Time dependent increase in myocardial distensibility after an acute preload elevation.

• Type: Summary of Presentation in an International Conference
• Date: 2007

Authors

Martins J (Author) Other; Pires AL (Author) FMUP; Ladeiras-Lopes R (Author) FMUP; Monteiro-Sousa D (Author) Other; Brás-Silva C (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Journal of Heart Failure

Initial page: 9

Heart Failure 2007

Hamburgo, Alemanha, 09 a 12 de Junho de 2007

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Purpose: The acute response to myocardial stretch is classically described as inducing immediate and delayed increases in contractility, each one regulated by different molecular mechanisms. Despite the evidence that some of the latter mechanisms might be also regulating the myocardial diastolic properties after acute muscle stretch, their roles remain to be clarified in this setting. Methods: Rabbit papillary muscles (modified Krebs solution, 0.2Hz, 1.8mM Ca2+, 30°C) were acutely stretched from 92% Lmax to 100% Lmax (length at which maximal force is developed) in the absence (n=8) or presence of amiloride (a Na+/H+-exchanger inhibitor; n=6) or chelerytrine (a selective protein kinase C inhibitor, PKC; n=7). Immediate and delayed responses to muscle stretch were evaluated. Results presented as mean ± standard error (p<0.05). Results: At baseline conditions, myocardial stretch promoted an immediate increase in contractility, inducing a 33.4±5.4% increase in Active Tension (AT), followed by a 10 minute elevation of 35.5±14.5% over the immediate response, remaining then constant until the end of the protocol (60 minutes). While the delayed response was inhibited by amiloride and chelerytrine, none of these inhibitors affected the immediate increase in AT. On the other hand, after an initial and stretch-induced increase of myocardial Passive Tension (PT), this parameter showed a delayed and continuous decrease, reaching a maximum of 54.7±2.9% at 35 minutes, remaining then constant until the end of the experiment. This PT decrease was significantly attenuated by chelerytrine (-39.5±2.1%) but not by amiloride. Conclusion: Myocardial stretch induces a delayed and significant decrease in cardiac muscle stiffness (PT decrease at constant muscle length), which is partially mediated by PKC. On the other hand, the delayed increase in contractility is PKC and Na+/H+-exchanger dependent. Therefore, the decrease in myocardial stiffness that follows muscle stretch allows the ventricle to increase its contractility after an elevation of end-diastolic volume with filling pressures more than 50% lower, thus decreasing the odds of pulmonary congestion.

Language: English

Type (Professor's evaluation): Scientific

Notes: Heart Failure 2007, published in journal, Journal of Heart Failure. 2007; 6(Suppl1):9.