Sivelestat is a neutrophil elastase inhibitor and the effects of sivelestat on the contractile regulation of vascular smooth muscle(VSM) have not been reported. This study was designed to determine whether sivelestat affects the contractility of porcine coronary arteries, and if so, to elucidate the underlying mechanism(s) and particularly those involving the Ca2＋ sensitization of VSM. Sivelestat induced the concentration-dependent(3×10－5－3×10－4 M) vasorelaxation of porcine coronary arteries, with or without endothelium, when precontracted with U46619(G protein-coupled receptor agonist; 100 nM). Simultaneous measurements of tension and [Ca2＋]i demonstrated that sivelestat shifted the [Ca2＋]i-tension curve to the right and downward during stimulation with 118 mM K＋ and 100 nM U46619. In β-escin-permeabilized arterial strips, sivelestat abolished contractions induced by GTP plus U46619 at a constant [Ca2＋]i, whereas it had no effect on Ca2＋-induced contractions. These findings suggested that sivelestat induced vasorelaxation via selective inhibition of the Ca2＋ sensitization induced by U46619, without affecting Ca2＋-induced contractions. In conclusion, sivelestat relaxes porcine coronary artery smooth muscle via a selective inhibition of Ca2＋ sensitization induced by a G protein-coupled receptor agonist, without affecting Ca2＋-induced contractions.
Warming of crystalloid fluid can cause expansion of the fluid container, resulting in misevaluation of the fluid level. However, how warming modifies the estimation of remaining fluid volume in the containers, and how much pre-warmed fluid decreases its temperature after running down have not been well studied. In this study, we examined differences between the ruler and the fluid level, and fluid temperatures at the end of infusion among three fluid containers, USP in VIAFLEXTM(the Baxter), LACTECTM(the Otsuka), and USP in EXCELTM(the B. Braun), with and without warming to 38°C. In results, warming of the Baxter and the B. Braun at 38°C caused the fluid levels to be less than the corresponding ruler levels, whereas warming of the Otsuka did not cause the phenomenon. The fluid temperature at the end of infusion line was above 31.7°C without any differences among three containers. In conclusion, the remaining fluid volume of pre-warmed containers may be falsely informed during infusion due to changes in containers’ shapes upon warming in the Baxter and in the B. Braun, but not in the Otsuka. Pre-warmed fluids to 38°C may not be sufficiently effective to treat hypothermia.
We report two cases with severe ischemic coronary disease and ileus because of malignant neoplastic disease. (Case 1)A 72-year-old man who was diagnosed of ascending colonic cancer with ileus complained chest pain. Emergent cardiac catheterization showed left main trunk disease. He received at first off pump coronary artery bypass(OPCAB) and underwent ascending colectomy 15 days after OPCAB. (Case 2) A 79-year-old man with ileus by rectal cancer complained chest pain. Cardiac catheterization showed left main trunk disease. Echocardiogram showed low ejection fraction. He received OPCAB and PCI, and thereafter he underwent low anterior resection for the rectal cancer 26 days after coronary revascularization. Continuous infusions of nicorandil and ladiolol were used during surgeries for maintenance of their hemodynamics. Their postoperative recoveries were smooth and uneventful.
A 65-year-old man underwent a partial hepatectomy for metastatic liver cancer, with no marked changes in hemodynamic or respiratory status. However, severe respiratory insufficiency developed immediately after extubation. Chest radiography showed a butterfly shadow and frothy sputum was suctioned from the tracheal tube on reintubation, and acute pulmonary edema was diagnosed. When acute pulmonary edema occurs immediately after extubation, chest radiography and echocardiography must be performed first to distinguish between cardiogenic and non-cardiogenic pulmonary edema, because of the different potential underlying causes and treatments. In this patient, a cardiogenic cause was ruled out, and we concluded that upper airway obstruction and excessive negative intrathoracic pressure led to pulmonary edema.