A.B. Semerjyan, N.F. Krasnikov, A.R. Davtyan, A.G. Mkhitaryan and H.S. Sisakian

Microcirculatory alterations lead to cell and organ dysfunction. High levels of catecholamines induce tachycardia, coronary vasospasm, microcirculatory disruption, hypoxia, ventricular fibrillation. Hypercatecholaminemia increases pulmonary capillary resistance and permeability as well.

Aim of this research is to study adrenaline-induced alterations in myocardial and lung microcirculation, and gas exchange parameters in rats.

Experiments were performed in male Wistar rats divided into 2 groups: control (n=11), and animals (n=12) treated with histotoxic-dose adrenaline. Anesthetized animals were exposed to mechanical lung ventilation at a frequency of 40 breaths/min and were sacrified 20 min after adrenaline injection. Paraffin-embedded myocardial and lung tissues were stained by hematoxylin and eosin. Myocardial and pulmonary microcirculation was studied by Sisakyan and Chilingaryan methods for revealing intraorganic MCB based on detection of phosphatase enzymes’ activities (acid phosphatase and Ca²⁺-ATP-ase, respectively) in the vessel walls. Mean capillary diameter (MCD) was calculated using ocular-micrometer. Partial pressures of arterial blood O₂, CO₂ and pH were measured.

Histologicalstudiesshowed that adrenaline induced contraction band lesions of cardiomyocytes, diffuse pulmonary infiltrations, hemorrhages. Myocardial and lung microcirculation studies revealed inhomogeneous and less intensive staining, tortuous course of capillary walls and their destructive changes. Blood gas analysis data indicated hypoxemia and hypercapnia developing along with acidosis following adrenaline injection.

In conclusion, high-dose adrenaline induces acute myocardial and lung injuries, manifested in inflammatory and microcirculatory alterations, disorders of pulmonary gas exchange that may aggravate further development of cardiopulmonary pathology. The data achieved in present study may allow further adjustment of treatment strategies for stress-induced myocardial injury considering the role of lung microcirculation and gas exchange disorders in the given pathology.