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Renal vasoconstriction induced by arachidonic acid during burn shock in rats.
Acta Physiol Scand. 1990 May; 139(1):21-7.AP

Abstract

Metabolites of arachidonic acid are possible mediators of local renal vasoconstriction in burn shock. The prostanoid precursor arachidonic acid (AA) therefore was infused in the control period and at 1 and 2 h after scalding in anaesthetized rats. To avoid systemic effects. AA was infused at low doses directly into the renal artery through a thin cannula introduced through the aortic wall. After control observations 40% of the body surface was scalded in 80 degrees C water. Renal arterial blood flow (RBF), measured by an electromagnetic probe, fell to 70% and 58% of the control level at 1 h and 2 h after scalding respectively. Arterial blood pressure was almost maintained. Infusion of AA (5, 15 and 25 nmol) in the renal artery over 15 s caused no effects in the control period, whereas a dose-dependent decrease in RBF was observed after scalding, and was most pronounced 2 h post-burn. The highest dose of AA reduced RBF by 37% at 1 h and by 80% of preinfusion flow at 2 h after scalding. The AA-induced decrease in RBF was abolished by blocking the thromboxane A2 receptors with AH23848. In contrast, inhibition of prostacyclin synthesis or blocking of serotonin S2 receptors did not significantly influence the response to AA during shock. Thus, infusion of AA into the renal artery caused a marked reduction of RBF after scalding, at doses that did not induce a change during the control period. The augmented effect of AA infusion may be due to an increased capacity for synthesis of thromboxane A2 (TxA2), and possibly PGH2 and PGF2 alpha, after scalding.

Authors+Show Affiliations

Department of Physiology, University of Bergen, Norway.No affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

2113346

Citation

Haugan, A, and A Kirkebø. "Renal Vasoconstriction Induced By Arachidonic Acid During Burn Shock in Rats." Acta Physiologica Scandinavica, vol. 139, no. 1, 1990, pp. 21-7.
Haugan A, Kirkebø A. Renal vasoconstriction induced by arachidonic acid during burn shock in rats. Acta Physiol Scand. 1990;139(1):21-7.
Haugan, A., & Kirkebø, A. (1990). Renal vasoconstriction induced by arachidonic acid during burn shock in rats. Acta Physiologica Scandinavica, 139(1), 21-7.
Haugan A, Kirkebø A. Renal Vasoconstriction Induced By Arachidonic Acid During Burn Shock in Rats. Acta Physiol Scand. 1990;139(1):21-7. PubMed PMID: 2113346.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal vasoconstriction induced by arachidonic acid during burn shock in rats. AU - Haugan,A, AU - Kirkebø,A, PY - 1990/5/1/pubmed PY - 1990/5/1/medline PY - 1990/5/1/entrez SP - 21 EP - 7 JF - Acta physiologica Scandinavica JO - Acta Physiol Scand VL - 139 IS - 1 N2 - Metabolites of arachidonic acid are possible mediators of local renal vasoconstriction in burn shock. The prostanoid precursor arachidonic acid (AA) therefore was infused in the control period and at 1 and 2 h after scalding in anaesthetized rats. To avoid systemic effects. AA was infused at low doses directly into the renal artery through a thin cannula introduced through the aortic wall. After control observations 40% of the body surface was scalded in 80 degrees C water. Renal arterial blood flow (RBF), measured by an electromagnetic probe, fell to 70% and 58% of the control level at 1 h and 2 h after scalding respectively. Arterial blood pressure was almost maintained. Infusion of AA (5, 15 and 25 nmol) in the renal artery over 15 s caused no effects in the control period, whereas a dose-dependent decrease in RBF was observed after scalding, and was most pronounced 2 h post-burn. The highest dose of AA reduced RBF by 37% at 1 h and by 80% of preinfusion flow at 2 h after scalding. The AA-induced decrease in RBF was abolished by blocking the thromboxane A2 receptors with AH23848. In contrast, inhibition of prostacyclin synthesis or blocking of serotonin S2 receptors did not significantly influence the response to AA during shock. Thus, infusion of AA into the renal artery caused a marked reduction of RBF after scalding, at doses that did not induce a change during the control period. The augmented effect of AA infusion may be due to an increased capacity for synthesis of thromboxane A2 (TxA2), and possibly PGH2 and PGF2 alpha, after scalding. SN - 0001-6772 UR - https://www.unboundmedicine.com/medline/citation/2113346/Renal_vasoconstriction_induced_by_arachidonic_acid_during_burn_shock_in_rats_ L2 - https://doi.org/10.1111/j.1748-1716.1990.tb08893.x DB - PRIME DP - Unbound Medicine ER -