Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock.

Hemorrhagic shock followed by resuscitation (HSR) causes oxidative stress, which results in multiple organ damage. The kidney is one of the target organs of HSR-mediated oxidative tissue injury. Heme oxygenase (HO)-1, the rate-limiting enzyme in heme catabolism, is induced by oxidative stress; it protects against oxidative tissue injuries. The aim of the present study was to examine the role of renal HO-1 induction after HSR. Rats were subjected to hemorrhagic shock to achieve a mean arterial pressure of 30 mmHg for 60 min, followed by resuscitation with the shed blood. HSR resulted in a significant increase in functional HO-1 protein in the tubular epithelial cells of the kidney, whereas HSR resulted in only a slight increase in gene expression of tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS), and in protein expression of activated caspase-3 solely in renal cells where HO-1 expression was absent. HSR also resulted in a significant increase in Bcl-2 gene expression. Pretreatment of HSR animals with tin-mesoporphyrin (0.5 micromol/kg), a specific competitive inhibitor of HO activity, resulted in a significant decrease in HO activity and exacerbated tissue inflammation and apoptotic cell death as judged by the marked increase in expression of TNF-alpha and iNOS, and in activated caspase-3-positive cells, and the significant reduction in Bcl-2 expression, respectively. These findings indicate that HO-1 induction is an adaptive response to HSR-induced oxidative stress and is essential for protecting tubular epithelial cells from oxidative damage through its anti-inflammatory and anti-apoptotic properties.

[Anesthetic management of awake off-pump coronary artery bypass grafting (ACAB) with remifentanil and thoracic epidural anesthesia].

Two patients with total occlusion of the right internal carotid artery, were anesthetized for ACAB with remifentanil and thoracic epidural anesthesia. Case 1: A 71-year-old man with hypertension and diabetes mellitus underwent single-vessel ACAB under IV remifentanil analgesia, the dose of which was adjusted to 0.04-0.05 microg x kg(-1) x min(-1), along with an epidural infusion of 10 ml x hr(-1) of a mixture of 2% lidocaine and 2.5 microg x ml(-1) of fentanyl, the PaCO2 being maintained at 52-55 mmHg. When the patient felt pain, the remifentanil dose was elevated to 0.08 microg x kg(-1) x min(-1) and PaCO2 increased to 60 mmHg. Case 2: A 66-year-old man with rheumatoid arthritis underwent ACAB for two grafts. An intraaortic balloon pump (IABP) was inserted preoperatively. The anesthetic method used was the same as in case 1, except for an additional right femoral block to provide anesthesia for extraction of the saphenous vein. Remifentanil was infused at 0.05 microg x kg(-1) x min(-1) and PaCO2 maintained at 49-53 mmHg. In response to the patient's pain and movement, the remifentanil dose was increased to 0.07-0.10 microg x kg(-1) x min(-1) and PaCO2 to 60 mmHg.

[Heparin resistance associated with elevated factor VIII].

An 84-year-old female patient was scheduled to undergo AVR, CABG, and Maze procedure. She had a history of hypertension, cerebral infarction, and branch retinal vein occlusion. Warfarin was administered preoperatively. Before the cardiopulmonary bypass (CPB), heparin 5,000 units was administered. Activated coagulation times (ACTs) before and after CPB were 123 sec and 157 sec, respectively. Additional heparin of 5,000 units extended ACT to 221 seconds, which was not enough for the CPB. Heparin 10,000 units was added, and ACT was 157 sec. AntithrombinIII (ATIII) and platelet counts were 75% and 270,000 mm(-3), respectively. ATIII 1,500 units was administered. ACT and ATIII became 133 sec and 123%, respectively. Because heparin resistance did not respond to ATIII, the operative method was changed to off-pump CABG. A postoperative examination revealed high factor VIII activity of 263%. Other results were as follows: protein C antigen, 40%; protein S antigen, 65%; factor VII, 50%; platelet factor 4, 12%; heparin cofactor II, 104%; von Willebrand factor antigen, 181%; heparin-PF4-IgG antibody, negative; factor VIII inhibitor, negative. The low values of protein C, protein S, and factor VII may have been caused by warfarin. Other values were normal, except for the von Willebrand factor antigen.