Effect of PGD2, PGE2, PGF2α and PGI2 on blood pressure, heart rate and plasma catecholamine responses to spinal cord stimulation in the rat
Laboratory of Clinical Science, National Institute of Mental Health Bethesda, Maryland 20205 USAProstaglandins 03/1981; 21(2):189-206. DOI: 10.1016/0090-6980(81)90137-4
The following experiments were designed in order to examine the inter-relationships of various prostaglandins (PG's) and the adrenergic nervous system, in conjunction with blood pressure and heart rate responses, in vivo. Stimulation of the entire spinal cord (50v, 0.3-3 Hz, 1.0 msec) of the pithed rat increased blood pressure, heart rate and plasma epinephrine (EPI) and norepinephrine (NE) concentration (radioenzymatic-thin layer chromatographic assay). Infusion of PGE2 (10-30 microgram/kg. min, i.v.) suppressed blood pressure and heart rate responses to spinal cord stimulation while plasma EPI (but not NE) was augmented over levels found in control animals. PGI2 (0.03-3.0 microgram/kg. min, i.v.) suppressed the blood pressure response to spinal cord stimulation without any effect on heart rate or the plasma catecholamine levels, PGE2 and PGF2 alpha (10-30 microgram/kg. min, i.v.) did not change the blood pressure, heart rate or plasma EPI and Ne responses to the spinal cord stimulation although PGF2 alpha disclosed an overall vasopressor effect during the pre-stimulation period. At the pre-stimulation period it was also observed that PGE2, PGF2 alpha and PGI2, had a positive chronotropic effect on the heart rate, the cardiac accelerating effect of PGE2 was not abolished by propranolol. These in vivo studies suggest that in the rat, PGE2 and PGI2 modulate sympathetic responses, primarily by interaction with the post-synaptic elements - PGE2 on both blood vessels and the heart and PGI2 by acting principally on blood vessels.
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ABSTRACT: In recent years, knowledge of the biochemistry of oxygenated metabolites of arachidonic acid has greatly increased. Their biological functions in acceleration and prevention of platelet aggregation and in inflammatory and immune reactions are becoming much clearer. The therapeutic value, particularly of PGI2 as well as selective inhibitors of synthesis, is also rapidly advancing. Despite much effort, the functional importance of prostaglandins and thromboxanes in the cNS in normal ongoing physiological processes is still quite uncertain. However, when parenchymal or vascular elements are damaged or invaded by extraneural cells, the synthesis of one or the other member of the eicosanoids is greatly increased and contributes significantly to pathophysiological reactions. Thus, prevention of synthesis is likely to have increasing importance in clinical neurology, particularly in cerebrovascular diseases.
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ABSTRACT: Acute hypovolemia induced by bleeding (5 ml/300 g body weight) halothane-anesthetized (0.8% in oxygen) rats is attended by hypotension, bradycardia, and increases in plasma renin, vasopressin, and catecholamine levels. Infusion of prostacyclin (PGI2, O.03 microgram/kg.min) to acutely hemorrhaged rats enhanced recuperation of heart rate, and potentiated the sympathetic response and vasopressin release without altering blood pressure of plasma renin concentration (PRC). Bleeding of bilaterally adrenal demedullated, splanchnicectomized rats resulted in prolonged hypotension and increased plasma levels of vasopressin and renin; epinephrine in the plasma was not detectable, and plasma norepinephrine concentration was not increased after hemorrhage. Prostacyclin infusion to the demedullated, splanchnicectomized rats had no effect on heart rate but enhanced blood pressure recovery after hemorrhage; in this experimental group, PRC was markedly elevated but prostacyclin had no effect on plasma vasopressin or catecholamine concentrations. In rats exposed to severe bleeding, resulting in a nonreversible shock and high mortality, PGI2 infusion after the bleeding increased the survival rate without effect on blood pressure, heart rate, or circulating levels of vasopressin and catecholamines. This study suggests that prostacyclin, through stimulation of the sympathoadrenal axis, enhances heart rate recuperation and vasopressin release in response to acute hemorrhagic shock. Furthermore, prostacyclin may stimulate renin secretion in sufficient amount to compensate for the inadequate sympathetic response during hemorrhagic shock. It is also shown that prostacyclin improves the survival rate to severe hemorrhage without overt hemodynamic or sympathetic effects.
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