ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017
The in vitro zebrafish heart as a model to investigate the chronotropic effects of vapor anesthetics.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- An Anesthesia-Free Pharmacological Assay for Zebrafish Heart Failure Models Using a Microfluidic Platform.Biomedicines · 2026Article
- Emergence of Functional Heart-Brain Circuits in a Vertebrate.bioRxiv : the preprint server for biology · 2025Article
- Pharmacological effects of caffeine on ventilation in adult zebrafish under free-swimming conditions.Scientific reports · 2022Article
- Drivers of Sinoatrial Node Automaticity in Zebrafish: Comparison With Mechanisms of Mammalian Pacemaker Function.Frontiers in physiology · 2022Article
- From Mice to Mainframes: Experimental Models for Investigation of the Intracardiac Nervous System.Journal of cardiovascular development and disease · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to their intended clinical actions, all general anesthetic agents in common use have detrimental intrasurgical and postsurgical side effects on organs and systems, including the heart. The major cardiac side effect of anesthesia is bradycardia, which increases the probability of insufficient systemic perfusion during surgery. These side effects also occur in all vertebrate species so far examined, but the underlying mechanisms are not clear. The zebrafish heart is a powerful model for studying cardiac electrophysiology, employing the same pacemaker system and neural control as do mammalian hearts. In this study, isolated zebrafish hearts were significantly bradycardic during exposure to the vapor anesthetics sevoflurane (SEVO), desflurane (DES), and isoflurane (ISO). Bradycardia induced by DES and ISO continued during pharmacological blockade of the intracardiac portion of the autonomic nervous system, but the chronotropic effect of SEVO was eliminated during blockade. Bradycardia evoked by vagosympathetic nerve stimulation was augmented during DES and ISO exposure; nerve stimulation during SEVO exposure had no effect. Together, these results support the hypothesis that the cardiac chronotropic effect of SEVO occurs via a neurally mediated mechanism, while DES and ISO act directly upon cardiac pacemaker cells via an as yet unknown mechanism.
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