{"title":"Changes in heart rate during electrical stimulation of the atrium in rainbow trout (Oncorhynchus mykiss) at low temperature","authors":"N. Kibler, V. Nuzhny, D. Shmakov","doi":"10.21638/spbu03.2022.204","DOIUrl":null,"url":null,"abstract":"In this work, we investigated the effect of high heart rate (HR) in vivo on the electrical properties and pumping functions of the heart ventricle of the rainbow trout (Oncorhynchus mykiss) at low ambient temperatures. HR was altered by atrial pacing. The electrocardiogram (ECG) parameters and hemodynamic parameters of the heart ventricle of rainbow trout adapted to a temperature of 5–7 °C were studied from the normal sinus rhythm (21.6 ± 4.9 bpm) to the maximum possible HR. Results show that a HR of about 60 bpm is the upper limit of the normal functional activity of the ventricle of the heart. An increase in heart rate up to 60 bpm leads to an increase in the PQ interval and QRS complex, a decrease in the QT interval on the ECG, and a violation of the rhythmic activity of the heart (i.e., the occurrence of extrasystole), as well as to a considerable change in the hemodynamic parameters of the ventricle of the heart and a decrease in its contractile properties. After a period of ventricular extrasystole for several minutes (10–15 min), the activity of the sinus node resumes but with a lower HR compared with the initial HR. The duration of the QRS complex recovers to the initial one, and the PQ and QT intervals increase. Maximum systolic pressure and end-diastolic pressure also return to their original values after extrasystolic contraction. After the experimental extrasystole, the phenomenon of the absence of an increase in HR is observed. The arising extrasystole probably has a functional nature and is one of the mechanisms of electromechanical homeostatic control in the heart.","PeriodicalId":8998,"journal":{"name":"Biological Communications","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological Communications","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21638/spbu03.2022.204","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Agricultural and Biological Sciences","Score":null,"Total":0}
引用次数: 0
Abstract
In this work, we investigated the effect of high heart rate (HR) in vivo on the electrical properties and pumping functions of the heart ventricle of the rainbow trout (Oncorhynchus mykiss) at low ambient temperatures. HR was altered by atrial pacing. The electrocardiogram (ECG) parameters and hemodynamic parameters of the heart ventricle of rainbow trout adapted to a temperature of 5–7 °C were studied from the normal sinus rhythm (21.6 ± 4.9 bpm) to the maximum possible HR. Results show that a HR of about 60 bpm is the upper limit of the normal functional activity of the ventricle of the heart. An increase in heart rate up to 60 bpm leads to an increase in the PQ interval and QRS complex, a decrease in the QT interval on the ECG, and a violation of the rhythmic activity of the heart (i.e., the occurrence of extrasystole), as well as to a considerable change in the hemodynamic parameters of the ventricle of the heart and a decrease in its contractile properties. After a period of ventricular extrasystole for several minutes (10–15 min), the activity of the sinus node resumes but with a lower HR compared with the initial HR. The duration of the QRS complex recovers to the initial one, and the PQ and QT intervals increase. Maximum systolic pressure and end-diastolic pressure also return to their original values after extrasystolic contraction. After the experimental extrasystole, the phenomenon of the absence of an increase in HR is observed. The arising extrasystole probably has a functional nature and is one of the mechanisms of electromechanical homeostatic control in the heart.