0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Effects of vasopressin during a pulmonary hypertensive crisis induced by acute hypoxia in a rat model of pulmonary hypertension

      , , ,

      British Journal of Anaesthesia

      Elsevier BV

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          <div class="section"> <a class="named-anchor" id="d5785704e123"> <!-- named anchor --> </a> <h5 class="section-title" id="d5785704e124">Background</h5> <p id="d5785704e126">A pulmonary hypertensive crisis (PHC) can be a life-threatening condition. We established a PHC model by exposing rats with monocrotaline (MCT)-induced pulmonary hypertension to acute hypoxia, and investigated the effects of vasopressin, phenylephrine, and norepinephrine on the PHC. </p> </div><div class="section"> <a class="named-anchor" id="d5785704e128"> <!-- named anchor --> </a> <h5 class="section-title" id="d5785704e129">Methods</h5> <p id="d5785704e131">Four weeks after MCT 60 mg kg <sup>−1</sup> administration i.v., right ventricular systolic pressure (RVSP), systolic BP (SBP), mean BP (MBP), cardiac index (CI), and pulmonary vascular resistance index (PVRI) were measured. PHC defined as an RVSP exceeding or equal to SBP was induced by changing the fraction of inspiratory oxygen to 0.1. Rats were subsequently treated by vasopressin, phenylephrine, or norepinephrine, followed by assessment of systemic haemodynamics, isometric tension of femoral and pulmonary arteries, cardiac function, blood gas composition, and survival. </p> </div><div class="section"> <a class="named-anchor" id="d5785704e136"> <!-- named anchor --> </a> <h5 class="section-title" id="d5785704e137">Results</h5> <p id="d5785704e139">PHC was associated with increased RV dilatation and paradoxical septal motion. Vasopressin increased MBP [mean (standard error)] from 52.6 (3.8) to 125.0 (8.9) mm Hg and CI from 25.4 (2.3) to 40.6 (1.8) ml min <sup>−1</sup> 100 g <sup>−1</sup> while decreasing PVRI. Vasopressin also improved RV dilatation, oxygenation, and survival in PHC. In contrast, phenylephrine increased MBP from 54.8 (2.3) to 96.8 (3.2) mm Hg without improving cardiac pump function. Norepinephrine did not alter MBP. Vasopressin contracted femoral but not pulmonary arteries, whereas phenylephrine contracted both arterial beds. Hence, improvements with vasopressin in PHC might be associated with decreased PVRI and selective systemic vasoconstriction. </p> </div><div class="section"> <a class="named-anchor" id="d5785704e147"> <!-- named anchor --> </a> <h5 class="section-title" id="d5785704e148">Conclusions</h5> <p id="d5785704e150">In this rat model of a PHC, vasopressin, but not phenylephrine or norepinephrine, resulted in better haemodynamic and vascular recovery. </p> </div>

          Related collections

          Author and article information

          Journal
          British Journal of Anaesthesia
          British Journal of Anaesthesia
          Elsevier BV
          00070912
          April 2019
          April 2019
          : 122
          : 4
          : 437-447
          Article
          10.1016/j.bja.2019.01.014
          6435915
          30857600
          © 2019

          Comments

          Comment on this article