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A V Samoilenko

Publications and source records attributed to A V Samoilenko.

4 recordsLinked to original sources

Role of vascular system adrenoceptors in formation of venous return.

In experiments on cats electromagnetic flowmetry showed that contribution of the blood flow in the anterior and posterior cava venae to the formation of venous return during stimulation of adrenoceptors with catecholamines is determined by the dynamics of systemic pressor reactions. At the moment of maximum elevation of blood pressure, the major role is played by blood flow changes in the anterior vena cava, while the posterior vena cave plays the predominant role during the period of maximum venous return. Under the action of alpha- and beta-adrenoceptor blockers, venous return is predominantly formed by the blood flow in the posterior vena cava independently on the dynamics of systemic depressor reactions. Adrenoceptor blockade modulates the structure of venous return formation in response to catecholamines: alpha-adrenoceptor blockade reduced the role of anterior vena cava blood flow and increased that of posterior vena blood flow in the formation of venous return, while beta-adrenoceptor blockade induced opposite changes. It is concluded that alpha- and beta-adrenoceptors predominantly control changes in the blood flow in the anterior and posterior cava venae, respectively.

Adrenergic alpha-Antagonists↗

[Hemodynamic changes after application of vasoactive substances in cats with unilateral renal artery constriction in addition to sinoaortal baroreceptor deafferentation].

The relationship between total peripheral resistance (TPR), cardiac output (CO) and venous return (VR) and their role in the response of mean arterial pressure (MAP) on intravenous adrenalin (10 micrograms/kg) and angiotensin II (0.5 micrograms/kg), resp., were investigated in normal cats (A), cats with unilateral renal artery stenosis (B) and cats with sinoaortal baroreceptor deafferentation (C). In the maximum MAP increase in group A there participated both TPR and VR through altered CO. In group B the MAP increased after angiotensin II only in consequence of an enhanced TPR, whereas the VR response was dampened; only after adrenalin the VR contributed a little to MAP increase through CO. In group C, the MAP increase after both substances was due exclusively to increased TPR; at a restricted ejection capacity of the heart the VR cannot act on the level of blood pressure.

Angiotensin II↗