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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxia-ischemia (HI) is a model of cerebral ischemia used to model neonatal hypoxia and to study brain damage. Interpreting the results of experiments that use HI rests partly on the assumption that only the brain suffers major damage. In this study, we demonstrate that HI also has adverse consequences on the heart. Both infarction scoring and measurements of troponin I indicate cardiac damage subsequent to HI. These results indicate that the effects of HI on the heart may confound the interpretation of experiments that have used HI to study neuroprotection or other aspects of brain damage.
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PMID:Cerebral hypoxia-ischemia causes cardiac damage in a rat model. 2484 Sep 31

Carbon monoxide intoxication is the most prevalent cause of death from carbon monoxide poisoning. We herein report the case of a 56-year-old man who was found unconscious and smelled of smoke after exposure to carbon monoxide from a heater. He scored 5 on the Glasgow Coma Scale, and had respiratory insufficiency and elevated troponin I, creatine kinase-MB fraction and carboxyhaemoglobin levels. He was treated by mechanical ventilation. After regaining consciousness, brain magnetic resonance imaging showed diffusion restriction in the left occipital lobe; there was a loss of vision (right temporal hemianopsia), which improved by the follow-up session. Carbon monoxide intoxication may cause neurologic and cardiac sequelae, and the initial treatment includes oxygen therapy. Acute carbon monoxide poisoning can cause serious injury to the brain, heart and other organs; the most severe damages that could be inflicted to the brain include cerebral ischaemia and hypoxia, oedema, and neural cell degeneration and necrosis.
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PMID:Cerebrovascular ischaemia after carbon monoxide intoxication. 2582 Aug 56

Background: Following aneurysmal subarachnoid hemorrhage, peripherally-drawn lactic acid has been associated with poor outcomes; however, its clinical significance is unknown. We investigated admission factors and patient outcomes associated with serum lactic acid in this population. Methods: This was a retrospective observational study of 105 consecutive patients with serum lactate collected within 24 h of admission. Primary objectives were to determine the incidence of admission lactic acidemia, and factors positively and negatively associated with lactate levels. We also sought to determine if admission lactic acidemia was associated with patient outcomes, including vasospasm, delayed cerebral ischemia, mortality, and discharge disposition. Results: Admission serum lactic acid was elevated in 56 patients (53% of the cohort). Levels were positively associated with Hunt & Hess and modified Fisher grade, glucose, troponin I and white blood cell counts, and negatively associated with GCS and ventilator-free days. Admission lactate was not associated with the development of vasospasm or delayed cerebral ischemia. Patients with elevated lactic acid more often died during hospitalization, and less often were discharged home. After adjusting for other predictors of poor outcome, the adjusted odds of inpatient mortality (OR 0.97, 95% CI 0.79-1.20; p = 0.80) and discharge to home (OR 1.00, 95% CI 0.80-1.26; p = 0.97) was not associated with admission lactic acid. Conclusions: Early serum lactic acid elevation is common following aneurysmal subarachnoid hemorrhage and is associated with the clinical and radiographic grade of hemorrhage. Levels did not independently predict short-term outcomes when adjusted for established predictors of poor outcome. Further study is needed to determine the clinical significance of peripherally-drawn lactic acid in aneurysmal subarachnoid hemorrhage.
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PMID:Serum Lactic Acid Following Aneurysmal Subarachnoid Hemorrhage Is a Marker of Disease Severity but Is Not Associated With Hospital Outcomes. 3008 30