Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Apr 1992
Autoregulation of cerebral blood flow in response to adenosine-induced hypotension in dogs.
During induced hypotension for surgical procedures, cerebral blood flow (CBF) autoregulation and cerebrovascular responsivity to CO2 may be impaired-changes that appear to be agent-specific. Adenosine is a potent endogenous systemic vasodilator and has been investigated as a hypotensive agent. In this study in dogs we investigated cerebral vascular responses to graded decreases of cerebral perfusion pressure (CPP) (100%, 60%, 45%, and 35% of control CPP) during normocapnia (PaCO2 = 37 mm Hg) and hypocapnia (PaCO2 = 21 mm Hg). ⋯ CBF was significantly greater during normocapnia compared with hypocapnia at all levels of CPP, except at 35% of control when the values were similar. Cerebral metabolic rate was unchanged throughout the study. We conclude that neither CBF nor CO2 responsivity is appreciably altered during adenosine-induced hypotension when GPP remains above the lower limit of autoregulation of CBF.
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J Neurosurg Anesthesiol · Dec 1991
A comparison of the cerebral and hemodynamic effects of mannitol and hypertonic saline in a rabbit model of acute cryogenic brain injury.
There has recently been an increased interest in the use of hypertonic saline solutions in the fluid resuscitation of trauma victims and patients with uncontrollable intracranial hypertension. In this study, the cerebral and hemodynamic effects of 3.2% hypertonic saline solution were compared with those of an equiosmolar (20%) mannitol solution or 0.9% saline in a rabbit model of acute cryogenic brain injury. Forty-five minutes following the creation of a left hemispheric cryogenic brain lesion, equal volumes (10 ml/kg) of hypertonic saline, 0.9% saline, or mannitol were infused over a 5-min period. ⋯ However, there appeared to be no significant differences in ICP between animals receiving mannitol or hypertonic saline at any time point following infusion of solutions. We conclude that following acute cryogenic brain injury, infusions of equal volumes of equiosmolar solutions of hypertonic saline or mannitol will transiently reduce ICP as compared to equal volumes of normal saline. However, hypertonic saline is not superior to mannitol in its ability to reduce ICP in this model of intracranial hypertension.
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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.