Phenomenon of the adaptive stabilization of structures and protection of the heart

To study the role of heat shock proteins in the mechanism of adaptive stabilization of structures.

Double-blind randomized trial.

Wistar male rats weighting between 250 and 300 g.

Adaptation to restraint stress. Animals were heparinized and anesthetized with nembutal. Experiments on isolated heart included ischemia, reperfusion, adrenergic damage and heat shock. Biochemical investigations studied calcium transport from sarcoplasmic reticulum and mitochondria, and cytofluorimetrical analysis of DNA using the O'Farrell method.

In reperfusion, the contraction amplitude of the hearts from adapted animals was 8.8 times higher than control. This acceleration of the contractile function recovery was due to a more rapid disappearance of the contracture. The duration of ventricular tachycardia and fibrillation was 246 +/- 16 s in control and 119 +/- 12 s in adaptation (P < 0.001). The creatine kinase release was 719 +/- 34 mU/min/g wet weight in control and 302 +/- 120 mU/min/g wet weight in adaptation (P < 0.05). In adaptation, the heat shock-induced contraction amplitude was 2.4 times higher than control and the enzyme yield was practically absent. Adaptation reduced the duration of atrioventricular blockade from 385 to 233 s per group and decreased the number of extrasystoles by 6.5 times. The calcium leakage from intracellular stores during storage proceeded slower in adaptation than in control. During storage of mitochondria at 4 degrees C, oxygen consumption fell much slower in adaptation than in control. As a result, the capacity of mitochondria (isolated from hearts of adapted animals stored for two days) to consume oxygen was 50% higher than in controls; in controls, almost one-half of nuclei were already damaged at one-chain DNA concentration of 50 micrograms/mL, while this phenomenon was 5.5 times less pronounced in adaptation. Adaptation resulted in the accumulation of five polypeptides (molecular weight 72 kDa and pl from 6.3 to 5.7).

The mechanism providing adaptive increase of the heart resistance is apparent both at the central level and at the level of heart cells, and is accompanied by accumulation of inducible polypeptides.