Resuscitation
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No accurate, independent biomarker has been identified that could reliably predict neurological outcome early after cardiac arrest. We speculated that brain natriuretic peptide (BNP) measured at hospital admission may predict patient outcome. ⋯ Brain natriuretic peptide levels on admission predict neurological outcome at 6 months and survival after cardiac arrest.
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To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. ⋯ Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.
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In animal models of cardiocirculatory arrest (CA) it is of major interest to establish tests that can assess neurological damage after global cerebral ischaemia following CA. We evaluated a tape removal test with regard to detection of sensorimotor deficit, comparing it to the Neurological Deficit Score (NDS) in an established model of global cerebral ischaemia after CA in rats. ⋯ In the present study, a clinically relevant sensorimotor deficit after global cerebral ischaemia following cardiac arrest in rats has been quantified for the first time by using a tape removal test. The tape removal test is a sensitive method that can be easily applied to test large numbers of animals in future studies.
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It has been shown that the inflammatory response and cellular damage after hemorrhagic shock are influenced by resuscitation strategies. Toll-like receptors (TLRs) play an important role in signal transduction in inflammatory conditions. However, alterations in TLR expression following hemorrhagic shock and resuscitation have not been well documented. This study was conducted to measure the impact of different resuscitation strategies on TLR expression and downstream signaling in key organs. ⋯ Hemorrhagic shock activates TLR signaling in lung, but not the spleen, probably through an up-regulation of TLR gene expression, and activation of NF-kappaB pathway. Resuscitation modulates this response in a fluid- and tissue-specific fashion.