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)

Effects of halothane/N2O anesthesia and in situ freezing of the brain on mean arterial blood pressure (MABP), pH, pCO2 and pO2 were evaluated in rabbits with either Streptococcus pneumoniae or Escherichia coli meningitis. Prior to anesthesia infected rabbits had, compared to controls, significantly lower values for MABP and pCO2, either with a compensated (S. pneumoniae group) or decompensated (E. coli group) metabolic acidosis. In most animals a slight additional decrease in MABP was observed during anesthesia. With maintained pre-anesthetic hypocapnia no further disturbance in acid-base balance occurred during anesthesia. After one minute of freezing MABP increased towards preanesthetic levels. We conclude that the technique for in situ freezing of the brain under halothane/N2O anesthesia may be applied for studies of cerebral metabolism in rabbit with experimental meningitis.
 ...
PMID:Experimental meningitis in the rabbit. I. Arterial blood pressure and acid-base balance during halothane anesthesia and in situ freezing of the brain. 311 54

Several authors have observed that nitrous oxide increases cerebral blood flow (CBF) and/or intracranial pressure (ICP) in experimental situations and in humans. However, the effects of hypocapnia on the cerebrovascular responses to N2O have not been investigated. Therefore, six New Zealand White rabbits were anesthetized with approximately equal to 1.0 MAC halothane (mean end-tidal concentration 1.26%) and surgically prepared for recording of ICP, the EEG, and both cortical and global CBF (by the H2-clearance method). After preparation was complete, measurements were obtained during ventilation with 70% nitrogen (in O2), and after the inspired gas mixture was changed to 70% N2O (still with 1.0 MAC halothane). Two such data pairs (N2-N2O) were obtained, one during hypocarbia (PaCO2 approximately equal to 20 mm Hg) and the other during normocarbic (PaCO2 approximately equal to 40 mm Hg) conditions. Mean arterial pressure (MABP) was held constant within each data pair by infusing angiotensin II as needed. Nitrous oxide resulted in a consistent increase in EEG frequency and decrease in amplitude as compared with N2, and produced small (approximately equal to 1 mm Hg) but statistically significant increases in ICP during both hypo- and normocarbic conditions. Nitrous oxide administration also increased CBF as measured both in frontal cortex and globally, with similar changes seen during hypo- and normocarbic conditions, e.g., cortical CBF increased from 42 +/- 8 to 59 +/- 15 ml.100 gm-1.min-1 during hypocarbia, and from 61 +/- 13 to 75 +/- 15 ml.100 gm-1.min-1 during normocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effects of PaCO2 on the cerebrovascular response to nitrous oxide in the halothane-anesthetized rabbit. 311 86

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 relationships between pHi (intracellular pH) and phosphate compounds were evaluated by nuclear magnetic resonance (NMR) in normo-, hypo-, and hypercapnia, obtained by changing fractional inspired concentration of CO2 in dogs anesthetized with 0.75% isoflurane and 66% N2O. Phosphocreatine (PCr) fell by 2.02 mM and Pi (inorganic phosphate) rose by 1.92 mM due to pHi shift from 7.10 to 6.83 during hypercapnia. The stoichiometric coefficient was 1.05 (r2 = 0.78) on log PCr/Cr against pHi, showing minimum change of ADP/ATP and equilibrium of creatine kinase in the pH range of 6.7 to 7.25. [ADP] varied from 21.6 +/- 4.1 microM in control (pHi = 7.10) to 26.8 +/- 6.3 microM in hypercapnia (pHi = 6.83) and 24.0 +/- 6.8 microM in hypocapnia (pHi = 7.17). ATP/ADP X Pi decreased from 66.4 +/- 17.1 mM-1 during normocapnia to 25.8 +/- 6.3 mM-1 in hypercapnia. The ADP values are near the in vitro Km; thus ADP is the main controller. The velocity of oxidative metabolism (V) in relation to its maximum (Vmax) as calculated by a steady-state Michaelis-Menten formulation is approximately 50% in normocapnia. In acidosis (pH 6.7) and alkalosis (pH 7.25), V/Vmax is 10% higher than the normocapnic brain. This increase of V/Vmax is required to maintain cellular homeostasis of energy metabolism in the face of either inhibition at extremes of pH or higher ATPase activity.
 ...
PMID:Relationship between intracellular pH and energy metabolism in dog brain as measured by 31P-NMR. 359 78

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)
 ...
PMID:The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide. 391 14

In this study we report our clinical experience with supplementary thiopental loading, based on 30 patients undergoing surgery for intracranial aneurysm after a recent episode of subarachnoid haemorrhage. As standard procedure we used pentobarbitone induction, pancuronium relaxation, endotracheal intubation, maintenance with halothane 0.5%, N2O 66% in oxygen, fentanyl, and moderate hypocapnia. A thiopental load of up to 20 mg X kg-1 was supplied while the aneurysm was approached. Satisfactory and well-controlled hypotension was obtained in five cases after thiopental alone, and after thiopental and sodium nitroprusside (SNP) (means +/- s.d.) 1.3 +/- 0.9 microgram X kg-1 X min-1 in the remaining 25 patients. No ECG sign of myocardial ischaemia was observed. One disadvantage was a prolonged recovery period, which in some cases necessitated controlled ventilation for some hours. We conclude that thiopental loading can be used safely as a supplement to neuroanaesthesia for aneurysm surgery.
 ...
PMID:Thiopental loading during controlled hypotension for intracranial aneurysm surgery. 649 3

This study is based on the same group of neurosurgical patients as our previous publication. All, except one, had suffered from head injury. We made a first measurement of rCBF under N2O anesthesia, a second under N2O + 1% enflurane anesthesia, both at a PaCO2 of 40 Torr. A third measurement was performed under N2O + 1% enflurane but at a PaCO2 of 30 Torr. The method we used consists of the intracarotid injection of 133Xe and recording of the radioactivity by a gammacamera. Mean arterial pressure was maintained constant by an intravenous phenylephrine drip. For each measurement of each patient, a map was drawn, representing the distribution of the regional cerebral blood flows (rCBF), compared to the mean value of the hemisphere. We have studied rCBF in one case of normal hemisphere, and in cases of traumtic lesions in acute and chronic states, taking into account that the normal brain exhibits areas with higher flow in the frontoparietal and insular regions. In the normal brain, introduction of 1% enflurane decreases uniformally mean CBF, rCBF repartition not being changed. Hyperventilation to 30 Torr shows that regions with previously higher flow react more to hypocapnia by a slightly more decreased flow. In severe brain trauma, mean CBF is generally low, and it is difficult to visualize the lesions under N2O and N2O + 1% enflurane anesthesia. Neither mean CBF, nor rCBF repartition are significantly modified. On the other hand, in the acute phase, hypocapnia causes a more decreased flow in the previously well irrigated areas, and shows a lack of vascular reactivity in the damaged region. Passing to the chronic state, the patient clinically recovering, the rCBF repartition is normalized and the contused area becomes agains vasoactive. Severe losses of neuronal tissue are characterized by definitive low flows without reactivity by hyperventilation.
 ...
PMID:Influence of 1% enflurane (Ethrane) anesthesia on regional cerebral blood flow repartition under normo-and hyperventilation. 677 96

Interregional differences in intracellular pH (pHi) in brain tissue, and its regulation following 1 and 5 h of respiratory alkalosis (with and without hypoxemia) were determined in N2O anesthetized dogs. Two techniques for pHi estimation were used (TCO2 and 14C-DMO) and included corrections for measured extracellular fluid (35SO4(2-)) space (ECS). Cortical pHi by the two techniques agreed closely in control and in 3 of the 4 experimental conditions, suggesting: (a) our estimation of extracellular fluid (ECF) [HCO3-] from measured CSF [HCO3-] was a valid assumption; and (b) our method had sufficient resolution to determine the magnitude of brain pHi regulation during respiratory acid-base disturbances. When moderate normoxic respiratory alkalosis (PaCO2 approximately 25 mm Hg) was imposed for 5 h, pHi (in most brain regions) was well regulated and always exceeded the incomplete regulation noted in bulk CSF. When moderate hypoxemia (PaO2 approximately 45 mm Hg) accompanied hypocapnia, pHi was more closely regulated during the early phase (1 h) of respiratory alkalosis. Increased levels of metabolic acids (especially lactic acid) were critical to brain pHi regulation during the initial hour of respiratory alkalosis and accounted for much of the independent effect of hypoxemia on pHi regulation. However, these metabolic acids remained unchanged as pHi was more completely regulated between 1 and 5 h of continued hypocapnia or hypoxic hypocapnia. This time-dependent regulation of pHi may involve some regulatory role for changed transmembrane fluxes of H+ and/or HCO3-. Significant interregional differences were observed in both pHi and in ECS; with tendencies toward more alkaline pHi and lower ECS in brain stem and white matter. With respiratory alkalosis ECS fell and intracellular fluid increased in both cortex and caudate nucleus, possibly reflecting an osmotic effect of increased metabolic acid levels or reduction in cell membrane ion pumping.
 ...
PMID:Interregional differences in brain intracellular pH and water compartmentation during acute normoxic and hypoxic hypocapnia in the anesthetized dog. 678 4

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
 ...
PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

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


<< Previous 1 2 3 Next >>