Abstract

BACKGROUND: Vascular endothelial growth factor (VEGF) is a signaling peptide released in response to hypoxia that induces the influx of calcium into endothelial cells. Decreases in serum levels of ionized calcium (iCa2+) are observed following resuscitation from cardiac arrest. We hypothesized that elevations in VEGF would correlate with the decrease in iCa2+ observed in a swine model of cardiac arrest. METHODS: Thirty-five mixed breed Yorkshire swine were premedicated, intubated, and placed under general anesthesia with inhaled isoflurane and nitrous oxide. Under fluoroscopic guidance, balloon occlusion of the left anterior descending coronary artery was performed, just distal to the first septal perforator to induce ventricular fibrillation (VF). Following 7 minutes of untreated VF, standard ALS resuscitation was attempted. Upon return of spontaneous circulation, blood was sampled at 0, 15, and 30 min post arrest for levels of iCa2+ and VEGF. RESULTS: iCa2+ demonstrated an inverse correlation with VEGF levels, with a Spearman rank correlation of rho=-0.52, p<0.0001. In generalized linear mixed modeling (FIGURE 1), a 1 pg/mL increase in VEGF concentrations was associated with a decrease in iCa2+ of 0.001 mg/dL (95% CI 0.003-0.001, p<0.0001). CONCLUSIONS: VEGF is inversely associated with iCa2+ during the early post arrest period. Its production may be responsible for the observed decrease in circulating iCa2+, which may in turn contribute to post arrest hypotension and myocardial dysfunction.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call