Abstract
The aim was to identify sex differences in the cardiac response to cholinergic stimuli in the development of myocardial necrosis and light desynchronosis.Materials and methods. Experiments were conducted in 144 albino rats (72 males, 72 females). Myocardial necrosis was induced by adrenaline (0.5 mg/kg, intramuscularly).The intensity of bradycardia that occurred as a response to intravenous acetylcholine injection and electrical stimulation of vagus nerve was measured. The animals were divided into 4 groups: 1 – rats that were in a light balance (day/night); 2 – rats exposed to light deprivation for 10 days; 3 – rats exposed to permanent lighting for 10 days; 4 – animals exposed to permanent lighting for 10 days and injected with melatonin (5 mg/kg) intraperitoneally 1 hour before the necrosis modeling.Results. The development of myocardial necrosis when occurring in light deprivation was characterized by an increased responsiveness of the rat heart to cholinergic stimulation due to an increase in both cholinoreceptors sensitivity and release of acetylcholine from the vagus nerve terminals in females, and due to only an increased cholinoreceptors sensitivity in males. The development of myocardial necrosis in rats exposed to permanent lighting was characterized by significantly higher sensitivity of cholinergic structures of the heart than that in light balance, especially in females. Melatonin injection in the development of myocardial necrosis contributed to the heart cholinergic structures response to the stimulation, which was close to that observed in conditions of light balance, though it remained somewhat higher: due to the facilitation of acetylcholine release from vagus nerve in females, and it was combined with a higher sensitivity of cholinoreceptors in males.Conclusions. The development of myocardial necrosis in light desynchronosis (light deprivation or permanent lighting) causes an increased heart response to cholinergic stimulation in rats. Such effects are stronger, especially in females in conditions of permanent lighting. The injection of melatonin in rats with myocardial necrosis and permanent lighting results in an approximation (but not restoration) of the heart sensitivity to cholinergic stimuli parameters to those that are observed in light balance. However, the heart response to cholinergic stimulation remains higher, especially in males.
Highlights
The aim was to identify sex differences in the cardiac response to cholinergic stimuli in the development of myocardial necrosis and light desynchronosis
The animals were divided into 4 groups: 1 – rats that were in a light balance; 2 – rats exposed to light deprivation for 10 days; 3 – rats exposed to permanent lighting for 10 days; 4 – animals exposed to permanent lighting for 10 days and injected with melatonin (5 mg/kg) intraperitoneally 1 hour before the necrosis modeling
Melatonin injection in the development of myocardial necrosis contributed to the heart cholinergic structures response to the stimulation, which was close to that observed in conditions of light balance, though it remained somewhat higher: due to the facilitation of acetylcholine release from vagus nerve in females, and it was combined with a higher sensitivity of cholinoreceptors in males
Summary
Experiments were conducted in 144 albino rats (72 males, 72 females). Myocardial necrosis was induced by adrenaline (0.5 mg/kg, intramuscularly).The intensity of bradycardia that occurred as a response to intravenous acetylcholine injection and electrical stimulation of vagus nerve was measured. The animals were divided into 4 groups: 1 – rats that were in a light balance (day/night); 2 – rats exposed to light deprivation for 10 days; 3 – rats exposed to permanent lighting for 10 days; 4 – animals exposed to permanent lighting for 10 days and injected with melatonin (5 mg/kg) intraperitoneally 1 hour before the necrosis modeling. Animals were divided into 4 groups: 1 – rats that were in a light balance (day/ night); 2 – rats exposed to light deprivation for 10 days; 3 – rats exposed to permanent lighting for 10 days; 4 – animals exposed to permanent lighting for 10 days and injected with melatonin (a single dose of 5 mg/kg) intraperitoneally 1 hour before the myocardial necrosis (MN) modeling [7]. On the 11th day, adrenaline-induced myocardial necrosis was modeled by adrenaline intramuscular injection (0.5 mg/kg)
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