Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1993
Randomized Controlled Trial Clinical TrialCerebral awakening concentration of sevoflurane and isoflurane predicted during slow and fast alveolar washout.
We studied 49 patients of ASA physical status I to determine cerebral anesthetic concentration on awakening calculated with end-tidal anesthetic concentration, when the end-tidal concentration decreased spontaneously. We also attempted to explain the difference in the average of the bracketing alveolar anesthetic concentration that allows and prevents the response to verbal command during recovery from anesthesia (MAC-Awake) between slow and fast alveolar washout by comparing the cerebral anesthetic concentrations with MAC-Awake determined by fast and slow washout. Slow washout was obtained by decreasing anesthetic concentrations in predetermined steps of 15 min, assuming equilibration between brain and alveolar partial pressures. ⋯ MAC-Awake values obtained by fast washout (0.22 +/- 0.07 MAC for sevoflurane, 0.22 +/- 0.05 MAC for isoflurane) were significantly smaller than those obtained by slow washout. Anesthetic concentrations in the brain at first eye opening calculated with end-tidal concentrations during fast alveolar washout (0.34 +/- 0.08 MAC for sevoflurane, 0.30 +/- 0.08 MAC for isoflurane) were nearly equal to MAC-Awake obtained by slow alveolar washout. The difference in MAC-Awake between fast and slow alveolar washout could be explained by arterial-to-cerebral and end-tidal-to-arterial anesthetic differences.
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Anesthesia and analgesia · Nov 1993
Effects of isoflurane, fentanyl, or thiopental anesthesia on regional cerebral blood flow and brain surface PO2 in the presence of a focal lesion in rabbits.
These studies were conducted to determine the effect of anesthetic drugs on tissue perfusion and O2 supply in the brain with focal cerebral edema. Using an open cranium preparation, we studied the effects of isoflurane (I; 1 minimum alveolar anesthetic concentration), of fentanyl (F; 0.5-1 microgram.kg-1 x min-1), or of thiopental (T; 32.5 mg.kg-1 x h-1) on regional cerebral blood flow (rCBF) and regional brain tissue PO2 in albino rabbits (n = 6 per group) with a focal brain lesion (cold injury). The doses of anesthetics were sufficient to suppress nociception. rCBF (H2 clearance) and tissue PO2 (multiwire surface electrode) were studied adjacent to and distant from the lesion. ⋯ The heterogeneity of the tissue PO2 in fentanyl anesthesia, as well as the increased frequency of hypoxic PO2 values with thiopental, might have resulted from microcirculatory disturbances. Thus, although isoflurane seemed to facilitate hyperemia with an increased O2 supply to the brain, fentanyl tended to induce the opposite response. Although these properties suggest the potential to manipulate perfusion and O2 supply in cerebral ischemia or hyperemia after head injury, the effects of such measures on intracranial pressure, neurologic status, and outcome have yet to be proven.
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Anesthesia and analgesia · Nov 1993
N omega-nitro-L-arginine methyl ester prevents cerebral hyperemia by inhaled anesthetics in dogs.
The mechanism by which halothane, isoflurane, and nitrous oxide increase cerebral blood flow (CBF) is unknown. We assessed the cerebrovascular effects of nitrous oxide (70%; n = 6), isoflurane (1 minimum alveolar anesthetic concentration: 1.4%; n = 6) or halothane (1 minimum alveolar anesthetic concentration: 0.8%; n = 6) before and after blockade of nitric oxide (NO) synthase with 40 mg/kg N omega-nitro-L-arginine methyl ester (L-NAME) intravenously in dogs with baseline pentobarbital anesthesia. Baseline CBF (microspheres) was determined after 1 h of pentobarbital anesthesia. ⋯ On the contrary, nitrous oxide increased CBF similarly (40 +/- 6 to 57 +/- 8 mL.min-1 x 100 g-1), but increased cerebral oxygen consumption (2.2 +/- 0.3 to 3.0 +/- 0.3 mL.min-1 x 100 g-1). L-NAME decreased blood flow in the neurohypophysis by 80% with no change in blood flow in other brain regions. After L-NAME, reexposure to nitrous oxide, halothane, or isoflurane resulted in no change in CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
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Anesthesia and analgesia · Nov 1993
Effects of nitric oxide synthase inhibition on regional cerebral blood flow and vascular resistance in conscious and isoflurane-anesthetized rats.
Nitric oxide is an important regulator of the regional cerebral vascular tone. We compared the magnitude of nitric oxide-related changes in the vascular tone by studying the regional cerebral blood flow (rCBF) and vascular resistance in conscious and isoflurane-anesthetized rats by using a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). In the conscious group (n = 12), after cannulation of a femoral artery and two veins under isoflurane anesthesia, rats were allowed to remain awake for 90 min. ⋯ Regional vascular resistance was determined by the ratio of mean arterial blood pressure and rCBF which was measured by [14C]iodoantipyrine. L-NAME significantly increased mean arterial blood pressure in both the conscious (123 to 158 mm Hg) and anesthetized (82 to 144 mm Hg) rats. Regional vascular resistance increased significantly in all 12 brain regions studied with the average value increasing from 1.19 +/- 0.33 mm Hg.mL-1 x min x 100 g to 2.22 +/- 0.48 (P < 0.0001) in the conscious and from 0.78 +/- 0.27 to 1.61 +/- 0.48 (P < 0.0001) in the isoflurane-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)