The multifunctional mast cells (MC), located in the myocardium, actively react to the pathology of a cardiovascular system. We investigated MC density in the pericardium and myocardium of rats in intact and experimental heart failure (HF) 24 h and 14, 28, and 60 days after two (at 24 h intervals) injections of Isoproterenol (IP) inducing necrosises in the myocardium. An expressiveness of HF was estimated with the help of ultrasonic scanning of the heart after 28 and 60 days after two IP injections. MC of different degrees of maturity were identified cytochemically on paraffin sections stained with Alcian blue-Safranine. The MC density in the myocardium of intact and experimental rats was relatively low, ranging from 4 to 6 cells/mm2, thus the ratio of cells of a different degrees of maturity during HF development was reliably unchanging. In the fibrous layer of pericardium, the MC density was higher than in the myocardium and, for the intact rats, it amounted 48.6 ± 13.0 cells/mm2. 24 h to 14 days after IP injections, the MC density in pericardium in contrast to intact sample increased on the average in 1.5 times (P < 0.05) at the expense of increase of density of more differentiated cells stained with Safranine, without density change of less differentiated cells stained with Alcian blue. After 28 days, the MC density in pericardium was 2 times higher than in the intact sample (P < 0.01) and, at the same time, the density of cells of a different maturity degree (P < 0.05) was considerably increased. For 60 days, the MC density and the balance of Alcian-and Safranine-positive cells did not differ reliably from the intact sample. The dynamic of behavior of the MC population of pericardium was corresponding to HF injury on functional parameters. The data obtained indicate the active reaction of MC pericardium on a dysfunction of the myocardium; it stimulates the maturation of resident MCs and the reinforcement of the population at the expense of the migration of cells from the outside, which allows us to propose an intensification of the MC secretory function. © MAIK Nauka 2008.