The relative role of protein synthesis and degradation in determining postprandial net protein deposition in human muscle is not known. To this aim, we studied forearm leucine and phenylalanine turnover by combining the arteriovenous catheterization with tracer infusions, before and following a 4 h administration of a mixed meal in normal volunteers. Forearm amino acid kinetics were assessed in both whole blood and plasma. Fasting forearm protein degradation exceeded synthesis ( P Ͻ 0.01) using either tracer, indicating net muscle protein loss. The net negative forearm protein balance was quantitatively similar in whole blood and in plasma. After the meal, forearm proteolysis was suppressed ( P Ͻ 0.05-Ͻ 0.03), while forearm protein synthesis was stimulated ( P Ͻ 0.05-Ͻ 0.01). However, stimulation of protein synthesis was greater ( P Ͻ 0.05-Ͻ 0.01) in whole blood (leucine data: ϩ 50.4 Ϯ 7.8 nmol/min ϫ 100 ml of forearm; phenylalanine data: ϩ 30.4 Ϯ 11.6) than in plasma (leucine data: ϩ 17.8 Ϯ 5.6 nmol/min ϫ 100 ml of forearm; phenylalanine data: ϩ 5.7 Ϯ 2.1). Consequently, the increment of net amino acid balance was approximately two to fourfold greater ( P Ͻ 0.04-Ͻ 0.03) in whole blood than in plasma.
Our pilot study shows that the administration of PC concentrate to patients having contraindications to the treatment with activated PC was safe and possibly useful to control the coagulopathy triggered and sustained by sepsis. A randomized, double blind study in patients with severe sepsis and contraindications to activated PC administration would be advisable to state the safety and the possible role of this product in the treatment of severe sepsis.
We investigated the incidence of post-intubation hypotension (PIH) in hemodynamically stable patients with STEMI requiring rapid sequences intubation (RSI) and medicated with ketamine or midazolam as induction agent. STEMI patients admitted between 1st January 2009 and 1st January 2017 who did not receive any type of inotropic support before the endotracheal intubation (ETI) was reviewed. PIH was defined as a reduction greater than 20% or a drop of systolic blood pressure (SBP) below 90 mmHg within 10 min from the administration of the induction agent [ketamine (1 mg/kg) or midazolam (0.3 mg/kg)]. Over the study period, 136 patients (66 male and 70 females, mean age 72.25 ± 7.33 years) met the inclusion criteria. Patients treated with midazolam and ketamine were 63 and 73, respectively. PIH was observed in 38 (27.9%) patients after 10 min from ETI. Midazolam patients had a significant lower SBP at both 5 and 10 min after induction (97.75 ± 8.06 vs 100.81 ± 8.08, p = 0.029 and 92.83 ± 7.53 vs 101.58 ± 7.29, p < 0.0001, respectively) (ANOVA p < 0.0001). Age (OR 1.91, 95% CI 1.87-1.97, p = 0.001), history of arterial hypertension (OR 2.27, 95% CI 2.21-2.35, p = 0.0001), multivessel coronary artery disease (OR 2.66, 95% CI 2.58-2.71, p = 0.001), SI ≥0.9 (OR 2.41, 95% CI 2.36-2.48, p < 0.0001) and anterior STEMI (OR 2.51, 95% CI 2.48-2.57, p = 0.0001) resulted independent predictors of PIH in STEMI patients treated with midazolam, as induction agent, before ETI. Midazolam was more likely than ketamine to cause significant PIH when used as an induction agent for RSI in hemodynamically stable patients with STEMI.
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