Effects of biliverdin administration on acute lung injury induced by hemorrhagic shock and resuscitation in rats.

Hemorrhagic shock and resuscitation induces pulmonary inflammation that leads to acute lung injury. Biliverdin, a metabolite of heme catabolism, has been shown to have potent cytoprotective, anti-inflammatory, and anti-oxidant effects. This study aimed to examine the effects of intravenous biliverdin administration on lung injury induced by hemorrhagic shock and resuscitation in rats. Biliverdin or vehicle was administered to the rats 1 h before sham or hemorrhagic shock-inducing surgery. The sham-operated rats underwent all surgical procedures except bleeding. To induce hemorrhagic shock, rats were bled to achieve a mean arterial pressure of 30 mmHg that was maintained for 60 min, followed by resuscitation with shed blood. Histopathological changes in the lungs were evaluated by histopathological scoring analysis. Inflammatory gene expression was determined by Northern blot analysis, and oxidative DNA damage was assessed by measuring 8-hydroxy-2' deoxyguanosine levels in the lungs. Hemorrhagic shock and resuscitation resulted in prominent histopathological damage, including congestion, edema, cellular infiltration, and hemorrhage. Biliverdin administration prior to hemorrhagic shock and resuscitation significantly ameliorated these lung injuries as judged by histopathological improvement. After hemorrhagic shock and resuscitation, inflammatory gene expression of tumor necrosis factor-α and inducible nitric oxide synthase were increased by 18- and 8-fold, respectively. Inflammatory gene expression significantly decreased when biliverdin was administered prior to hemorrhagic shock and resuscitation. Moreover, after hemorrhagic shock and resuscitation, lung 8-hydroxy-2' deoxyguanosine levels in mitochondrial DNA expressed in the pulmonary interstitium increased by 1.5-fold. Biliverdin administration prior to hemorrhagic shock and resuscitation decreased mitochondrial 8-hydroxy-2' deoxyguanosine levels to almost the same level as that in the control animals. We also confirmed that biliverdin administration after hemorrhagic shock and resuscitation had protective effects on lung injury. Our findings suggest that biliverdin has a protective role, at least in part, against hemorrhagic shock and resuscitation-induced lung injury through anti-inflammatory and anti-oxidant mechanisms.

A fatal case of streptococcal toxic shock syndrome due to Streptococcus dysgalactiae subsp. equisimilis possibly caused by an intramuscular injection.

An 88-year-old man died of streptococcal toxic shock syndrome due to a group G streptococcus infection that was possibly caused by an intramuscular injection given 30 hours earlier in his right deltoid muscle. The causative pathogen was later identified to be Streptococcus dysgalactiae subsp. equisimilis (stG485). Although providing intramuscular injections is an essential skill of health care workers that is performed daily worldwide, it may constitute a port of entry for pathogens via skin breaches that can cause life-threatening infections. All invasive procedures should be carefully performed, especially when immunologically compromised patients are involved.

Emphysematous liver abscesses complicated by septic pulmonary emboli in patients with diabetes: two cases.

An emphysematous liver abscess is a fatal condition that often occurs in patients with uncontrolled diabetes mellitus. I herein describe two cases of Klebsiella pneumoniae-induced emphysematous liver abscesses complicated by septic pulmonary emboli in patients with poorly controlled diabetes mellitus. Both patients showed hemoglobin A1c levels of more than 10% and did not present with any abdominal symptoms on admission. However, they were diagnosed and successfully treated with percutaneous transhepatic abscess drainage and antibiotics. This fatal disease should be taken into consideration in patients with uncontrolled diabetes mellitus who suffer from prolonged fevers and uncharacteristic general malaise.

Inhalation of carbon monoxide following resuscitation ameliorates hemorrhagic shock-induced lung injury.

Even after successful resuscitation, hemorrhagic shock frequently causes pulmonary inflammation that induces acute lung injury (ALI). We previously demonstrated that when CO is inhaled at a low concentration both prior to and following hemorrhagic shock and resuscitation (HSR) it ameliorates HSR-induced ALI in rats due to its anti-inflammatory effects. In the present study, we administered CO to the same model of ALI only after resuscitation and examined whether it exerted a therapeutic effect without adverse events on HSR-induced ALI, since treatment of animals with CO prior to HSR did not prevent lung injury. HSR were induced by bleeding animals to achieve a mean arterial pressure of 30 mmHg for 1 h followed by resuscitation with the removed blood. HSR resulted in the upregulation of inflammatory gene expression and increased the rate of apoptotic cell death in the lungs. This was determined from an observed increase in the number of cells positive for transferase-mediated dUTP-fluorescein isothiocyanate (FITC), nick-end labeling staining and activated caspase-3. HSR also resulted in prominent histopathological damage, including congestion, edema, cellular infiltration and hemorrhage. By contrast, CO inhalation for 3 h following resuscitation significantly ameliorated these inflammatory events, demonstrated by reduced histological damage, inflammatory mediators and apoptotic cell death. The protective effects of CO against lung injury were notably associated with an increase in the protein expression level of peroxisome proliferator-activated receptor (PPAR)-γ, an anti-inflammatory transcriptional regulator in the lung. Moreover, CO inhalation did not affect the hemodynamic status or tissue oxygenation during HSR. These findings suggest that inhalation of CO at a low concentration exerts a potent therapeutic effect against HSR-induced ALI and attenuates the inflammatory cascade by increasing PPAR-γ protein expression.

[Impact of beach chair position on the value of bispectral index during general anesthesia].

BACKGROUND: Although the bispectral index (BIS) has been established as a common index of anesthetic depth, there is a possibility that head-up position may influence BIS values under general anesthesia. This study examined whether beach chair position with 57 degrees head-up would cause the variation of BIS values during shoulder surgery. METHODS: Two groups of patients were scheduled for surgery, one was supine position group, and the other was beach chair position group. Anesthesia was induced with propofol and rocuronium, and maintained with sevoflurane (end-tidal concentration 1.0-1.2%). The BIS values were recorded manually until 120 minutes after the onset of positioning and evaluated at each 30 min interval. RESULTS: There was no time-dependent difference in BIS values during supine position. In contrast, BIS values in beach chair position group showed a marked downward-trend through the measurement period. End-tidal anesthetic gas concentration and mean blood pressure did not significantly differ between the groups consistently. CONCLUSIONS: To our knowledge, this is the first report of the effect of beach chair position on BIS values intraoperatively. This result indicates that the beach chair position causes a time-dependent decrease in BIS under general anesthesia.

[Case of coronary vasospasm during lumbar discectomy in prone position].

A 62-year-old man with hypertension was scheduled for discectomy at L4-5 in prone position. Anesthesia was induced with propofol 70 mg, fentanyl 0.75 mg and rocuronium 40 mg and maintained with sevoflurane 0.8-2.0% in oxygen 2 l x min(-1) and nitrous oxide 2 l x min(-1). Just before the end of surgery, ST elevation with hypotension on the ECG was observed for only a few seconds, followed by ventricular fibrillation (Vf). Immediately, lidocaine 50 mg, nitroglycerine 0.5 mg and methoxamine 6 mg were administered intravenously, and sinus rhythm and normal blood pressure returned from Vf within one minute. This case achieved a complete response to quick administration of the coronary vasodilator and antiarrhythmic agent, in this case whose coronary spasm was suspected on the basis of ST elevation in the first place. We have to be careful of various initiating factors for coronary spasm each time during anesthesia as it is difficult to assess its clinical risk, especially in prone position because actual coronary flow is much lower and cardiac resuscitation is difficult in a sudden cardiac complication.

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.

[The efficacy of intravenous lidocaine for acute herpetic pain--placebo controlled trial].

BACKGROUND: Acute herpetic pain (AHP) which is considered not only nociceptive pain but also neuropathic pain, is often severe and intractable. Although there have been reports of the efficacy of intravenous lidocaine (IVL) for neuropathic pain, the efficacy of lidocaine for AHP is not known. Therefore, the effect of IVL for AHP was examined. METHODS: The study included 43 patients, who visited our pain management office within 90 days after skin eruption of herpes zoster. This study was a randomized, placebo-controlled design. In group A, a continuous infusion of saline 100 ml for 30 min was given followed by a continuous infusion of IVL 3 mg x kg(-1) for 30 min. In group B, IVL 3 mg x kg(-1) for 30 min was given followed by saline 100 ml for 30 min. A pain relief score (PRS) was assessed at the end of each infusion. RESULTS: In group A, PRS decreased significantly with saline and decreased furthermore with IVL. In group B, PRS decreased significantly with IVL and did not change with saline. A reduction of PRS with IVL in group B was significantly greater than that with saline in group A. CONCLUSIONS: This study demonstrates that IVL has a significant analgesic effect in patients with AHP.

[Successful anesthetic management of a patient with thyroid storm using landiolol].

We report successful anesthetic management of a 38-year-old man with thyroid storm using an ultra-short acting beta blocker, landiolol. The patient was admitted to the hospital for severe abdominal pain. An emergency laparotomy was scheduled for perforated gastric ulcer under a condition of uncontrolled thyrotoxicosis. On arriving the operating room, he showed tachycardia of 140 beats x min(-1) and blood pressure of 140/75 mmHg and high fever of 39 degrees C with tremor, sweating and diarrhea. He was anesthetized with oxygen, nitrous oxide, sevoflurane and fentanyl. Heart rate was around 130 beats x min(-1), and the landiolol was given continuously at a rate of 0.02-0.04 microg x kg(-1) x min(-1). Heart rate was controlled bellow 120 beats x min(-1) without hypotension during anesthesia. Thiamazole and inorganic iodine were given through an enterostomy tube postoperatively, and heart rate decreased gradually. He was extubated on the third postoperative day without any sequelae.

[A case of ligating both upper and anomalous lower left pulmonary veins in the left upper lobectomy].

A 53-year-old male was anesthetized for left upper lobectomy under one-lung ventilation using a double-lumen endobronchial tube in the lateral position. When the upper left pulmonary vein was ligated, Pao2/FIo2 ratio (PF ratio) was elevated despite the one-lung ventilation. After the operation, the patient was repositioned onto spine position and massive bleeding occurred from the anomalous lower left pulmonary vein, which was ligated during the operation. The lower left pulmonary vein was restored and the bleeding stopped. Because the pulmonary shunt flow from the lower left pulmonary vein had stopped, the PF ratio was unusually elevated. We urge anesthesiologists to pay attention to the arterial blood gas data even when it is better than expected.

[A case of ligation of the left pulmonary artery during total arch replacement for aortic arch aneurysm].

Pulmonary artery embolism is one of the most severe complications that can occur in the perioperative period. We report a case of left pulmonary artery obstruction during total arch replacement, which occurred during cardiopulmonary bypass (CPB) for severely invasive procedures. A 59-year-old male was anesthetized for total arch replacement using a double-lumen endobronchial tube (Bronco-Cath 39 F left) in the supine position. The surgery was performed under deep hypothermic circulatory arrest and CPB. When the CPB was finished and mechanical ventilation was started, PaCO2 was unusually elevated. Furthermore, end-tidal CO2 was decreased and no CO2 was expired from the left side of the double-lumen tube. Left pulmonary embolism was highly suspected and pulmonary artery angiography was performed. As the complete obstruction of the left pulmonary artery was demonstrated, pulmonary artery reconstruction was performed. The reason for the obstruction was the surgical ligation during CPB. The wall of the aneurysm was attached to the left pulmonary artery and when it was removed, the left pulmonary artery was injured. The systemic circulation remained stable, however, despite reports that pulmonary embolism was very dangerous and often caused the patient's death.