Effect of Isoflurane-Induced Hypotension on Cerebral Autoregulation in the Anesthetized Pig

Seven normoventilated and five hyperventilated healthy adults undergoing cholecystectomy and anaesthetized with methohexitone, fentanyl and pancuronium were studied with measurement of cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and quantified electroencephalography (EEG) under two sets of conditions: 1) 1.7% end-tidal concentration of isoflurane in air/oxygen; 2) 0.85% end-tidal concentration of isoflurane in nitrous oxide (N2O)/oxygen. The object was to study the effects of N2O during isoflurane anaesthesia on cerebral circulation, metabolism and neuroelectric activity. N2O in the anaesthetic gas mixture caused a 43% (P less than 0.05) increase in CBF during normocarbic conditions but no significant change during hypocapnia. CMRO2 was not significantly altered by N2O. EEG demonstrated an activated pattern with decreased low frequency activity and increased high frequency activity. The results confirm that N2O is a potent cerebral vasodilator in man, although the mechanisms underlying the effects on CBF are still unclear.

Section: Discussionmentioning

confidence: 99%

Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anaesthesia in man

Algotsson

Messeter

Rosén

et al. 1992

“…Effects on MAP must be taken into consideration when comparing CBF values obtained under inhalational anaesthesia, since impairment of cerebrovascular autoregulation may occur with high doses of volatile anaesthetic agents (17)(18)(19). Since the differences in MAP between normocapnia and hypocapnia were small, the decline in CBF on hyperventilation indicates that none of the agents abolished CO 2 -reactivity at either MAC level although hypocapnia was induced after the intended steady-state concentration of inhalational agent had been achieved.…”

Section: Cerebral Vasoreactivity To Hypocapniamentioning

confidence: 99%

Desflurane results in higher cerebral blood flow than sevoflurane or isoflurane at hypocapnia in pigs

Holmström¹,

Rosén

Åkeson³

2004

Desflurane results in higher cerebral blood flow than sevoflurane or isoflurane at hypocapnia in pigs. Link to publication Citation for published version (APA): Holmström, A., Rosén, I., & Åkeson, J. (2004). Desflurane results in higher cerebral blood flow than sevoflurane or isoflurane at hypocapnia in pigs. Acta Anaesthesiologica Scandinavica, 48(4), 400-404. DOI: 10.1111400-404. DOI: 10. /j.0001-5172.2004 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Background: In clinical neuroanaesthesia, the increase in cerebral blood flow (CBF) and intracranial pressure caused by the cerebral vasodilative effects of an inhalational anaesthetic agent is counteracted by the cerebral vasoconstriction induced by hypocapnia. Desflurane and sevoflurane may have advantages over the more traditionally used isoflurane in neuroanaesthesia but their dose-dependent vasodilative effects at hypocapnia have not been compared in the same model using truly equipotent minimal alveolar concentrations (MACs). Method: Desflurane, sevoflurane and isoflurane were administered in a randomized order to six pigs at 0.5 and 1.0 MAC. The intra-arterial xenon clearance technique was used to calculate CBF. Blood pressure was invasively monitored. Cerebral and systemic physiological variables were recorded first at normocapnia (PaCO 2 5.6 kPa) and then at hypocapnia (PaCO 2 3.5 kPa). Electroencephalographic (EEG) activity was continuously recorded. Results: None of the three agents abolished cerebrovascular reactivity to hyperventilation, and at 0.5 MAC all had similar

“…To our knowledge, vasoactive drugs (24-27), controlled hemorrhage (12) or venous balloon catheters (24)(25)(26)(27) have been used to increase or decrease MAP levels in all available experimental models designed for this purpose except one (28), where xenon was studied with a model similar to ours and including both venous and arterial balloon catheters. By entering the target organ to be studied, e.g.…”

Section: Effects Of Confounding Factorsmentioning

confidence: 99%

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

Schmidt

Ryding

Åkeson

2003

Background: Little is known about the influence of racemic ketamine on autoregulation of cerebral blood flow (CBF), and available reports regarding its influence on cerebral hemodynamics are contradictory. This study was designed to evaluate cerebrovascular responses to changes in the mean arterial pressure (MAP) during ketamine anesthesia. Methods: In eight normoventilated pigs anesthesia was induced with propofol and maintained by i.v. infusion of ketamine (15.0 mg kg À1 .h À1 ) during measurements. The intra-arterial xenon clearance technique was used to calculate CBF. Balloon-tipped catheters were introduced in the inferior caval vein and mid-aorta, and increases or decreases by up to 40% in mean arterial pressure (MAP) in random order were achieved by titrated inflation of these balloon catheters. Cerebral blood flow was determined at each MAP level. Regression coefficients of linear pressure-flow curves were calculated in all animals. Results: From the mean baseline level (101 mmHg) MAP was reduced by 20% and 40%, and increased by 26% and 43%. The maximal mean increase and decrease in MAP induced a 12% increase and a 15% decrease, respectively, of CBF from the