (n = 16) subjected to the same stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide does not mediate autoregulation of retinal blood flow in newborn pig. 757 3

MRI is a powerful tool for measuring cerebral blood flow (CBF) longitudinally. However, most animal studies require anesthesia, potentially interfering with normal physiology. Isoflurane anesthesia was used here to study CBF regulation during repetitive scanning in rats. MR perfusion images were acquired using FAIR (flow-sensitive alternating inversion recovery) arterial spin labeling, and absolute CBF was calculated. CBF changes in response to a hypoxic (12% O2) and hypercapnic (5% CO2) gas stimulus were monitored. Hypercapnia led to a robust increase in CBF compared with baseline (195.5+/-21.5 vs 123.6+/-17.9 ml/100 g/min), and hypoxia caused a smaller non-significant increase in mean CBF values (145.4+/-13.4 ml/100 g/min). Strikingly, when measurements were repeated 5 days later, CBF was dramatically reduced in hypoxia (93.2+/-8.1 ml/100 g/min) compared with the first imaging session. Without application of the hypoxic and hypercapnic gases during the first MRI, baseline CBF and CBF changes in response to hypoxia at the second MRI were similar to naive rats. Blood gas analyses revealed a slight reduction in arterial oxygenation during the second period of anesthesia compared with the first. These findings indicate that, in isoflurane-anesthetized rats, even a short hypoxic episode can have long-lasting effects on cerebrovascular regulation.
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PMID:Longitudinal MRI studies in the isoflurane-anesthetized rat: long-term effects of a short hypoxic episode on regulation of cerebral blood flow as assessed by pulsed arterial spin labelling. 1827 45

Isoflurane is currently the most common volatile anaesthetic used in laboratory mice, whereas in human medicine the more modern sevoflurane is often used for inhalation anaesthesia. This study aimed to characterize and compare the clinical properties of both anaesthetics for inhalation anaesthesia in mice. In an approach mirroring routine laboratory conditions (spontaneous breathing, gas supply via nose mask, preventing hypothermia by a warming mat) a 50 min anaesthesia was performed. Anaesthetics were administered in oxygen as carrier gas at standardized dosages of 1.5 minimum alveolar concentrations, which was 2.8% for isoflurane and 4.9% for sevoflurane. Both induction and recovery from anaesthesia proceeded quickly, within 1-2 min. During anaesthesia, all reflex testing was negative and no serious impairment of vital functions was found; all animals survived. The most prominent side-effect during anaesthesia was respiratory depression with hypercapnia, acidosis and a marked decrease in respiration rate. Under anaesthesia, heart rate and core body temperature remained within the normal range, but were significantly increased for 12 h after anaesthesia. Locomotor activity, daily food and water consumption and body weight progression showed no abnormalities after anaesthesia. No significant difference was found between the two anaesthetics. In conclusion, isoflurane and sevoflurane provided an equally reliable anaesthesia in laboratory mice.
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PMID:Isoflurane and sevoflurane provide equally effective anaesthesia in laboratory mice. 2050 78

We encountered a 2-year-old child with life-threatening hypercapnia, with a PaCO(2) of 238 mm Hg and severe respiratory and metabolic acidosis, due to status asthmaticus that was refractory to steroid and bronchodilator therapy. Suspecting ventilatory failure and excessive ventilation-induced obstructive shock, we started respiratory physiotherapy in synchrony with her respiration, to facilitate exhalation from her over-inflated lungs. Isoflurane inhalation was commenced in preparation for extracorporeal circulation, to reduce the hypercapnia. The combination of respiratory physiotherapy and isoflurane inhalation resulted in a rapid decrease in ventilatory resistance and PaCO(2) levels within a few minutes, with recovery of consciousness within 60 min. Isoflurane inhalation was gradually discontinued and steroid and aminophylline therapy were commenced. The patient recovered completely without any recurrence of her bronchospasm and without any residual neurological deficits. In our patient with a severe asthmatic attack, decreased exhalation secondary to asthma and overventilation during artificial ventilation resulted in overinflation of the lungs, which in turn led to cerebral edema and obstructive cardiac failure. The favorable outcome in this case was due to the short duration of hypercapnia. Hence, we conclude that the duration of hypercapnia is an important determinant of the morbidity and mortality of status asthmaticus-induced severe hypercapnia.
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PMID:Treatment of life-threatening hypercapnia with isoflurane in an infant with status asthmaticus. 2431 Aug 52