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Biomedical subjects

J G Wade

Publications and source records attributed to J G Wade.

5 recordsLinked to original sources
PubMed1979

Regional cerebral blood flow changes during severe fetal asphyxia produced by slow partial umbilical cord compression.

We studied the effects of severe partial asphyxia on regional cerebral blood flow and arterial blood pressure in the unanesthetized, physiologically stable fetal lamb. Cerebral blood flow was measured by the microsphere technique before and during partial umbilical cord compression. Asphyxia sufficient to decrease pH from 7.40 to 7.04 and reduce oxygen saturation from 50% to 19% increased cerebral blood flow to all areas of the brain with the largest increases going to the brain stem (275% of control) and deep cerebral structures (240% of control). Fetal arterial blood pressures increased from a mean of 58 mm Hg to a mean of 71 mm. Hg during asphyxia. The blood pressure increases correlated closely with the regional cerebral blood flow increases. There was a poor correlation between cerebral blood flow increases and changes in Paco2' pH, or oxygen saturation. We conclude that during severe fetal asphyxia arterial blood pressure is the critical factor in determining cerebral blood flow.

Acidosis↗
PubMed1978

Effect of anaesthetic agents on the ionic composition of cerebrospinal fluid following total cerebral ischaemia.

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.

Anesthetics↗
PubMed1977

Halothane depresses baroreflex control of heart rate in man.

Baroreflex control of heart rate was determined during three awake control situations and during two depths of halothane anesthesia in man. Baroreflex function was quantiated by calculating the pressor test slope from the R-R interval change on the ECG produced by a pharmacologically induced pressor response. During the three awake control situations the subjects breathed room air or 100 per cent O2 spontaneously or 100 per cent O2 with ventilation controlled. Mean (+/- SD) slopes obtained were 15.1 +/- 4.5, 15.6 +/- 6.8 and 18.4 +/- 9.9, respectively. No significant difference in baroreflex function slope was observed. During light halothane anesthesia (0.7 per cent endtidal) baroreflex function was significantly depressed (mean slope = 2.5 +/- 1.5), and it was abolished at 1.1 per cent end-tidal halothane (mean slope = 0.03 +/- 0.04). It is concluded that halothane anesthesia produces depression of baroreflex control of heart rate in man.

Adult↗
PubMed1977

Mechanisms of the "low-flow" state during resuscitation of the totally ischemic brain.

Resuscitation of the brain following total circulatory arrest may be impeded by difficulty in establishing cerebral tissue perfusion, a postischemic "low-flow"state. We have confirmed this hypothesis in a rat model of total cerebral ischemia and have demonstrated marked imporvement in post-ischemic brain tissue perfusion following epinephrine injection. This is mainly due to the systemic vascular effects of epinephrine, resulting in improved central arotic pressure and cerebral perfusion pressure. Hyperkalemic induced vasoconstriction has also been postulated as a cause of the "low-flow/. We have, therefore, investigated the in vitro effects of increasing potassium ion concentration on cerebrovascular smooth muscle strips. Large arteries constrict, while small arteries dilate in response to hyperkalemia. The net effect on cerebral blood flow remains unsettled. Our research to date suggests that resuscitation of the totally ischemic brain, in animal models at least, is enhanced by epinephrine, mainly via its effects on central aortic pressure.

Animals↗