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

The effect of isoflurane 1.0% and 1.5% with nitrous oxide on ventricular cerebrospinal fluid pressure was studied in 17 patients who underwent intracranial shunt procedures. Isoflurane at both concentrations caused significant increases in cerebrospinal fluid pressure during normocapnic ventilation, but these could be prevented by simultaneous hyperventilation or by the prior induction of hypocapnia. Decreases in mean arterial pressure occurred also, and resulted in a significant reduction in cerebral perfusion pressure in normocapnic patients.
 ...
PMID:Isoflurane and cerebrospinal fluid pressure--a study in neurosurgical patients undergoing intracranial shunt procedures. 249 3

Isoflurane (ISF)-induced hypotension causes equal reductions of cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) so that no disturbance of cerebral energy stores or metabolites occurs. While hypocapnia during ISF-induced hypotension causes a further reduction of CBF, the effects on cerebral energy stores and metabolites produced by combining hypocapnia with ISF-induced hypotension are not known. This study examined the effect of hypocapnia (PaCO2 = 20 mmHg) on CMRO2, the electroencephalogram (EEG), and levels of adenine nucleotides, phosphocreatine, lactate, pyruvate, and glucose in brain tissue in 12 dogs during ISF-induced hypotension. All dogs were examined at: normocapnia with normotension; hypocapnia with normotension; hypocapnia combined with ISF-induced hypotension to cerebral perfusion pressures of 60, 50, and 40 mmHg; and restoration of normocapnia with normotension. In six dogs CMRO2 was determined, and the EEG was evaluated using compressed spectral analysis. In the other six dogs brain tissue metabolites were determined. Hypocapnia combined with ISF-induced hypotension (all levels) caused a decrease of the power of the beta-2 spectra, an increase of the power of the alpha and beta-1 spectra, but no change in total power of the EEG. There was no change in cerebral energy stores or brain tissue metabolites. CMRO2 was reduced by approximately 27%. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites remained unchanged and CMRO2, and the power of the alpha, beta-1, and beta-2 spectra of the EEG returned to control values. These results suggest no adverse effect on cerebral metabolism or function during hypocapnia combined with ISF-induced hypotension.
 ...
PMID:Cerebral metabolism and EEG during combination of hypocapnia and isoflurane-induced hypotension in dogs. 309 38

Positron emission tomography was used to study the effects of nitrous oxide (N2O) and isoflurane on regional cerebral blood volume (rCBV) in dogs during normocapnia and hypocapnia. Regional cerebral blood volume was measured serially during the addition of 50% N2O to a background anesthetic of fentanyl in normocapnic (group 1) and hypocapnic (PaCO2 25 mmHg, group 2) dogs. In each group, after 15 min of N2O administration accompanied by rCBV measurement, elimination of N2O with 100% O2 was continued for 15 min. This was followed by introduction of 2% isoflurane (no N2O), again accompanied by serial measurements of rCBV. In the normocapnic animals, the addition of 50% N2O caused an 11% increase in rCBV (6.1 +/- 1.4 to 6.8 +/- 1.0 ml/100 g, P less than 0.02) while 2% isoflurane caused a 36% increase (6.1 +/- 1.3 to 8.0 +/- 1.7 ml/100 g, P less than 0.02). The initial induction of hypocapnia during infusion of fentanyl in group 2 animals was associated with a 17% decrease in rCBV. In the hypocapnic dogs, there was no change in rCBV when N2O was introduced; however, an increase of 15% occurred following the addition of isoflurane (3.9 +/- 0.6 to 4.5 +/- 0.7 ml/100 g, P less than 0.02). Isoflurane, even during hypocapnia, may increase cerebral blood volume which in some circumstances may lead to an increase in ICP.
 ...
PMID:Cerebral blood volume is increased in dogs during administration of nitrous oxide or isoflurane. 311 42

The effects of isoflurane (1 MAC) and enflurane (1 MAC) on cerebral blood flow and cerebral oxygen consumption were studied in 20 male patients without intracranial disease undergoing coronary artery bypass surgery (mean age 57 and 59 years respectively). The aim of the study was to investigate whether both agents diminish autoregulation of cerebral blood flow and CO2 reactivity of cerebral blood vessels. Patients were randomly assigned to one of two groups (10 patients each) receiving either isoflurane 1.15 vol.% or enflurane 1.68 vol.% endexpiratory. Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). Cerebral blood flow was measured by the argon wash-in technique. Isoflurane and enflurane produced a significant drop in cardiac index and cerebral perfusion pressure and reduced cerebral blood flow significantly by 35% and 39% respectively. Cerebral oxygen consumption was also significantly decreased by 49% (isoflurane) and 50% (enflurane). Induced hypertension with norepinephrine increased cerebral blood flow significantly by 32% (isoflurane) and 26% (enflurane), while hypocapnia reduced cerebral blood flow significantly by 26% (isoflurane) and 29% (enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The effects of isoflurane and enflurane on cerebral hemodynamics and cerebral oxygen consumption in humans]. 326 82

It is important to know the effects of anaesthetics on cerebral blood flow and cerebral metabolism to enable appropriate selection of agents for the brain injured patient. Thiopental possesses favourable cerebrovascular and metabolic properties but has not been shown to improve outcome in head injured patients. Propofol has properties similar to thiopental. Its rapid metabolism as well as its ability to reduce intracranial pressure and its antiemetic properties render it a very favourable drug. Despite controversies surrounding the effects of short-acting narcotics on intracranial pressure, they continue to be used because they provide stable haemodynamic conditions when used with care. Isoflurane is currently advocated as the best inhalational agent for neuroanaesthesia because of its lesser effects on cerebral blood flow and intracranial pressure. The effects of nitrous oxide on cerebral blood flow and intracranial pressure appear to vary according to the background anaesthetic used. Nitrous oxide is still widely used in most neuroanaesthetic practices, as its effects can be blunted by barbiturates, narcotics and/or hypocapnia. There is no convincing human study on the cerebral protective properties of anaesthetic agents although mild hypothermia has been shown experimentally to offer significant protection against global and focal ischaemia.
 ...
PMID:Cerebrovascular and cerebral metabolic effects of commonly used anaesthetics. 771 Feb 26

Desflurane-induced increase of intracranial pressure (ICP) does not appear to be completely explained by desflurane-induced changes in cerebral blood flow, cerebrospinal fluid (CSF) formation and reabsorption, or brain tissue water content. The present study was designed to determine whether desflurane alters intracranial volume/pressure relationships sufficiently to account for desflurane-induced increase of ICP. In 24 dogs, infusions of mock CSF were used to determine the CSF pressure increase due to increase of CSF volume, and the capacity of CSF pressure to return to baseline after a CSF pressure increase (CSF pressure normalization). CSF pressure increase was assessed by determining (a) CSF pressure prior to volume infusion (P(o)), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance (C, calculated as the ratio of change of intracranial volume [delta V] to change of CSF pressure [delta P]), (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of delta P to delta V, (e) the pressure/volume index (PVI, calculated as the ratio of delta V to log Pp/P(o)), and (f) estimated intracranial compliance (C(e), calculated from PVI as 0.4343PVI/P(o)). CSF pressure normalization was assessed by determining the first (S1) and second (S2) phase slopes of decrease of CSF pressure from Pp, the duration of S1 (DS1), and the intersection of extrapolated S2 with the P(o) to Pp slope (delta Ps). During normocapnia (Group 1, n = 6) and hypocapnia (Group 2, n = 6), two infusions were made at each of four experimental conditions: 0.5 minimum alveolar anesthetic concentration (MAC) desflurane and normal or increased CSF pressure, and 1.0 MAC desflurane and normal or increased CSF pressure. For comparison to these two desflurane-anesthetized groups, intracranial volume/pressure values were determined at the same experimental conditions during 0.5 MAC isoflurane (Group 3, n = 6) and in controls (Group 4, n = 6) anesthetized with thiopental 12 mg/kg then 12 mg.kg-1.h-1 intravenously combined with halothane 0.5% inspired. In comparison to controls, both desflurane and isoflurane decreased Ce at normal CSF pressure but not at increased CSF pressure. However, desflurane and isoflurane had no consistent effect on the other measures of CSF pressure increase caused by increase of CSF volume. Isoflurane also decreased the capacity for CSF pressure normalization at normal CSF pressure as indicated by decreased S1 and increased delta Ps. It is concluded that, under conditions of normal ICP, desflurane may decrease Ce, favoring an increase of ICP.
 ...
PMID:Intracranial volume/pressure relationship during desflurane anesthesia in dogs: comparison with isoflurane and thiopental/halothane. 794 87

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.
 ...
PMID:Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 819 13

Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.
 ...
PMID:The effect of hypocapnia on the autoregulation of cerebral blood flow during administration of isoflurane. 1584 6