The effects of halothane on maternal and fetal hemodynamics, distribution of fetal cardiac output, regional cerebral blood flow, and fetal cerebral oxygen consumption were studied in the ewe (N = 9) using radionuclide-labeled microspheres. An adjustable uterine artery occluder was used to produce a controlled state of fetal asphyxia. Measurements were taken during three periods of study: 1) control, 2) asphyxia, and 3) asphyxia plus 15 min of 1% maternal halothane. The fetal cardiovascular response to asphyxia was acidosis, hypoxia, hypertension, bradycardia, and preservation of vital organ blood flows. There was a significant drop in maternal blood pressure when halothane was administered but uterine blood flow was maintained, 308 ml ± min−1 during asphyxia versus 275 ml ± min−1 with halothane. Fetal blood pressure during asphyxia plus halothane (54 mmHg) was significantly lower than that during asphyxia alone (59 mmHg), while heart rate was significantly higher: 172 beats per minute (bpm) versus 125 bpm (P < 0.05). Despite these changes, the administration of halothane during asphyxia did not produce a reduction in vital organ flows. Cerebral blood flow was maintained: 357 ± 37 ml ± 100 g−1 • min−1 during asphyxia alone and 344 ± 26 ml ± 100 g−1 min−1 after halothane administration (P = NS, mean ± SEM). Cerebral oxygen delivery also was maintained: 8.3 ± 0.8 ml ± 100 g−1 during asphyxia alone versus 9.7 ± 1.5 ml ± 100 g−1 • min−1 after halothane, compared with 11.2 ± 1.1 ml ± 100 g−1 • min−1 during the control period. Cerebral oxidative metabolism (CMRO2) decreased significantly from 4.1 ± 0.6 ml ± 100 g−1 • min−1 during control to 2.8 ± 0.4 ml ± 100 g−1 • min−1 during asphyxia alone, but no further significant change occured after halothane (2.0 ± 0.3 ml ± 100 g−1 • min−1). Fetal myocardial blood flow was maintained: 625 ± 93 ml ± 100 g−1 ml−1 during asphyxia alone versus 529 ± 79 ml ± 100 g−1 • min−1 after halothane administration. The authors conclude that the addition of 1% maternal halothane in the briefly asphyxiated fetal lamb does not abolish the protective reflexes of increased coronary and cerebral blood flow and decreased CMRO2.
Effect of Halothane on Regional Cerebral Blood Flow and Cerebral Metabolic Oxygen Consumption in the Fetal Lamb In Utero
Received from the Department of Anesthesia, University of California, San Francisco, San Francisco, California. Accepted for publication April 17, 1987. Supported by NIH Grant GM29922-02. Presented in part at the 1985 Annual Meeting of the American Society of Anesthesiologists, San Francisco, California.
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D. B. C. Cheek, S. C. Hughes, P. A. Dailey, D. R. Field, S. Pytka, M. A. Rosen, J. T. Parer, S. M. Shnider; Effect of Halothane on Regional Cerebral Blood Flow and Cerebral Metabolic Oxygen Consumption in the Fetal Lamb In Utero. Anesthesiology 1987; 67:361–366 doi: https://doi.org/10.1097/00000542-198709000-00014
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