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Effect of Halothane on Regional Cerebral Blood Flow and Cerebral Metabolic Oxygen Consumption in the Fetal Lamb In Utero

Title: Effect of Halothane on Regional Cerebral Blood Flow and Cerebral Metabolic Oxygen Consumption in the Fetal Lamb In Utero
Authors: Cheek, D. B. C.; Hughes, S. C.; Dailey, P. A.; Field, D. R.; Pytka, S.; Rosen, M. A.; Parer, J. T.; Shnider, S. M.
Source: Anesthesiology ; volume 67, issue 3, page 361-366 ; ISSN 0003-3022 1528-1175
Publisher Information: Ovid Technologies (Wolters Kluwer Health)
Publication Year: 1987
Description: 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 (CMRO 2 ) 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% ...
Document Type: article in journal/newspaper
Language: English
DOI: 10.1097/00000542-198709000-00014
Availability: https://doi.org/10.1097/00000542-198709000-00014; https://pubs.asahq.org/anesthesiology/article-pdf/67/3/361/528883/19870900.0-00014.pdf; https://journals.lww.com/00000542-198709000-00014
Accession Number: edsbas.6FACB841
Database: BASE