[Effect of renin-angiotensin system inhibitors on the density of myocardial, pericardial and pulmonary rat mast cells under experimental heart failure].

Activation of the renin-angiotensin system (RAS) plays a critical role in the pathogenesis of heart failure (HF). We studied the effect of lisinopril (LP) and fosinopril (FP), the inhibitors of angiotensin-converting enzyme, and of losartan (LT), the antagonist of Angiotensin II receptors, on the behavior of multifunctional mast cells (MCs) under experimental HF. The inhibitors of RAS were daily injected during 4 weeks in 4 weeks after two (at 24-h interval) isoproterenol injections. MCs of different degrees of maturity were identified on paraffin sections stained with Alcian blue and Safranin. Expressiveness of HF was estimated by functional parameters with the help of echocardiogram and by morphological markers. The MC density in the myocardium of the intact rats as well as of the rats with HF, both treated and untreated with the preparations, was relatively low: from 3 to 4 cells/mm2. The MC density in the pericardium of the intact rats was several times higher than in the myocardium: 35 +/- 7 cells/mm2. The density ofpericardial MC under HF was 1.7 higher than that in the intact rats at the expense of the increase in the density of Alcian-positive immature cells (P < 0.05). The injections of LP increased the MC density still in 1.4 times at the expense of the density of Safranin-positive mature cells (P < 0.01). The injections of FP and LT had no influence on the MC density and the balance of cells of different degrees of maturity in the pericardium. 96-99% of MCs in lung were Alcian-positive cells. The density of such cells in the intact rats, in the rats with HF, and in the rats with HF treated with FP was 30 cells/mm2. The injections of LP and LT decreased the density of pulmonary MCs up to 7 cells/mm2 (P < 0.01) and 19 cells/mm2 (P < 0.05), respectively. Functional parameters of the hearts were consistent with the data of morphological analyses. Myocardium function improvement was noted only in the rats with HF treated with FP and LT. The reaction of MCs (as cell elements of "tissue" RAS) to injections of inhibitors of RAS was various in the myocardium, pericardium and lung of the rats with HF. The injections of LP stimulated maturation of the resident MCs in the pericardium and the replenishment of the population through immature cells migrating from the outside. It allows us to suppose an intensification of secretory activity of the cells. In contrast, the injections of LP and LT reduced the pulmonary MC population.