Early recognition of minor myocardial cell injury and appropriate treatment may prevent development of myocardial infarction as one of the most severe postoperative cardiac complications. Troponins have been shown to be sensitive biochemical markers for the assessment of myocardial cell injury. We investigated prospectively 67 cardiac risk patients undergoing elective non-cardiac surgery. Troponin T (TNT) concentrations were measured during the perioperative period, and in those patients with increased TNT (cut-off 0.2 ng ml-1), troponin I (TNI) concentrations were measured additionally (cut-off 0.6 ng ml-1). Patients were allocated to one of three groups: group I, all patients with normal TNT concentrations had a good cardiac outcome (80.5%). In those patients with increased TNT concentrations (19.5%) TNI was also positive; group II, patients (8.8%) with only slightly increased TNT concentrations (0.32-0.99 ng ml-1) also had a good outcome, indicating minor myocardial cell injury, whereas patients with cardiac complications (11.9%) had higher TNT concentrations (0.47-9.8 ng ml-1) (P < 0.05) (group III). With a TNT cut-off at 0.2 ng ml-1, the positive predictive value for adverse outcome was 61.5%; the negative predictive value was 100%. With a TNT cut-off at 0.6 ng ml-1, the positive predictive value for adverse outcome increased to 87.5%, but the negative predictive value was still high (98%). Most of the patients showed an increase in TNT content from the day of surgery until the third postoperative day. We conclude that serial troponin measurements during the perioperative period identify pre-, intra- and postoperative myocardial cell injury. The concentration of troponin T may reflect the degree of injury and help categorize the subsequent risk.
This study demonstrates that increased post-operative release of fNA and fA as well as of cNA and cA correlates with high post-operative serum levels of troponins in cardiac risk patients undergoing non-cardiac surgery.
The enteric nervous system (ENS) has to respond to continuously changing microenvironmental challenges within the gut and is therefore dependent on a neural stem cell niche to keep the ENS functional throughout life. In this study, we hypothesize that this stem cell niche is also affected during inflammation and therefore investigated lipopolysaccharides (LPS) effects on enteric neural stem/progenitor cells (NSPCs). NSPCs were derived from the ENS and cultured under the influence of different LPS concentrations. LPS effects upon proliferation and differentiation of enteric NSPC cultures were assessed using immunochemistry, flow cytometry, western blot, Multiplex ELISA and real-time PCR. LPS enhances the proliferation of enteric NSPCs in a dose-dependent manner. It delays and modifies the differentiation of these cells. The expression of the LPS receptor toll-like receptor 4 on NSPCs could be demonstrated. Moreover, LPS induces the secretion of several cytokines. Flow cytometry data gives evidence for individual subgroups within the NSPC population. ENS-derived NSPCs respond to LPS in maintaining at least partially their stem cell character. In the case of inflammatory disease or trauma where the liberation and exposure to LPS will be increased, the expansion of NSPCs could be a first step towards regeneration of the ENS. The reduced and altered differentiation, as well as the induction of cytokine signalling, demonstrates that the stem cell niche may take part in the LPS-transmitted inflammatory processes in a direct and defined way.
SummarySupraglottic airway devices such as the ProSeal Laryngeal Mask Airway TM (PLMA) and Laryngeal Tube-Suction TM Airway (LTS) that provoke the least stress responses could be beneficial in many situations, especially in patients with cardiovascular disease. We compared the haemodynamic and catecholamine stress response of the LTS and PLMA in a randomised study of 36 patients. Mean arterial pressure, heart rate, epinephrine and norepinephrine levels were all reduced following induction of anaesthesia with no significant differences between the two groups. Following insertion of LTS, mean arterial pressure, heart rate, epinephrine and norepinephrine levels increased to pre-induction levels. However, following the insertion of the PLMA, mean arterial pressure, heart rate, epinephrine and norepinephrine levels remained significantly lower than pre-induction values. Mean arterial pressure, heart rate and epinephrine were significantly greater in the LTS group than in the PLMA group. We conclude that the LTS produces a greater and more sustained haemodynamic and catecholamine stress response than does the PLMA.
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