Changes in CO2 responsiveness and in autoregulation of the cerebral circulation during and after halothane-induced hypotension.

Abstract

SYNOPSIS C02 responsiveness of the cerebral circulation has been measured in baboons before, during, and after halothane-induced hypotension. At a systolic blood pressure (BP) of 60 mmHg, CO2 responsiveness was abolished, but was maintained at higher levels of BP. After hypotension, CO2 responsiveness returned to control values. Autoregulation to BP increases induced by intravenous noradrenaline was impaired when cerebral perfusion pressure during the hypotensive period had been below 30-40 mmHg. It is concluded that at levels of halothane-induced hypotension commonly employed clinically, CO2 responsiveness of the cerebral circulation may be absent. The return of CO2 responsiveness in the post-hypotensive phase argues in favour of controlled hyperventilation after neurosurgery which has involved induced hypotension.Harper and Glass (1965) reported loss ofcerebrovascular responsiveness to Paco2 changes during haemorrhagic hypotension, while Haggendal and Johansson (1965) reported that some degree of response was retained in these circumstances. Recent evidence (Fitch et al., 1973) shows that the cerebral circulation responds differently during drug-induced hypotension compared with hypotension produced by haemorrhage.It seemed important, therefore, to establish whether changes in cerebrovascular responsiveness to PaC02 occurred during drug-induced hypotension, since the combination of hypotension and hyperventilation could, by a combined action on cerebral perfusion, be clinically undesirable. Consequently, we decided to investigate cerebrovascular responses to changes in PaCO2 during hypotension induced with halothane at a level of systolic blood pressure commonly employed clinically. METHODSFive baboons weighing between 7.2 and 13.8 kg were premedicated with phencyclidine (0.8-1.0 mg/kg) intramuscularly and anaesthesia was induced and (Accepted 22 October 1975.) 221 maintained with halothane, N20, and 02. After intramuscular injection of suxamethonium (50 mg), the animals were intubated and ventilated by intermittent positive pressure (Starling ventilator

Effects of nicardipine-induced hypotension on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus under sevoflurane anesthesia

“…There have been contradictory data regarding the effects of induced hypotension on cerebrovascular CO 2 reactivity under anesthesia in animal studies and in studies of patients without diabetes mellitus [5,[16][17][18]. Artru and Colley [4] and Artru [5] reported that cerebral vascular responses to hypocapnia during [16] showed the absence of cerebrovascular CO 2 responsiveness after halothaneinduced hypotension at a systolic blood pressure of 60 mmHg in baboons.…”

“…Artru and Colley [4] and Artru [5] reported that cerebral vascular responses to hypocapnia during [16] showed the absence of cerebrovascular CO 2 responsiveness after halothaneinduced hypotension at a systolic blood pressure of 60 mmHg in baboons. Regarding the effects of nicardipine-induced hypotension on cerebrovascular CO 2 reactivity in humans, Kawaguchi et al [6] examined the effects of nicardipine on cerebral vascular responses to hypocapnia (manipulation of the Pa CO 2 level during hypocapnia, 36 ± 1 mmHg), and showed that cerebrovascular CO 2 reactivity was maintained during nicardipine-induced hypotension under fentanyl/diazepam/nitrous oxide anesthesia in patients without diabetes mellitus.…”

Checkpoints and pitfalls in the experimental neuropathology of circulatory disturbance

“…Cerebral autoregulation is impaired under most inhalation anesthetics 20,57 . However, vascular reactivity to Pco 2 is maintained reasonably well 23,58 . Halothane and isoflurane increase CBF and decrease oxygen consumption 59 .…”

“…In brain ischemia research, maintenance of Pao 2 is, of course, essential. Under physiological conditions CBF is dependent on Paco 2 23 . Maintenance of blood gas tensions at a constant level is therefore crucial.…”