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Mitochondrial injury in sepsis
Critical Carevolume 11, Article number: P17 (2007)
Sepsis-induced multiple organ failure is the major cause of mortality and morbidity in critically ill patients. However, the precise mechanisms by which this dysfunction is caused remain to be elucidated. It seems that, in sepsis, mitochondria dysfunction results in raised tissue oxygen tensions and organ failure. Possibly due to oxide nitric, that is produced in excess in sepsis, and is known to inhibit mitochondrial respiration in vitro.
To analyze cellular damage to electronic microscopy and evaluated its possible relation with serum cardiac markers (troponin, MB-creatin phosphate kinase), and homodynamic data.
We selected all consecutive patients who met the criteria for septic shock, and we collected blood samples from the first through the 12th day, or until death. We also analyzed homodynamic parameters by pulmonary catheter. From the patients that died, a fragment of the left ventricle was sent for electronic microscopy. The exclusion criteria were previous coronary artery disease or dilated miocardiopathy.
We studied 22 patients, age 53 ± 4 years, APACHE scores 22 ± 2; mortality was 45%. The patients who died showed data of cardiac damage from the first day. This was shown by troponin (0.54 ± 0.08 U/Ml vs 1.7 ± 0.3 U/Ml) and the left ventricular systolic worth index (64.2 ± 3.7 vs 37.6 ± 1.3), respectively, in survivor and nonsurvivor groups. The electronic microscopy from the myocardial of the nonsurvivor group showed a significant injury in the mitochondria, represented by an increase in its numbers. There was an alteration on organelle organization and mitochondria crest lesions. The histology of the heart demonstrated inflammatory infiltration and increases of collagen fibers.
Septic patients with impaired cardiac function demonstrate inflammatory alterations and mitochondrial damage. We hypothesize that mitochondrial damage may, in part, be responsible for the cardiac depression seen in severe septic patients.