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Sergeev IYu

Publications and source records attributed to Sergeev IYu.

3 recordsLinked to original sources

Role of sympathetic cholinergic pathway in the neurogenous control of tissue-type plasminogen activator release into the blood.

The changes in conductivity of skeletal muscle vessels of the hind leg and tissue-type plasminogen activator (t-PA) activity in outflowing blood after electrostimulation (5 V, 0.5 ms, 20 Hz, 30 s) at the L4-L5 level of the peripheral end of the transected isolated sympathetic chain were studied in experiments on anaesthetized cats. Stimulation of the sympathetic chain induced vasoconstriction and release of t-PA from the vascular wall into the blood. Pretreatment with the beta-adrenoblocker propranolol neither changed the character of vascular reactions nor blocked t-PA secretion. Efferent stimulation of the sympathetic chain against a background of alpha-adrenoceptor blockade by dihydroergotoxin increased blood flow and was accompanied by a rise in t-PA activity. The M-cholinergic blocker atropine suppressed both vascular relaxation and release of t-PA into the blood. Vasodilatation accompanied by t-PA secretion could be induced by intraarterial infusion of acetylcholine and blocked by atropine. The existence of a neurogenic mechanism controlling t-PA release from the vascular wall involving a sympathetic cholinergic pathway and connected with excitation of vascular M-cholinoceptors by acetylcholine is suggested.

Acetylcholine↗

Increase in osmolality of venous blood from skeletal muscle during cholinergic vasodilatation.

The arterio-venous difference in the osmolality of blood plasma of cat m. triceps surae was studied during sympathetic cholinergic nerve excitation. The vasodilatation was induced by stimulation of hypothalamus or the sympathetic chain, the latter after alpha-adrenoceptor blockade. The vasodilator effect induced by intraarterial injection of acetylcholine was also tested. In all cases studied the vasodilatation was associated with an increase in osmolality (on the average by 10 mOsm/kg H2O with a maximum at the 30-40th s after the beginning of stimulation). Atropine (0.1 mg/kg) considerably decreased the vasodilator effect elicited by hypothalamic stimulation. The increase in osmolality was much smaller after atropine, a small peak remaining at the 50-60th s after the beginning of stimulation. The latter effect was blocked by propranolol (0.5 mg/kg). Atropine similarly almost completely abolished the vasodilator effect and the increase in osmolality produced by lumbar sympathetic stimulation and acetylcholine. The increase in osmolality was caused by a rise in the contents of Na+ (7.4%), lactate (8.2%) and K+ (13.2%); Ca2+, inorganic phosphate and total protein concentrations remained unchanged. Our data indicate that acetylcholine released by sympathetic endings activates muscle fibre metabolism via the muscarin-receptors. The increase in tissue osmolality resulting from activation of metabolism causes, at least partly, the vasodilator effect.

Acetylcholine↗