| Abstrakt: |
Pneumonia occurs in approximately 50% of intubated patients in burn intensive care units and carries a mortality as high as 40%. A model was developed to study altered cardiopulmonary function in burn complicated by pneumococcal pneumonia. Sprague–Dawley rats were given a 43% total body surface area scald burn or sham burn; 24 h later they were transtracheally inoculated with either 107Streptococcus pneumoniaein 0.5 ml phosphate buffer solution (PBS) or 0.5 ml PBS alone. The four groups were: Sham (N= 7), Burn alone (N= 10), Pneumonia alone (N= 11), and Burn and Pneumonia (N= 12). A fifth group of burned rats (N= 10), given an identical fluid resuscitation regimen, was sacrificed 24 h postburn to examine the early cardiac responses to burn injury alone. Shams and burned animals had normal lung histology, negative bronchoalveolar lavage (BAL) cultures, and negative blood cultures. Pneumonia and burn plus pneumonia animals had abnormal lung histology, positive BAL cultures, and positive blood cultures. Cardiac function was assessed 24 h afterS. pneumoniaechallenge (48 h after burn) (Langendorff preparation). Compared to the Sham group, Pneumonia group, and Burn group, the Burn plus Pneumonia group had the lowest left ventricular pressure (LVP: 94 ± 4, 71 ± 3, and 87 ± 3 mm Hg vs 63 ± 4 mm Hg,P< 0.05), the lowest maximal rate of LVP rise (+dP/dtmax: 1932 ± 115, 1419 ± 71, and 1772 ± 96 mm Hg vs 1309 ± 59 mm Hg/s,P< 0.05), and the lowest maximal rate of LVP fall (−dP/dtmax: 1704 ± 120, 1263 ± 73, and 1591 ± 83 mm Hg vs 1025 ± 98 mm Hg/s,P< 0.05). Cardiac contraction and relaxation deficits were confirmed in animals 24 h postburn (group 5), as indicated by a significantly lower LVP and ±dP/dtmax(62 ± 3 mm Hg, 1210 ± 60, and 909 ± 50 mm Hg/s, respectively,P< 0.05 compared to Sham group). Tumor necrosis factor-alpha (TNF-α) concentrations in serum, but not bronchoalveolar lavage, were greater in burned animals with aspiration pneumonia-induced sepsis than in animals with either burn alone or aspiration pneumonia-induced sepsis alone. While our data suggest that elevated circulating TNF-α levels may contribute, in part, to depressed cardiac function, further studies are needed to fully define the mechanisms underlying cardiac contractile deficits in this model. We speculate that depressed cardiopulmonary function due to burn complicated by pneumonia and sepsis contributes to the high mortality of this patient population. |
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