Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Ozaki, Suzuko; Nakaya, Haruaki; Gotoh, Yasuyuki; Azuma, Mitsue; Kemmotsu, Osamu; Kanno, Morio

doi:10.1213/00000539-199006000-00007

Cited by 8 publications

(3 citation statements)

References 19 publications

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“…Our latencies are also faster than those measured during antidromic activation of cortical neurons in rodents (∼1.6 ms) 17. This is likely based upon the following: (1) Isoflurane and ketamine were used together for anesthesia, both of which slow the conduction velocity30, 31; (2) the brain may have been cooled toward the ambient temperature during surgical exposure, further slowing the conduction velocity28; and (3) stimulation artifact may have obscured the fastest responses. Regardless of these mechanistic and technical considerations, our results demonstrate a short latency scalp potential associated with symptomatically effective, high‐frequency subthalamic DBS in humans with PD.…”

Section: Discussionmentioning

confidence: 64%

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

et al. 2012

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Background Subthalamic deep brain stimulation is superior to medical therapy for the motor symptoms of advanced Parkinson’s disease, and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for Parkinson disease. Methods In 5 subjects (6 hemispheres) electroencephalography measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event related potentials to suppress the stimulation artifact. Results Subthalamic brain stimulation at 20 Hertz activates somatosensory cortex at discrete latencies (mean latencies 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 milliseconds, denoted R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high frequency stimulation is nonlinearly dependent on stimulation voltage (p < 0.001, repeated measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 milliseconds, p < 0.001, Levene’s test). Conclusions Clinically effective subthalamic brain stimulation in humans with Parkinson disease activates cerebral cortex at one millisecond after stimulus onset, most likely by antidromic activation. Our findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region is an important component of the therapeutic mechanism of subthalamic brain stimulation.

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Section: Discussionmentioning

confidence: 64%

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

et al. 2012

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“…Isoflurane is a commonly used inhalant anesthetic in small animal experiments due to its ease of control over both the duration and depth of anesthesia. Although it may potentially affect cardiac function and electrophysiological metrics, its cardiac effects are generally less disadvantageous than those of other anesthetics ( 48 , 49 ).…”

Section: Discussionmentioning

confidence: 99%

A comprehensive protocol combining in vivo and ex vivo electrophysiological experiments in an arrhythmogenic animal model

Nyman,

Stølen,

Johnsen

et al. 2024

American Journal of Physiology-Heart and Circulatory Physiology

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Ventricular arrhythmias contribute significantly to cardiovascular mortality, with coronary artery disease as the predominant underlying cause. Understanding the mechanisms of arrhythmogenesis is essential to identify proarrhythmic factors and develop novel approaches for antiarrhythmic prophylaxis and treatment. Animal models are vital in basic research on cardiac arrhythmias, encompassing molecular, cellular, ex vivo whole heart and in vivo models. Most studies employ either in vivo protocols lacking important information on clinical relevance, or exclusively ex vivo protocols, thereby missing the opportunity to explore underlying mechanisms. Consequently, interpretation may be difficult due to dissimilarities in animal models, interventions, and individual properties across animals. Moreover, proarrhythmic effects observed in vivo are often not replicated in corresponding ex vivo preparations during mechanistic studies. We have established a protocol to perform both an in vivo and ex vivo electrophysiological characterization in an arrhythmogenic rat model with heart failure following myocardial infarction. The same animal is followed throughout the experiment. In vivo methods involve intracardiac programmed electrical stimulation and external defibrillation to terminate sustained ventricular arrhythmia. Ex vivo methods conducted on the Langendorff-perfused heart include an electrophysiological study with optical mapping of regional action potentials, conduction velocities, and dispersion of electrophysiological properties. By exploring the retention of the in vivo proarrhythmic phenotype ex vivo, we aim to examine whether the subsequent ex vivo detailed measurements are relevant to in vivo pathological behavior. This protocol can enhance greater understanding of cardiac arrhythmias by providing a standardized, yet adaptable model for evaluating arrhythmogenicity or antiarrhythmic interventions in cardiac diseases.

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“…Isoflurane was introduced into the oxygen through Isoflurane Vapour (ACOMA I type MKIII, Tokyo, Japan) and dissolved in the external solution. From the data of a previous study in which isoflurane was vaporized into a physiological solution (Ozaki et al , 1990), the concentration of isoflurane in the solution dissolved at 4% would be expected to be around 1.36 m M .…”

Section: Methodsmentioning

confidence: 99%

A key role for the subunit SUR2B in the preferential activation of vascular K_ATP channels by isoflurane

Fujita

Ogura

Tamagawa

et al. 2006

British J Pharmacology

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Background and purpose: It has been postulated that isoflurane, a volatile anaesthetic, produces vasodilatation through activation of ATP-sensitive K þ (K ATP ) channels. However, there is no direct evidence for the activation of vascular K ATP channels by isoflurane. This study was conducted to examine the effect of isoflurane on vascular K ATP channels and compare it with that on cardiac K ATP channels. Experimental approach: Effects of isoflurane on K ATP channels were examined in aortic smooth muscle cells and cardiomyocytes of the mouse using patch clamp techniques. Effects of the anaesthetic on the K ATP channels with different combinations of the inward rectifier pore subunits (Kir6.1 and Kir6.2) and sulphonylurea receptor subunits (SUR2A and SUR2B) reconstituted in a heterologous expression system were also examined. Key results: Isoflurane increased the coronary flow in Langendorff-perfused mouse hearts in a concentration-dependent manner, which was abolished by 10 mM glibenclamide. In enzymically-dissociated aortic smooth muscle cells, isoflurane evoked a glibenclamide-sensitive current (i.e. K ATP current). In isolated mouse ventricular cells, however, isoflurane failed to evoke the K ATP current unless the K ATP current was preactivated by the K þ channel opener pinacidil. Although isoflurane readily activated the Kir6.1/SUR2B channels (vascular type), the volatile anesthetic could not activate the Kir6.2/SUR2A channels (cardiac type) expressed in HEK293 cells. Isoflurane activated a glibenclamide-sensitive current in HEK293 cells expressing Kir6.2/SUR2B channels. Conclusion and implications: Isoflurane activates K ATP channels in vascular smooth muscle cells and produces coronary vasodilation in mouse hearts. SUR2B may be important for the activation of vascular-type K ATP channels by isoflurane.

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Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Cited by 8 publications

References 19 publications

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

A comprehensive protocol combining in vivo and ex vivo electrophysiological experiments in an arrhythmogenic animal model

A key role for the subunit SUR2B in the preferential activation of vascular K_ATP channels by isoflurane

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Effects of Isoflurane on Conduction Velocity and Maximum Rate of Rise of Action Potential Upstroke in Guinea Pig Papillary Muscles

Cited by 8 publications

References 19 publications

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

A comprehensive protocol combining in vivo and ex vivo electrophysiological experiments in an arrhythmogenic animal model

A key role for the subunit SUR2B in the preferential activation of vascular KATP channels by isoflurane

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A key role for the subunit SUR2B in the preferential activation of vascular K_ATP channels by isoflurane