Effect of hyperventilation on the platelet aggregation induced by ADP.
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This study in dogs determined the effect of systemic cooling and arterial hypocarbia during cardiopulmonary bypass (CPB) on the requirements for enflurane anaesthesia (MAC) before and after CPB. Twelve mongrel dogs were each anaesthetized with enflurane in oxygen on two separate occasions. End-tidal enflurane concentration was measured with a Puritan-Bennett Anaesthesia Agent Monitor. Using the tail-clamp method, MAC was determined twice with a one-hour interval between measurements (MAC 1 and MAC 2). Partial CPB was then initiated using femoral arterio-venous cannulation and maintained for one hour. Following separation from CPB, MAC was again determined twice with a one hour interval between measurements (MAC 3 and MAC 4). Dogs were randomly assigned according to PaCO2 management during CPB (low, 17.6 +/- 8.6 mmHg vs high, 38.9 +/- 11.5 mmHg), and then subjected to two experimental conditions. The first experiment on each dog was undertaken using normothermia during CPB (warm, 35-37 degrees C) while the second experiment (at least two weeks later) was conducted using hypothermia during CPB (cold, 30 degrees C). Analysis of the data, using ANOVA for repeated measures, revealed MAC 3 (1.95 +/- 0.33%, post-CPB) to be reduced when compared with MAC 1 (2.18 +/- 0.28%, P < 0.01) or MAC 2 (2.10 +/- 0.22%, P < 0.01), determined before CPB. Multivariate repeated measures analysis revealed no independent effects of hypothermia or arterial hypocarbia during CPB, on MAC reduction. By the time of the second experiment in each dog (two weeks later), MAC had returned to baseline levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PURPOSE: Although it has been suggested that the rate at which the cerebral circulation responds to changes in PaCO2 is different with differing anesthetics, there have been no attempts to measure this. Transcranial Doppler allows the continuous measurement of cerebral blood flow velocity (CBFV) and any changes over time. Our aim was to compare the rate of change of CBFV when end-tidal CO2 (P(ET)CO2) was rapidly altered during halothane or isoflurane anesthesia. METHODS: Twenty-eight unpremedicated healthy patients were randomly assigned to receive air/O2 and either 1-1.5 MAC halothane or isoflurane as the primary anesthetic. After 15 min of steady state, P(ET)CO2 was rapidly reduced from 45 mm Hg to 30 mm Hg. CBFV and P(ET)CO2 were recorded every 30 sec for the next 10 min. RESULTS: The rate of change of normalized CBFV (delta CBFV vs. delta time) was more rapid in the isoflurane group (P <0.0001) especially in the initial few minutes. In all patients anesthetized with isoflurane, and in all but two patients anesthetized with halothane, the reduction in P(ET)CO2 produced a corresponding decrease in CBFV However, there were no differences in the magnitude of cerebrovascular CO2 reactivity (delta CBFV vs. delta P(ET)CO2) between the two groups. CONCLUSIONS: The rate of change of CBFV was faster in the isoflurane than in the halothane group especially in the initial few minutes. Indeed, for two patients in the halothane group Vmca did not change despite a change in P(ET)CO2. This may be of clinical importance when cerebrovascular tone needs to be changed rapidly.
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