The nasal cavity surgery are usually traumatic surgery. Septoplasty leads to reactive inflammation, edema and hypoxemia. In the present study, we study the response of the autonomic nervous system (ANS), its role in changing behavioral reactions, as well as possible mechanisms of impairment of cognitive and adaptive reactions in rats after trauma to the nasal septum mucosa. The nasal septum mucosa was scarified in 10 adult mongrel male rats. The day before surgery and 2 days after surgery animals were tested in the square-shaped “open field” (OF) and electrocardiogram (ECG) in 1 hour before OF. ANS condition was analyzed by the high-frequency component of the heart rate (HF) and the low-frequency component of the heart rate (LF). The correlation of HF & LF with rat behavior in the open field before and after surgery was performed. Simulation of septoplasty in rats provokes a powerful stress response in the form of a sharp imbalance of ANS towards its PNS on the 2 postoperative day. Changes in behavioral and research reactions of rats in OF are manifested in a decrease in research activity, a display of uneasiness, depression-like state, as well as anxiety.
Experiments employing ultrasound technique showed that nonselective blockade of central muscarinic cholinoceptors with amizyl significantly increases the number and lifespan of rats highly resistant to acute massive blood loss. This pretreatment increased individual resistance of the circulatory system to posthemorrhagic hypoxia (blood pressure and portal blood flow rate). Preliminary blockade of central nicotinic cholinoceptors and peripheral muscarinic cholinoceptors with cyclodol and methacin, respectively, had no effect on the percentage of rats highly and low resistant to acute blood loss. Preliminary blockade of peripheral muscarinic cholinoceptors with methacin prevented the decrease in the cardiac output in low resistant animals during the posthemorrhagic period.
Study of the dynamics of cardiac output in rats with different tolerance to acute massive blood loss showed that the pumping ability of the heart remains intact during the entire posthelnorrhagic period in "all high-resistant and in 65% low-resistant rats. In 35% rats that were low-resistant to blood loss, the cardiac output deficiency syndrome developed after cessation of bleeding against the background fall in arterial pressure and a decrease in the hepatic blood flow, which are the signs of rapid variant of the dysfunction produced by acute blood loss.
Variations of blood flow and vascular resistance in the common carotid arteries and of blood flow in the hepatic artery and portal vein are examined during and after acute massive blood loss in rats with low and high resistance to circulatory hypoxia. In rats with low resistance, arterial pressure and the rates of cerebral and hepatic blood macro-and microflow, which have decreased during blood loss, continued to fall during the posthemorrhagic period. After cessation of bleeding, a transient arterial pressure rise to 70 mm Hg is observed in rats with high resistance, while the blood flow via carotid arteries increases to 65% of its initial value, being maintained at this level throughout the period of changes in carotid vascular resistance; intrinsic hepatic arterial blood flow increases to 115% of baseline value, while the portal vein blood flow and hepatic microflow increase to 75%.
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