Search results
Results from the WOW.Com Content Network
Myocardial contractility represents the innate ability of the heart muscle (cardiac muscle or myocardium) to contract.It is the maximum attainable value for the force of contraction of a given heart.
A molecule, called adenosine triphosphate (ATP) which is produced by an intracellular structure called a mitochondrion, is then used, as a source of energy, to help move the myosin head, carrying the actin. As a result, the actin slides across the myosin filament shortening the muscle. This is called a power stroke.
Contraction that squeezes blood towards the exit is more efficient than a simple squeeze from all directions. Although the ventricular stimulus originates from the AV node in the wall separating the atria and ventricles, the Bundle of His conducts the signal to the apex. Depolarization propagates through cardiac muscle very rapidly.
The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. [1] It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. [1]
It is a region of cardiac muscle on the wall of the upper right atrium near to the superior vena cava entrance. The cells that make up the SA node are specialized cardiomyocytes known as pacemaker cells that can spontaneously generate cardiac action potentials. These signals are propagated through the heart's electrical conduction system.
The main role of a sinoatrial node cell is to initiate action potentials of the heart that can pass through cardiac muscle cells and cause contraction. An action potential is a rapid change in membrane potential , produced by the movement of charged atoms ( ions ).
First, atrial contraction feeds blood into the ventricles, then ventricular contraction pumps blood out of the heart to the body systems, including the lungs for resupply of oxygen. Cardiac systole is the contraction of the cardiac muscle in response to an electrochemical stimulus to the heart's cells (cardiomyocytes).
Unlike skeletal muscle, E-C coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release, [35] which is based on the junctional structure between T-tubule and sarcoplasmic reticulum. Junctophilin-2 (JPH2) is essential to maintain this structure, as well as the integrity of T-tubule.