Implication of vasopressin in the vascular response to myocardial infarction and cardiogenic shock in a rat model
Introduction Acute heart failure (AHF) due to acute myocardial infarction (AMI) is likely to involve cardiogenic shock (CS), with neuro-hormonal activation, when early revascularization is not efficient. The increase of vasopressin (VP) release has been associated with poor prognosis in AHF and may be involved in microcirculation alteration with inadequate tissue oxygenation. Objective The aim of the experimental study was to investigate the implication of VP in the alterations of circulation and tissue oxygenation observed in AMI with suspected CS. Methods Surgical left coronary artery ligation was performed (PMI, n = 38) or not (Sham, n = 26) on male Wistar rats treated (PMI-SR, n = 6 and Sham-SR, n = 6) or not with the VP antagonist SR-49059. Animals were sacrificed the day after the surgery. Echocardiography was performed to validate AHF and to determine ejection fraction (EF). Mesenteric oxygenation (MO) was measured by abdominal near infrared spectroscopy to estimate tissue oxygenation. Contractile response to VP were evaluated ex vivo on aortic rings. Results expressed as mean were compared between Sham and PMI with EF Results In sham and PMI groups, mortality rates were respectively 4 and 36%. In animals treated with SR-49059, no death was noticed. In all groups, MO decreased immediately after surgery. We observed a significant ( P P = 0.12). Ex vivo contractile response of aorta to VP was impaired in PMI group. The maximal contraction induced by the agonist represented 57% of the maximal response to KCl in PMI groups while it represented 70% in Sham group ( P = 0.04). Conclusion CS after severe AMI was associated with a prolonged decreased in mesenteric oxygenation and a decreased in the contractile response to VP. Antagonist treatment appeared to provide better microcirculatory recovery and to reduce mortality.
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