Effects of hyperbaric oxygen preconditioning on cardiac stress markers after simulated diving.

Arve Jørgensen,Philip P Foster,Alf O Brubakk,Ingrid Eftedal

doi:10.1002/phy2.169

Abstract

Hyperbaric oxygen preconditioning (HBO-PC) can protect the heart from injury during subsequent ischemia. The presence of high loads of venous gas emboli (VGE) induced by a rapid ambient pressure reduction on ascent from diving may cause ischemia and acute heart failure. The aim of this study was to investigate the effect of diving-induced VGE formation on cardiac stress marker levels and the cardioprotective effect of HBO-PC. To induce high loads of VGE, 63 female Sprague–Dawley rats were subjected to a rapid ambient pressure reduction from a simulated saturation dive (50 min at 709 kPa) in a pressure chamber. VGE loads were measured for 60 min in anesthetized animals by the use of ultrasonography. The animals were divided into five groups. Three groups were exposed to either diving or to HBO-PC (100% oxygen, 38 min at 303 kPa) with a 45 or 180 min interval between HBO-PC and diving. Two additional groups were used as baseline controls for the measurements; one group was exposed to equal handling except for HBO-PC and diving, and the other group was completely unexposed. Diving caused high loads of VGE, as well as elevated levels of the cardiac stress markers, cardiac troponin T (cTnT), natriuretic peptide precursor B (Nppb), and αB-crystallin, in blood and cardiac tissue. There were strong positive correlations between VGE loads and stress marker levels after diving, and HBO-PC appeared to have a cardioprotective effect, as indicated by the lower levels of stress marker expression after diving-induced VGE formation.

Highlights

The formation of gas emboli as a result of a reduction in ambient pressure is a major cause of injury associated with diving (Vann et al 2011)
Hyperbaric oxygen preconditioning (HBO-PC) had no effect on venous gas emboli (VGE) formation, which was measured as the maximum amount of emboliÁcm2Áheart cycleÀ1 (Dive: 3.9, HBO45: 4.1, HBO180: 4.4, P = 0.92, n = 12 in each group, Fig. 1)
The primary findings of this study were that strenuous simulated diving with subsequent VGE formation resulted in increased levels of cardiac stress marker expression in rat serum and cardiac tissue

Summary

Introduction

The formation of gas emboli as a result of a reduction in ambient pressure (decompression) is a major cause of injury associated with diving (Vann et al 2011). Circulating VGE is effectively trapped in the lungs, and may cause increased pulmonary artery pressure, cardiac overload, and heart failure (Muth and Shank 2000). Blood perfusion and pulmonary gas exchange are impaired, and the arterial partial pressure of oxygen decreases relative to the increased number of VGE, resulting in hypoxia with subsequent cardiac ischemia and cell death (Butler and Hills 1985; Vik et al 1990). Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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