Anesthetic-dependent pial arteriolar response to ethanol

Abstract

Anesthetic agents are often administered in the presence of ethyl alcohol, both in research and in the clinical setting. The authors tested the hypothesis that anesthetic agents may affect cerebrovascular responses to ethanol. A closed cranial window preparation in the rat was used to compare the response of pial arterioles to topically applied ethanol (0.01% to 1% vol/vol) in the presence of alpha-chloralose/urethane (50 and 600 mg/kg, respectively) or halothane (0.5% to 1%) anesthesia. Heart rate, mean arterial blood pressure, and blood gas levels were maintained stable and within the physiological range throughout each experiment. Ethanol induced significant vasoconstriction in alpha-chloralose/urethane-anesthetized animals (multivariate analysis of variance (MANOVA), p = 0.039); conversely, ethanol induced significant vasodilation of the pial arterioles in halothane-anesthetized animals (MANOVA, p = 0.017). These responses were significantly different from one another (MANOVA, p = 0.001). Thus, the choice of anesthetic agent alters the cerebrovascular response to ethanol, and care should be taken to ascertain the influence of anesthesia in both research and clinical settings.

A systematic review of physiological methods in rodent pharmacological MRI studies

“…The major effects of the main anaesthetic types reported upon neurotransmitter systems as well as cerebrovascular and systemic effects are summarised in Table 1 . Since evidence suggests that phMRI data are likely to be affected by the choice of anaesthetic regime due to differential actions of anaesthetic agents (Gordon et al 1995 ; Gozzi et al 2008 ; Du et al 2009 ; Liu et al 2012 ; Hodkinson et al 2012 ), the apparent laboratory dependence of these important aspects of research methodology is a major concern. Specifically, interpretation of the neurotransmitter effects of a drug under investigation should consider likely interactions with neurotransmitter effects of the anaesthetic (Table 1 ), especially when comparing between different studies.…”

“…Caution is thus required when interpreting preclinical phMRI data, where observed signal changes may reflect an interaction of the effects of the anaesthetic agent and those of the drug under study. Indeed several studies have presented differential responses to pharmacological challenge under varying anaesthetic regimes (Gordon et al 1995 ; Gozzi et al 2008 ; Du et al 2009 ; Liu et al 2012 ; Hodkinson et al 2012 ). Intravenous cocaine, for instance, evoked CBF increases in alpha-chloralose-anaesthetised rats, but reduced CBF under isoflurane (Du et al 2009 ).…”

Mesoscopic Mapping of Ictal Neurovascular Coupling in Awake Behaving Mice Using Optical Spectroscopy and Genetically Encoded Calcium Indicators

“…Different anesthetics work through distinct mechanisms and can have a variety of effects on NVC mechanisms leading to drastically different responses to the same experimental conditions (Lindauer et al, 1993;Bonvento et al, 1994;Gordon et al, 1995;Jones and Diamond, 1995;Linde et al, 1999;Kaisti et al, 2003;Oz et al, 2004;Austin et al, 2005;Du et al, 2009). Moreover, fluctuating levels of anesthesia can lead to intra-experimental variations in results (Masamoto and Kanno, 2012).…”