Experimental Study On Acute Heart Failure Following Seawater Immersion In Dog With Open Abdominal Injury

BackgroundPrevious studies show that injury is worsen after seawater immersion due to the following reasons: symptoms caused by compression after seawater into the abdominal cavity,hypertonic dehydration,hypothermia and pathogen infection. Unlike ordinary trauma, seawater immersion injury has a unique pathophysiology and clinical manifestation. Previous studies focuses on effect of hypothermia and the ways of rewarming. Institute of Field Surgery in The Third Military Medical University and Naval General Hospital Battle Injury Research Center do a lot of experiments regarding to seawater immersion injury, most of those studies are about the hepatic function or respiratory function; there are few reports about the effect of seawater immersion on heart, especially on the failure heart.The pathogenesis of heart failure is complex, it could not be explained by the known theories, including Frank-Starling mechanism,neurohumoral compensatory mechanism and myocardial energy depletion. In the failure heart, there is always accompanied with abnormal cellular and molecular transduction. There are evidences that tumor necrosis factor (TNF)-αplays an important role in the pathogenesis of heart failure.Based on the above-mentioned evidences, after successfully establishment of heart failure dog model, we observed plasma TNF-α, nitric oxide (NO) and brain natriuretic peptide (BNP) levels to explore the possible mechanisms of acute heart failure and hope to provide a new theoretical basis and clinical target for acute heart failure after injury and immersion in the seawater (for possible future war across the Taiwan Strait).Objective1. To establish an experimental animal model of acute heart failure with open abdominal injury and seawater immersion.2. To explore the mechanisms of acute heart failure caused by the open abdominal injury and seawater immersion. MethodsSixteen healthy adult dogs were divided randomly into two groups: control group (n=8) and seawater immersion group (n=8), all dogs are with abdominal injury, while the immersion group also got treated with seawater immersion. Artery catheter (5F) and four-chamber thermodilution Swen-Ganz catheter were placed into anatomized animal jugular vein and carotid artery. Mean artery pressure (MAP), pulmonary artery wedge pressure (PAWP), central vein pressure (CVP) and cardiac output (CO) were obtained and blood samples were taken at different time intervals before and after injury to determine K+, Na+, Cl-, plasma osmolality, blood gas, BNP and TNF-αfor both groups. Doppler Echocardiography was performed to measure the left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), stroke volume (SV) and left ventricular ejection fraction (LVEF) respectively.Results1. There were significant hemodynamic changes in the dogs with open abdominal injury and seawater immersion. After seawater immersion, MAP, CVP and CO was going down in a time-dependent manner in the immersion group. After 2 hour-point of immersion, PAWP went to the highest level (25mmHg); CO was decreased about 60.61% as compared with pre-injury state and decreased about 55.17% as compared with the control dog.2. Cardiac function, determined by echocardiography, was abnormal in the immersion group. As compared with the pre-injury, after 2 hours of immersion, LVESV was increased 72.73%; SV decreased 30.88%, LVEF decreased 39.16% at 2-hour point in the immersion group (P < 0.01). As compared with control dogs, LVESV was increased 42.77% (P < 0.01); SV and LVEF decreased 25.98% and 29.12% in the immersion group. No significant difference was found in the control group before and after injury (P > 0.05).3. Dogs in immersion group had water-electrolyte acid-base balance disorders. Na⁺, K⁺, Cl^- levels and plasma osmolality levels were significantly increased; the degree of acidosis was increased during the experiment in the immersion group. Blood PH value and HCO₃^- were reduced as compared with the control group at the same time point (P <0. 05). No significant difference was noted in control group.4. Plasma cytokines were changed significantly in immersion group. BNP level was gradually increased, reached its maximal level (447.95 pg/ml) at out-water time point in the immersion group. No significant change was noted in the control group. In immersion group, plasma TNF-αlevel was gradually increased, and significant difference was noted at 0.5h point (P <0. 05), and reached the highest value (5.68 ug / L) at out-water 1h time point. Plasma NO was significantly increased, reached its maximum (156.75 umol/L) at out-water time point.Conclusion1. Animal model of acute heart failure with open abdominal injury and seawater immersion was successfully established.2. Seawater immersion and open abdominal injury reduces the body blood volume, leads to electrolyte acid-base balance disorder and changes of various cytokine concentrations. All of those factors result in cardiac myocyte ischemia and hypoxia, energy metabolism abnormality, cardiac electrical activity disorder and reduction of cardiac excitability and myocardial contractility, leading to the heart failure.