Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jun 1991
Intracranial volume-pressure relationship following flumazenil in anesthetized dogs.
A series of infusions of mock cerebrospinal fluid (CSF) was used to determine intracranial volume-pressure relationships in 12 anesthetized dogs. Measures of intracranial volume-pressure relationships included (a) CSF pressure prior to volume infusion (Po), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance [C, calculated as the ratio of change of intracranial volume (DeltaLV) to change of CSF pressure (DeltaLP)], (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of DeltaLP to DeltaLV), (e) the pressure-volume index (PVI, calculated as the ratio of DeltaLV to log Pp/Po), and (f) estimated intracranial compliance (Ce, calculated from PVI as 0.4343PVI/Po). Measurements were made before giving flumazenil and after flumazenil doses of 0.0025 and 0.16 mg/kg in dogs receiving midazolam and in dogs not receiving midazolam (controls). ⋯ In dogs receiving midazolam at normal CSF pressure, 0.16 mg/kg of flumazenil (but not 0.0025 mg/kg) increased Po (by 4 +/- 2 cm H2O) and PVI, decreased Ce, and did not significantly changes C or VPR. Neither does of flumazenil caused consistent changes in dogs receiving midazolam when CSF pressure was increased prior to giving flumazenil, or in dogs not receiving midazolam. It is concluded that, in the presence of a benzodiazepine effect, large does of flumazenil increase CSF pressure from preflumazenil values and may be interpreted as worsening the intracranial volume-pressure relationship when the relationship is assessed by measures strongly affected by Po (PVI and Ce) but not when the relationship is assessed by indices that are relatively independent of Po (C and VPR).
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J Neurosurg Anesthesiol · Mar 1991
Changes in cerebral CO2 responsivity over time during isoflurane anesthesia in the dog.
We assessed cerebrovascular responsivity to changes in arterial carbon dioxide tension (PaCO2) during 3 h of 1 MAC isoflurane anesthesia to determine whether it parallels previously reported time-dependent decrease in normocapnic cerebral blood flow (CBF). Twelve dogs were studied under pentobarbital anesthesia (30 mg kg iv bolus) and twelve dogs under isoflurane anesthesia (1.4% end-tidal). In six animals of each anesthetic group, hypocapnia was compared to normocapnia; in the remaining six animals, hypercapnia was compared to normocapnia. ⋯ CO2 responsivity during hypocapnia decreased from over the same period decreased from 9.0 +/- 1.0 to 5.1 +/- 0.9 ml min 100 g mm Hg (p <0.05). Similar time-dependent trends were observed in most brain regions. We conclude that normocapnic CBF and cerebral CO2 responsivity decrease over time during isoflurane anesthesia and that these changes are not caused by changes in brain metabolism.
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J Neurosurg Anesthesiol · Mar 1991
Cerebrovascular effects of small volume resuscitation from hemorrhagic shock: comparison of hypertonic saline and concentrated hydroxyethyl starch in dogs.
To determine if hypertonic and hyperoncotic resuscitation solutions exerted comparable effects on cerebral hemodynamics following hemorrhagic shock, we compared randomly assigned, equal volumes (6.0 ml/kg) of hypertonic (7.2%) saline (HS) and hyperoncotic (20%) hydroxyethyl starch (HES) for resuscitation from acute experimental hemorrhage in 12 anesthetized dogs. Regional cerebral blood flow (radiolabeled microspheres), intracranial pressure (cisternal catheter), and systemic hemodynamics were recorded. Rapid hemorrhage reduced the mean arterial pressure to 45 mm Hg for 30 min. ⋯ Regional cerebral blood flow was similar following both fluids. Neither fluid restored cerebral oxygen transport to baseline values. Based on these data, the authors conclude that, following severe hemorrhagic shock of brief duration, systemic and cerebral hemodynamic values are restored equally well by highly concentrated colloid or by hypertonic saline, although hypertonic saline only transiently improves cardiac output.
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J Neurosurg Anesthesiol · Mar 1991
Detection of venous air embolism by continuous mixed venous oximetry in dogs.
Continuous mixed venous oxygen saturation (SvO 2) was evaluated as a monitor of venous air embolism in a canine model. Nineteen dogs were anesthetized, paralyzed, and mechanically ventilated. Invasive monitoring included SvO 2, systemic and pulmonary artery blood pressures, and thermodilution cardiac outputs. ⋯ Peak changes in pulmonary artery pressure occurred at 1.2 +/- 0.8 min. In the present study, time to maximum change was greater for SvO 2 than for pulmonary artery pressure changes. Use of fiberoptic pulmonary artery catheters for continuous measurement of SvO 2 can add a new diagnostic modality to venous air embolism detection in patients who require a pulmonary artery catheter for other medical indications.
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J Neurosurg Anesthesiol · Dec 1990
In vitro demonstration of the antidotal efficacy of hydroxocobalamin in cyanide poisoning.
The effects of sodium cyanide (1 mM) and the antidotal action of hydroxocobalamin (1 mM) were studied on rat cardiac papillary muscle. A 10-min period of exposure to cyanide induced a marked decrease in inotropy as shown by a decrease in the maximum unloaded shortening velocity (Vmax: 64 +/- 11% of precyanide values, p <0.01) and active isometric force (AF/s: 35 +/- 13%, p <0.01). The impairment of contraction-relaxation coupling under low load and the nearly complete disappearance of the load sensitivity of relaxation suggested a decrease in sarcoplasmic reticulum function. ⋯ The effects of hydroxocobalamin developed very quickly, beat to beat. The main toxic target of cyanide is brain and heart cytochrome oxidase, and brain damage appears only a few minutes after the onset of anoxia. Because hydroxocobalamin is a rapid and powerful antidote, it may be useful in the treatment of acute cyanide poisoning.