अमूर्त

Cardiac ventricular diastolic phase and papillary muscle lusitropic response to Aurelia venom in abdominal arteriovenous fistulas induced murine circulation volume overloading heart.

Yang Wang, Dorothy Pokuaa, Han Wang, Annie Christel Bell, Zhihao Shen, Shouyan Fan, Linghua Piao, Zhibin Chen, Lingfeng Gao

Purpose: Aurelia venom was reported to inhibit muscle cholinergic receptor elicited cross cellular membrane currents and introduced muscle physiologic tetanus. However, the recording and analyzing of inotrope effectiveness in cardiac muscles was not well established. In this study, we investigated Aurelia venom and its analogue intervene induced cardiovascular hemodynamics variations in cardiac cycle in vivo and cardiac papillary muscle passive tension responsiveness in vitro.

Methods: Aurelia venom was separated by 10% acrylamide gel. CfTX-1 homology 11 amino acid sequence was identified. The sequence was resin solid-phase synthesized subsequently, and defined as CfTX-1 analogue. In vivo fistulas mice left ventricle haemodynamics were measured through carotid artery cannula and venom intervene by local irrigation. Arterial pressure waveforms, diastole and systole dP/dt_max were evaluated. Cardiac papillary muscle lusitrope was investigated in vitro. Myogenic activities during passive tension deceleration and deceleration velocity were determined in several step length stretching.

Results: 100 μl volume challenge with Aurelia venom or CfTX-1 analogue reduced 10% diastolic pressures, however systolic pressure did not significantly increased with significant enhancing of pulse pressure. Furthermore, −dP/dt_max in diastolic phase was improved rather than systolic dP/dt_max in CfTX-1 analogue intervened fistulas heart. The cardiac papillary muscle velocity attenuation after active stretching was significantly accelerated in severe stretched higher preload muscle.

Conclusion: Aurelia crude venom especially CfTX-1 analogue significantly improved ventricle lusitropic responses in diastolic phase, induced a rapidly relaxation velocity reducing. This further promoted ventricular filling to fit volume and pressure strained having great worth to provide accommodation to protect ventricle from mechanical stressing.