Stress cardiomyopathy is a unique heart syndrome that is characterized by reversible left ventricular apical wall motion abnormalities and is commonly known as Takotsubo syndrome. In transient left ventricular apical ballooning, myocardium lengthening stress is in a high energy-demand state. The increased passive tension and force enhancement conducted asynergically are associated with severe hypokinesis on the ventricular wall and reduced the blood ejection fraction. Ventricular myocardial deformation and global longitudinal strain have significant mechanotemporal alteration characteristics. Membrane potential dominant mechanisms related to akinesia are considered from multiple effects of variation of calcium transients, myocardium metabolism, which is relative to the ST segment lift in an ECG, and in the weakness of contraction of the ventricular muscle. Ventricular filling, not pressure,-determine the strengthening from stretching; thus, in stress cardiomyopathy, ventricular apical ballooning (takotsubo-shaped ventricle) strengthens the mechanical stress on the wall. Muscle fiber tolerance of lengthening is a high energy consumption process. Ventricular apical akinesia further aggravates passive tension. Depleted ATP and high inorganic phosphate inhibit Ca 2+-activated development, terminates the crossbridge detachment process in its early stage, and facilitates the occurrence of myogenic force enhancement. Comprehensive analysis of the above mechanisms, in lengthening stress, increased cardiac fibers energy demand, and Ca 2+ transient variation interruption of the diastolic cycle, delayed the onset of systole and aggravated the occurrence of apical ballooning in stress cardiomyopathy.

Toad urothelium barrier is the model to mimic and investigate urothelium permeability. Thiazide blocked ionic transportation in polarized membrane state. Jellyfish venom causes pores to be adjusted to urothelium permeability which improved polarization. This study aimed at CfTX-1 peptide in urothelium permeability evoked polarizations. Thiazide pretreated toad urothelium permeability to ions were investigated in modified Ussing chamber. Thiazide urothelium were further intervened by CfTX-1 peptide and treated with G-protein receptor agonists. 0.1 mol CaCl 2 activated transurothelium potential differences were recorded by unipolar lead and computerized by fast Fourier transform technique. Apical chamber was settled as anode. The amplitude of potential differences were evaluated to determine the urothelium polarizations. The results indicated that CaCl 2 activation induced a positive monophasic wave in thiazide urothelium, which suggested the urothelium was slightly polarized and significantly enhancive in adrenergic receptor treated urothelium. Furthermore, CfTX-1 peptide enhanced transurothelium potential difference in thiazide urothelium, therefore, urothelium were supra polarized. NPPB treatment significantly attenuated this supra polarization, which suggested that the Cl influx was the main stream ionic compound of this polarization. It is concluded that CfTX-1 peptide was considered to generate supra polarization in thiazide urothelium. This mechanism is useful to study the improvement of drug delivery crossing urothelium barrier.

Force enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart. In excessive preload heart, force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. In this study, the force enhancement occurrence in mouse cardiac papillary muscle was evaluated by a microstepping stretch method. The intracellular Ca2+ redistribution during occurrence of force enhancement was monitored in real-time by a Flou-3 (2 mM) indicator. The force enhancement amplitude, the enhancement of the prolongation time, and the tension–time integral were analyzed by myography. The results indicated that the force enhancement occurred immediately after active stretching and was rapidly enhanced during sustained static stretch. The presence of the force and the increase in the amplitude synchronized with the acquisition and immediate transfer of Ca2+ to adjacent fibres. In highly preloaded fibres, the enhancement exceeded the maximum passive tension (from 4.49 ± 0.43 N/mm2 to 6.20 ± 0.51 N/mm2). The occurrence of force enhancement were unstable in each static stretch. The increased enhancement amplitude combined with the reduced prolongation time to induce a reduction in the tension–time integral. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. During the cardiac muscle in its passive relaxation period, the occurrence of this interruption affected the rhythmic stability of the cardiac relaxation cycle.