Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reduction in cerebral blood flow (CBF) caused by hypocapnia is an important element of neuroanesthetic techniques. While it has been demonstrated previously that the CO2 response of the cerebral circulation (CO2 X R) is enhanced (i.e., greater delta CBF/delta PaCO2) during halothane administration, the effect of isoflurane on CO2 X R has not been evaluated completely. Accordingly, the authors examined CO2 X R in cats during anesthesia with 1.0 MAC isoflurane (with 75% N2O) and compared it with CO2 X R during anesthesia with 1.0 MAC halothane (with 75% N2O) and with CO2 X R during the administration of 75% N2O alone. CO2 X R during anesthesia with isoflurane-N2O was enhanced relative to that observed during administration of both halothane-N2O (P less than 0.025) and N2O alone (P less than .001). CO2 X R during anesthesia with halothane-N2O was, in turn, greater than that observed during the administration of N2O alone (P less than 0.025). Furthermore, at similar levels of hypocapnia (PaCO2 18-20 mmHg), CBF was significantly lower (P less than 0.01) during administration of isoflurane-N2O (29.0 +/- 4.5 ml X 100 g-1 X min-1) than during administration of either N2O (40.6 +/- 5.5 ml X 100 g-1 X min-1) or halothane-N2O (39.6 +/- 7.8 ml X 100 g-1 X min-1). CBF values during administration of the N2O alone and halothane-N2O were not different during hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide. 391 14

Inhalation anesthetics diminish cerebrovascular resistance, augmenting cerebral blood flow (CBF) and hematic volume. This may lead to a dangerous increase in intracranial pressure (ICP). It has been observed that isoflurane used in hypocapnia does not appear to cause an increase in ICP equal to that caused by other inhalation anesthetics. The authors aimed to evaluate the effects of isoflurane on ICP and on intracranial vessel reactivity to changes in CO2 using a pulsed intracranial Doppler technique which measures cerebral flow velocity (CFV). A prospective study was performed at the Neurosurgery Clinic of the University of Milan in 10 in-patients due to undergo surgical removal of supratentorial intracranial expansion. Patients were anesthetised with isoflurane 1 MAC in air and O2. The following parameters were monitored: ICP at a spinal subarachnoid level; mean arterial pressure (MAP); cerebral perfusion pressure (CPP); ECG; CFV; EtCO2. The study was subdivided into 5 stages: basal (before induction); hypocapnia lasting 30 min; registration of data for 10 min; stabilisation phase in normocapnia; registration in normocapnia. The results show that during hypocapnia isoflurane causes significant reductions in MAP and CCP whereas ICP and CFV tend to diminish but not significantly. On the contrary, isoflurane in normocapnia causes an increase in ICP and a further and more marked reduction in CPP with a corresponding but not significant increase in CFV. In conclusion, in the light of these results the increase in ICP and the contemporary reduction of MAP would appear to restrict the use of isoflurane in normocapnia in patients with intracranial pathologies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of inhalation anesthetics on intracranial pressure and cerebral blood flow velocity]. 776 Oct 12

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when Paco2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.
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PMID:Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations. 827 58

We have studied the effects of hypocapnia on cerebrovascular changes in two MAC-equivalent anaesthetic regimens, using the transcranial Doppler technique as an index of cerebral blood flow (CBF) in 24 healthy ASA I patients undergoing spinal surgery. Eight of the patients were subjected to carbon dioxide reactivity challenges in the awake state. Before surgery, the other 16 patients received, in random order, either 1.15% isoflurane in oxygen or 0.5% isoflurane with 70% nitrous oxide. Carbon dioxide reactivity was calculated for each group as the increase in flow velocity per kPa change in PE'CO2 (cm s-1 kPa-1). It was significantly greater for the isoflurane group (14.09 (SD 2.44) cm s-1 kPa-1) and significantly less for the isoflurane-nitrous oxide group (7.95 (1.32) cm s-1 kPa-1) compared with the awake group (11.24 (0.95) cm s-1 kPa-1). We conclude that cerebrovascular responsiveness to changes in arterial carbon dioxide concentration is influenced markedly by the anaesthetic procedure. Hyperventilation is more likely to affect CBF during isoflurane anaesthesia than during an MAC-equivalent isoflurane-nitrous oxide anaesthesia.
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PMID:Cerebrovascular carbon dioxide reactivity during exposure to equipotent isoflurane and isoflurane in nitrous oxide anaesthesia. 812 6

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC50 value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F2 alpha was unchanged (unaffected EC50 value). However, the Emax value for prostaglandin F2 alpha at normocapnia (mean PCO2 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2)%, 91 (3)% and 84 (4)% at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3)%. During hypocapnia (PCO2 2.7 (0.1) kPa, pH 7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F2 alpha.
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PMID:Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 819 13

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a PaCO2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a PaCO2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when PaCO2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a PaCO2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations. 806 34

Intracranial pressure (ICP) has been shown to increase dramatically during desflurane anesthesia, possibly as a result in part of an increase in the rate of cerebrospinal fluid (CSF) formation (Vf) or a decrease in the rate of CSF reabsorption. To examine this phenomenon, I designed a study to measure Vf, resistance to reabsorption of CSF (Ra), brain tissue water content, and the electroencephalographic activity (EEG) during desflurane anesthesia in dogs. Vf and Ra were determined using ventriculocisternal perfusion of mock CSF labeled with blue dextran. EEG activity was determined using aperiodic analysis. At the end of the study, brain tissue water contents of gray and white matter were determined by dry/wet weight ratios. Eighteen dogs were allocated into three groups. Group 1 (n = 6) was examined at five experimental conditions during normocapnia; group 2 (n = 6) was examined at five experimental conditions during hypocapnia. The experimental conditions for groups 1 and 2 were (a) baseline (halothane 0.5-1.0% inspired plus thiopental 12 mg.kg-1 i.v. given over 15 min followed by i.v. infusion at 12 mg.kg-1 x h-1), (b) 0.5 MAC (3.5 +/- 0.1% expired) and (c) 1.0 MAC (7.0 +/- 0.1% expired) desflurane at normal CSF pressure, and (d) and (e) 0.5 and 1.0 MAC desflurane at increased CSF pressure (> 30 cm H2O). Group 3 (n = 6), the control group, was examined over the same time period as groups 1 and 2. In the control group, desflurane was not administered; instead, the baseline condition (i.e., halothane plus thiopental) was maintained throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rate of cerebrospinal fluid formation, resistance to reabsorption of cerebrospinal fluid, brain tissue water content, and electroencephalogram during desflurane anesthesia in dogs. 840 Jul 57

We have examined cerebral pressure autoregulation while awake, and during 0.5 and 1.5 MAC of sevoflurane anaesthesia in 10 patients undergoing non-intracranial neurosurgical procedures. All patients received a standardized anaesthetic comprising premedication with temazepam 20 mg orally, a sleep dose of propofol, fentanyl 1 microgram kg-1 and vecuronium 0.1 mg kg-1. After tracheal intubation, the lungs were ventilated with a mixture of air and oxygen to mild hypocapnia. Routine monitors included ECG, continuous and intermittent non-invasive arterial pressure, pulse oximetry and end-tidal capnography. In addition, blood flow velocity (vmca) was measured by insonating the middle cerebral artery transtemporally using a 2-MHz transcranial Doppler probe. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by approximately 20 mm Hg using an infusion of phenylephrine and simultaneously recording vmca. The index of autoregulation (IOR) during each period of the study, calculated as the ratio of percentage change in estimated cerebral vascular resistance (CVRe = MAP/vmca) to percentage change in MAP, was compared using ANOVA. vmca during 0.5 and 1.5 MAC of sevoflurane anaesthesia was significantly lower than that while awake (mean 79 (SD 24), 54 (15) and 51 (12) cm s-1, respectively; P < 0.05). There was no significant change in vmca with the increase in MAP while awake, or during 0.5 or 1.5 MAC of sevoflurane anaesthesia and IOR was similar under the three conditions (0.82 (0.11), 0.83 (0.04) and 1.0 (0.03), respectively). We conclude that cerebral pressure autoregulation remained intact during sevoflurane anaesthesia in humans.
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PMID:Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans. 938 65

The effects of halothane, isoflurane, sevoflurane (0.5, 1 and 2 MAC) and pentobarbital (10(-5) M, 10(-4) M and 3 x 10(-4) M) on hypocapnia- and bicarbonate-induced constriction of isolated dog middle cerebral arteries were investigated in vitro. The isometric tension of isolated cerebral arterial rings was measured in an organ bath containing Krebs bicarbonate solution, aerated with 5% CO2 and 95% O2. Hypocapnia, induced by replacing the bathing solution with one that had been equilibrated with 2.5% CO2 and 97.5% O2, produced a sustained vasoconstriction (268 +/- 36 mg, mean +/- SEM). Exposure of arterial rings to a bathing solution that contained double the concentration of NaHCO3 (50 mM) elicited a phasic constriction followed by a gradual decrease in tension (309 +/- 34 mg). Although halothane, isoflurane, and sevoflurane attenuated both hypocapnia- and bicarbonate-induced constrictions in a dose-dependent manner, the inhibition of these constrictions was greater in rings treated with halothane than in those treated with isoflurane or sevoflurane when compared at equipotent concentrations. These alkaline-induced constrictions were attenuated by pentobarbital only at the highest concentration of 3 x 10(-4) M. Halothane (1 and 2 MAC) attenuated the constriction induced by hypocapnia to a greater extent than that induced by 15 mM KCl, whereas pentobarbital (10(-4) M and 3 x 10(-4) M) attenuated hypocapnia-induced constriction less than KCl-induced constriction. These results indicate that alkaline-induced constriction is more vulnerable to halothane than other volatile anesthetics and pentobarbital. The mechanisms of the inhibitory effects of halothane and pentobarbital on alkaline-induced cerebral vasoconstriction seem to differ; the inhibitory effect of pentobarbital, but not of halothane may be, in part, ascribed to its inhibitory effect on the Ca++ influx.
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PMID:Inhibitory effects of halothane, isoflurane, sevoflurane, and pentobarbital on the constriction induced by hypocapnia and bicarbonate in isolated canine cerebral arteries. 1077 3

In this study, 33 female patients, scheduled for operative gynecological laparoscopies, were enrolled. Our aim was prospective, randomized comparison of the influence of two different management strategies, regarding end tidal CO2, on cerebral blood flow velocities and on pulsatility index, examined by means of transcranial Doppler ultrasonography, under sevoflurane anesthesia 1.3 MAC: permissive hypercapnia (up to 45 mmHg, Group I, n = 17) versus intervention to ensure mild hypocapnia, (around 33 mmHg, Group II, n = 16). Baseline measurements of investigated parameters were recorded and CO2 insufflation started. In Group I no further adjustment was performed and CO2 partial pressure rose, while in Group II it was kept stable, by ventilatory patterns adjustment. Hemodynamic, acid base balance and cerebrovascular variables were recorded during pneumoperitoneum and in post-desufflation period, at eight checking time points. In Group I cerebral blood flow velocities increased according to CO2 elevation (2.3%-3.9% per mmHg of increase in CO2 partial pressure), whereas in Group II no significant alterations were noticed. Pulsatility index was constant over time without clinical differences between groups. Our study suggests that under sevoflurane anesthesia 1.3 MAC, prophylactic hyperventilation limits the cerebral blood flow velocities enhancing effect of CO2 insufflation, during laparoscopies.
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PMID:Cerebral blood flow velocity alterations, under two different carbon dioxide management strategies, during sevoflurane anesthesia in gynecological laparoscopic surgery. 1287 Feb 62


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