Hepatitis C virus structural proteins induce liver cell injury in transgenic mice.

To develop an animal model of hepatitis C virus (HCV) infection, transgenic mice carrying part of the HCV cDNA (C980) encoding HCV-core and envelope proteins under control of the mouse class I major histocompatibility complex gene (H-2K) regulatory region were produced. HCV-C980 RNA and HCV-core protein were present in livers from line H36 as determined by RNase protection assay and immunostaining, respectively. More than 40 animals from line H36 were examined histologically. Most of these H36 mice after 10 months of age developed spontaneous focal infiltration of lymphocytes, hepatocyte necrosis, degeneration, and altered foci with mitotic hepatocytes. These pathological lesions were absent in livers from the age-matched control littermates. Liver cells from these H36 mice were sensitive to damage induced by intravenous administration of an anti-Fas antibody. It is suggested that HCV-C980 proteins by themselves may be one causative agent of liver cell injury in subjects with HCV infection.

[Postoperative nausea and vomiting after gynecologic abdominal surgery--a comparison of propofol versus inhalational technique].

Propofol has been reported to reduce emesis. This study was performed to evaluate the incidence of postoperative nausea and vomiting (PONV) in gynecologic abdominal surgery patients after propofol anesthesia and inhalational anesthesia. Sixty patients were evaluated for the incidence of PONV. Thirty patients received oxygen-propofol-epidural anesthesia (propofol group) and the others were maintained with nitrous oxide-oxygen-isoflurane/sevoflurane--epidural anesthesia (inhalational group). The incidence of PONV was 33.3% in propofol group and 60% in inhalational group (P < 0.05). The means of frequency of postoperative nausea were 0.63 and 1.97 in propofol-group and inhalational group, respectively (P < 0.05). Those of postoperative vomiting were 0.17 after propofol and 1.00 following inhalational anesthesia (P < 0.01). For the gynecologic abdominal surgery patients, PONV was significantly less following intravenous anesthesia with propofol than after isoflurane or sevoflurane inhalational anesthesia. This study indicated that propofol anesthesia was useful in reducing PONV after gynecologic abdominal surgery.

[Post dural puncture headache (PDPH) which occurred after the removal of an epidural catheter].

A 57-year-old man received gastrectomy under general anesthesia combined with epidural anesthesia. He showed no signs of dural puncture and catheter migration into the subarachnoid space. Cardiovascular status was stable with epidural injection of lidocaine, morphine during the operation. Although epidural morphine and buprenorphine infusions were continued for 1 to 6 postoperative days, respiratory depression and other side effects were not observed. However, severe headache in the upright position occurred after stopping these infusions and the removal of the catheter on the 7th postoperative day. The headache was thought to be caused by unintentional dural puncture. PDPH persisted over a period of 30 days and was treated with an epidural blood patch and stellate ganglion blocks since the other conservative therapy had been ineffective. We consider that administration of continuous epidural opioids for postoperative analgesia helped to prevent PDPH until the 7th postoperative day. We also conclude that prolonged PDPH after using a thick needle like a Touhy needle should be treated by an epidural blood patch.

Effects of surfactant on lung injury induced by hyperoxia and mechanical ventilation in rabbits.

We evaluated the effects of exogenous surfactant on lung injury caused by 100% oxygen and mechanical ventilation in rabbits. Surfactant-treated rabbits (n = 9) were ventilated with 100% oxygen for 36 hours and bovine surfactant was given via the trachea 12 hours after the start of mechanical ventilation. Saline-treated (n = 9) rabbits were treated identically, except that they received saline without surfactant. There were no significant changes in hemodynamics, lung mechanics, or arterial oxygen tension during artificial ventilation. Albumin concentration in the bronchoalveolar lavage fluid (BALF) of saline-treated rabbits was slightly higher than those in surfactant-treated rabbits and significantly higher than in non-treated rabbits. C3a concentration in BALF was significantly higher in saline-treated rabbits than in surfactant-treated and non-treated rabbits. In addition, the wet-to-dry lung weight ratio was significantly lower in surfactant-treated rabbits than in saline-treated rabbits (5.06 +/- 0.10 vs. 5.67 +/- 0.14, P < 0.05). Light microscopy revealed hyaline membrane formation in saline-treated rabbits, but fewer changes were observed in surfactant-treated rabbits. Electron microscopy revealed extensive endothelial cell destruction in saline-treated rabbits, while such changes except endothelial cell swelling were not observed in surfactant-treated rabbits. We conclude that exogenous surfactant attenuated lung injury caused by oxygen exposure and ventilation.

[Coronary artery spasm during coronary artery bypass surgery].

We report two cases of coronary artery spasm during coronary artery bypass surgery. As one of the complications during cardiac surgeries, coronary vasoconstriction occurs mainly after coming off cardiopulmonary bypass. The factors responsible for the spasm include high endogenous catecholamine levels due to inadequate anesthesia and hypothermia, exogenous catecholamines for circulatory support, various chemical mediators and combination of these factors. Coronary artery spasm was suspected strongly because of sudden ischemic change in electrocardiography and simultaneous aggravation of circulatory parameters, which improved immediately after direct injection of coronary vasodilators into vein graft. This method, popular in coronary angiography and catheterization, is effective for release of coronary-artery spasm observed particularly after cardiopulmonary bypass. Then mechanical circulatory assist is readily available to treat possible systemic side effect of the vasodilators.

[Protective effects of PGE1 on postoperative liver function after gastric cancer surgery].

The effects of PGE1 on liver function tests in patients who underwent gastric cancer surgery were studied. PGE1 was administered in 13 patients at a rate of 20-100 ng.kg-1.min-1 (PGE1 group) during surgery. Fourteen patients served as the control group. On the first postoperative day, SGOT and SGPT increased in both groups. But on the first and the third postoperative days, SGPT of the PGE1 group was significantly lower (P less than 0.05) than that of the control group. Five patients in the control group showed transaminase above 100 IU.l-1 in the postoperative period. In contrast, no patient showed this increase in the PGE1 group. These findings indicate that continuous infusion of PGE1 during surgery is beneficial in attenuating hepatic injury.

Effects of prostaglandin E1 on the cardiovascular response to tracheal intubation.

STUDY OBJECTIVE: To evaluate the efficacy of prostaglandin E1 in attenuating the hypertensive response to laryngoscopy and intubation. DESIGN: Controlled, comparative, and randomized study. SETTING: Induction of anesthesia for elective surgery at a university hospital. PATIENTS: Thirty normotensive patients (ASA physical status I) undergoing elective surgery divided into three groups. Each group consisted of ten patients. INTERVENTIONS: Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. Either 0.3 micrograms/kg of prostaglandin E1, 0.6 micrograms/kg of prostaglandin E1, or saline (control) was injected 15 seconds before starting direct laryngoscopy (within 30 seconds), which was attempted 2 minutes after administration of thiopental sodium and vecuronium. MEASUREMENTS AND MAIN RESULTS: Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were significantly less in prostaglandin E1-treated patients than in the control group (p less than 0.05). CONCLUSIONS: A single rapid intravenous administration of prostaglandin E1 is a practical pharmacologic and safe method to attenuate the hypertensive response to tracheal intubation. The use of 0.6 micrograms/kg of prostaglandin E1 as a supplement during induction is recommended for reducing the pressor response to intubation on the basis of rate-pressure product and mean arterial pressure following intubation as an index.

The effect of diltiazem on the cardiovascular response to tracheal intubation.

The efficacy of diltiazem in the attenuation of the cardiovascular response to laryngoscopy and tracheal intubation was studied in patients who received 0.2 or 0.3 mg/kg diltiazem 60 seconds before the start of laryngoscopy. These data were compared with a control group who received saline. Each group consisted of 10 patients who had elective surgery. Patients who received saline showed a significant increase in mean arterial pressure and rate pressure product associated with tracheal intubation. These increases after tracheal intubation were reduced in diltiazem-treated patients compared with those of the control group (p less than 0.05). The data suggest that a bolus injection of diltiazem is a simple, practical and effective method to attenuate the hypertensive response to laryngoscopy and tracheal intubation.

Perioperative effect of methylprednisolone given during lung surgery on plasma concentrations of C3a and C5a.

Methylprednisolone or saline (placebo) solution was infused intravenously in 28 patients undergoing elective lobectomy for lung cancer. The state of the complement system during and after surgery and the effects of methylprednisolone on biologically active products of complement were studied by measurements of plasma C3a and C5a anaphylatoxins and leukocyte counts in peripheral blood perioperatively. In the placebo group plasma concentrations of C3a were significantly increased on postoperative days 1 and 2, whereas C5a had risen significantly 6 hours after surgery and on days 1 and 2. Methylprednisolone infusion during surgery eliminated the postoperative elevation of C3a and C5a. The postoperative leukocyte count in peripheral blood was higher in the methylprednisolone group than in the controls. The observations indicated that methylprednisolone may reduce the influx of leukocytes from peripheral blood into the airways by attenuating production of biologically active complements.