Key result
Common anesthetic regimens induce distinct cardiovascular depression and biomarker profiles in preclinical models.
Why the study?
General anesthetics can affect cardiovascular and respiratory physiology, potentially biasing preclinical outcomes, but their integrated cardiorespiratory and biochemical effects in rats are not fully characterized.
Do different anesthetic regimens differentially affect cardiorespiratory physiology, autonomic variability, and biochemical markers in adult male Wistar rats?
Do different anesthetic regimens differentially affect cardiorespiratory physiology, autonomic variability, and biochemical markers in adult male Wistar rats?
Different anesthetic agents produce distinct profiles of cardiovascular depression, autonomic alteration, and biomarker release in rats, highlighting the need to carefully select anesthetics in preclinical experimental protocols.
Anesthetic choice may bias rat cardiorespiratory data; leaves open optimal regimen for unbiased translational studies.
General anesthetics enable invasive experimentation but can affect cardiovascular and respiratory physiology, biasing preclinical outcomes. We compared five anesthetic regimens in adult male Wistar rats, tribromoethanol (TBE, 250 mg/kg i.p.), chloral hydrate (CH, 400 mg/kg i.p.), ketamine-xylazine (KX, 80/10 mg/kg i.p.), thiopental (TP, 80 mg/kg i.p.), and isoflurane (ISO, 4% induction, 2% maintenance), to investigate integrated cardiorespiratory and biochemical markers. Femoral arterial catheterization allowed continuous blood pressure (BP) and derived heart rate (HR) recordings, while ventilation was assessed through pletysmography at baseline (awake), during induction, and early recovery phases of anesthesia. Variability was evaluated in the time and frequency domains, including HR, systolic blood pressure (SBP), and spontaneous baroreflex sensitivity. In an independent cohort of rats, butyrylcholinesterase (BChE), CK-MB, cTnI, and LDH were measured. Baseline BP was unchanged by TBE and TP, whereas all anesthetics affected HR. Minute ventilation and breathing frequency were reduced with all agents, while tidal volume decreased with KX and TBE only. LDH and cTnI were unaffected, BChE was reduced by KX, TBE, and ISO, and CK-MB increased with CH and KX. Variability analysis showed that all anesthetics depressed pulse-interval and SBP variability and shifted spectral power toward higher frequencies, while baroreflex sensitivity and effectiveness were consistently reduced. During early recovery, KX and TP restored most variability indices, whereas CH, TBE, and ISO showed continued suppression of these indices. These findings highlight distinct profiles of cardiovascular depression and biomarker responses across anesthetics and underscore the importance of accounting for autonomic variability when selecting different anesthetics in experimental protocols.
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Corrêa et al. (2026) studied this question. Five anesthetic regimens (tribromoethanol, chloral hydrate, ketamine-xylazine, thiopental, isoflurane) vs. Baseline (awake) was evaluated on Cardiorespiratory physiology and biochemical markers. Five anesthetic regimens produced distinct profiles of cardiovascular depression and biomarker responses in rats, highlighting the need to account for autonomic variability in experimental protocols.
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