Decreased contractility leads to an increase in the final systolic volume and a reduction in CO, leading to hypotension and activation of the β-adrenergic nervous system and RAAS. First, NMII must be enabled. A dominant signaling pathway involves phosphorylation of the myosin regulating light chain by kinase-mediated signaling pathways such as myosin light chain kinase (MLCK) and rho-dependent kinase (ROCK) (Heissler & Manstein, 2013). This is thought to promote F-actin bonding, the assembly of mini-filaments, and thus the formation of an efficient contractile unit. With this in mind, both MLCK and ROCK support junctional contractility and NMII recruitment for the junctional cytoskeleton (Smutny et al., 2010) and for medial-apical networks (Mason et al., 2013; Munjal et al., 2015). Cardiac contractility is a term that expresses the force of contraction or, more precisely, the change in force developed at a certain length of fiber at rest (Bern and Levy, 1988). An increase in the length of the fibers above rest increases the contraction force (Frank-Starling mechanism), but does not increase contractility. In vitro contractility measurements include isometric peak voltage and maximum shortening rate to a fixed initial length. The measurement of contractility in vivo is less accurate. DP/dt during the isonomic phase of the cardiac cycle (isometric contraction) and initial blood flow in the aorta are used as indirect clues. Davie et al. (1987) found that dP/dt values for ventricular contractions in teleasts ranged from 370 mm Hg/s to 480 mm Hg/s, about five times slower than those of mammalian hearts.
On the other hand, tuna has a higher heart rate and ventral aortic pressure, and dP/dt levels are much higher than those of other teleosts and are in the mammalian range (Jones et al., 1992). In contrast, ventricular dP/dt is more than 10 times slower for glutinosa and eptatretus cirrhatus hagfish (approximately 22 mm Hg/sec) than for teleosts (Davie et al., 1987). Ventricular dP/dt in leopard sharks (Triakis semifasciata) is also slow (25 mm Hg/sec) and only 36 mm Hg/sec when swimming (Lai et al., 1990a). The slowness of dP/dt in small-scale fish and elasmobranchia probably reflects low contractility and possibly slow rates of electrical conduction between myocytes. Slow conduction rates would be expected in Hagfish due to the absence of deep penetrating T tubules in the SL and poor electrical couplings between myocytes (Davie et al., 1987). Many forms are mobile – some due to thin filiform flagella and others due to the contractility of the protoplasm. A second set of cells should form muscles that are mainly equipped with contractility. Poor contractility is suspected when preload parameters (preload parameters (history of recent fluid load, ease of stretching of the jugular vein, central venous pressure, post-cavalal diameter, terminal diastolic ventricular volume) indicate normal or high preload and forward flow parameters (blood pressure, pulse quality, vasomotor tone indicators [capillary filling time] and indicators of tissue perfusion Appendix temperature, metabolic acidosis, lactate levels, central venous oxygen pressure indicate poor cardiac output in an animal without organic heart disease (e.B. hypertrophic cardiomyopathy, mitral insufficiency, aortic stenosis, pericardial tamponade, fibrosis).
If poor contractility is suspected, administration of a β1 agonist is indicated. If the animal is also hypotensive, dopamine (5-20 mcg / kg / min) is recommended; If blood pressure is acceptable, dobutamine (5-20 mcg/kg/min) is recommended. However, the case of emergency contractility is slightly better than that of ordinary contractility. The power of cardiac contraction is directly related to the amount of free intracellular Ca2+. The electrical excitation of the sarcolemma evaluates the size of intracellular Ca2+ in an excitation-contraction (e-c) coupling process to generate sufficient amounts of force and force to pump blood (Bers, 2002). As part of a physiologically integrated unit, the contractility and e-c coupling of the fish heart need to be refined to meet general physiological requirements under different environmental conditions and, therefore, we can expect changes in organs, cells and molecules in fish exposed to prolonged anoxia. The contractility of actomyosin in the apical cortex creates forces that lead to apical narrowing, but these cellular forces are also integrated through the tissue during tissue intussusception (Harris and Tepass, 2010; Heisenberg & Bellaïche, 2013; Lecuit et al., 2011). . . .