Histological study on the effect of heat stress on cardiac muscle of adult male albino rats and the possible role of mast cells

ABSTRACT

Heat stress causes serious physiological dysfunction that may result in heat related diseases. The cardiovascular system has been considered the primary target of heart stress. The mechanism of heat stress- induced myocardial damage remains unclear. Recent findings indicate that mast cells are not only necessary for allergic reaction, but they also involved in a variety of neuro inflammatory diseases especially those worsened by stress. This work was aimed to study the effect of heat stress on the myocardium of rats and to clarify the possible role of mast cells in this process. This study was performed on 30 adult male albino rats, divided into three equal main groups [10 rats/ each]; the first main group was control, divided into two equal subgroups [5 rats/ each], the first subgroup [A] was negative control, the second subgroup [B] received 1 ml sterile saline I.P daily for 15 days. The second main group was heat-stressed group which was exposed to heat stress [39°C for 2 hours daily] and the third main group was mast cell stabilized group that received 10 mg/kg/b.w of doxantrazole followed by exposure to heat stress [the same as the second main group], half an hour after drug intake. All rats were sacrificed after 15 days and heart sections were processed. Paraffin sections were stained with H and E, masson trichrom [M.T] and toluidine blue for histological study. Other sections were processed for immuno histochemical demonstration of actin and caspase- 3. Other very small pieces of heart sections were processed for electron microscopic study [E.M]. The cardiac muscle of stressed second group revealed focal areas of necrosis, areas of vaculations with loss of characteristic striations and mononuclear cell infiltration. Congestion and extravasation of blood with odema fluid between cardiac muscle fibers were evident. Excessive collagen fibers deposition was also seen. Decreased reaction for actin and strong+ve reaction for caspase-3 in the affected fibers were demonstrated. Moreover hyperplasia and activation with degranulation of mast cells were documented in C.T endomesium. On ultrastructural level, the same group showed disorganized and fragmented microfilaments and mitochondrial changes. Moreover, degranulated mast cells were documented in the C.T endomesium. On the other hand, non of these changes were observed in cardiac muscles of mast cell stabilized group with the exception of slight congestion and minimal fibrosis in the interstitium and perivascular areas at light microscopic level. It is concluded that heat stress induced histological and ultra structural changes in myocardium and these changes could be mast cell mediated. Such study provided further support for the role of mast cells in stress induced myocardial damage and therefore it might provide a novel medical strategy and therapeutic target in management of heat stress induced cardiomyopathy. Furthermore, stress exposure should be avoided or minimized as much as possible to seek for good health