Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters











Database
Language
Publication year range
1.
Drug Res (Stuttg) ; 69(7): 365-373, 2019 Jul.
Article in English | MEDLINE | ID: mdl-30609434

ABSTRACT

A study of potassium channels correlates the fundamentals of mechanistic pathways and various physiological functions. The knowledge of these pathways provides the background, how to determine unit cell functions and to affect cardio protection. ATP sensitive potassium channels adjust excitability of membrane and functions as per metabolic status of cell. A lot of energy consumption primarily occurred in skeletal muscles which also express high number of potassium channels. The increase in calcium release and high heat production is occurred due to loss of potassium channels. Such type of mediations determines metabolic changes and energy required in the dissipation. IPC reduces infarct size in anesthetized mice. In ischemic-reperfusion, pressure in left ventricle was watched while contractile power recovery did not happen. It was seen that elements of intact potassium channel are fundamental for Ischemic preconditioning (IPC). If more prominent is enactment of potassium channels and their cardiologic effects create high heart rate. All the more as of late, it has been suggested that mitochondrial ATP sensitive potassium channels are critical as closing stage effectors which trigger IPC as opposed to sarcolemmal potassium channels. Nevertheless, the importance of the potassium channels reconsidered in cardio-protection in present findings. These discoveries recommend that potassium channels in the adjusting ischemic-reperfusion damage in mice. The heart rate of the mouse occurred during ischemia; enhance watchful extrapolation applied to larger warm blooded animals.


Subject(s)
Energy Metabolism , Ischemic Preconditioning, Myocardial , KATP Channels/metabolism , Myocardial Infarction/prevention & control , Myocardial Reperfusion Injury/prevention & control , Animals , Cell Membrane/metabolism , Disease Models, Animal , Heart Rate , Heart Ventricles/cytology , Heart Ventricles/metabolism , Heart Ventricles/pathology , Mice , Mitochondria/metabolism , Myocardial Infarction/etiology , Myocardial Infarction/pathology , Myocardial Reperfusion Injury/etiology , Myocardial Reperfusion Injury/pathology , Myocardium/cytology , Myocardium/metabolism , Myocardium/pathology
SELECTION OF CITATIONS
SEARCH DETAIL