Prophylactic low-dose ketamine was found to be effective in preventing postoperative shivering.

Portopulmonary hypertension (PPHTN) is no longer an absolute contraindication to orthotopic liver transplantation (OLT).P ortopulmonary hypertension (PPHTN) is pathophysiologically distinct from hepatopulmonary syndrome. Whereas PPHTN is characterized by pulmonary vasoconstriction, hepatopulmonary syndrome is characterized by pulmonary vasodilation, shunting, and hypoxemia. 1 The early clinical recognition of PPHTN may be frustrated by nonspecific cardiopulmonary symptoms. Late PPHTN can be complicated by hemodynamic compromise and right heart failure.PPHTN is defined by a mean pulmonary arterial pressure (MPAP) greater than 25 mm Hg in a patient with a pulmonary capillary wedge pressure (PCWP) less than 15 mm Hg, portal hypertension, and no intrinsic or underlying lung disease. 2 PPHTN may be categorized further into mild (MPAP, 25 to 35 mm Hg), moderate (MPAP, 36 to 45 mm Hg), and severe (MPAP Ͼ 45 mm Hg). 3 Up to 12.5% of patients presenting for orthotopic liver transplantation (OLT) evaluation have PPHTN, 3-5 but 60% of these patients are asymptomatic at the time of diagnosis. 6 The prognosis for patients with PPHTN is dismal, with a mean and median survival after diagnosis of 15 months and 6 months, respectively. 6 The 6-month mortality rate is estimated to be approximately 50%. 6 In patients with severe PPHTN who proceed to OLT, perioperative mortality is very high. In 5 patients with severe PPHTN who underwent OLT at the University of Pittsburgh, PA, the perioperative mortality rate was reported at 80% and resulted primarily from right ventricular (RV) dysfunction. 7 It has been estimated that in patients who undergo OLT with an MPAP between 35 and 49 mm Hg and pulmonary vascular resistance (PVR) of 250 dynes ⅐ s ⅐ cm -5 or greater, the mortality rate is 50%. Patients with an MPAP of 50 mm Hg or greater have a cardiopulmonary mortality rate that approaches 100%. 2,8 It therefore has been recommended that moderate to severe PPHTN and significant RV dysfunction should be considered contraindications to OLT. 2 However, preoperative therapy to reduce pulmonary hypertension and RV dysfunction may improve clinical status and make OLT feasible. Continuous intravenous epoprostenol (prostacyclin, or prostaglandin I 2 ) is a potent vasodilator shown to improve exercise tolerance, reduce PVR, and improve mortality in patients with primary pulmonary hypertension. 9 Similar hemodynamic improvements have been achieved before OLT in patients with PPHTN. 10,11 Kuo et al 10 treated 4 patients with severe PPHTN (MPAP, 53 to 63 mm Hg) with 10 to 28 ng/kg/min of epoprostenol over 6 to 14 months and reported a 29% to 46% decrease in MPAP, a 22% to 71% decrease in PVR, and a 25% to 75% increase in cardiac output (CO).

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Myoclonic movements and pain on injection are common problems during induction of anesthesia with etomidate. We investigated the influence of pretreatment with magnesium and two doses of ketamine on the incidence of etomidate-induced myoclonus and pain. A prospective double-blind study was performed on 100 ASA physical status I-III patients who were randomized into 4 groups according to the pretreatment drug: ketamine 0.2 mg/kg, ketamine 0.5 mg/kg, magnesium sulfate (Mg) 2.48 mmol, or normal saline. Ninety seconds after the pretreatment, anesthesia was induced with etomidate 0.2 mg/kg. Vecuronium 0.1 mg/kg was used as the muscle relaxant. An anesthesiologist, blinded to group allocation, recorded the myoclonic movements, pain, and sedation on a scale between 0-3. Nineteen of the 25 patients receiving Mg (76%) did not have myoclonic movements after the administration of etomidate, whereas 18 patients (72%) in the ketamine 0.5 mg/kg, 16 patients (64%) in the ketamine 0.2 mg/kg, and 18 patients (72%) in the control group experienced myoclonic movements (P < 0.05). We conclude that Mg 2.48 mmol administered 90 s before the induction of anesthesia with etomidate is effective in reducing the severity of etomidate-induced myoclonic muscle movements and that ketamine does not reduce the incidence of myoclonic movements.

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Postmenopausal hormone replacement therapy (HRT) protects women from the risk of cardiovascular system disease, osteoporosis, and dementia. There are conflicting reports about the effects of HRT on insulin resistance. The purpose of this study was to investigate the effects of HRT on insulin resistance with the hyperinsulinemic euglycemic clamp technique, the most sensitive technique measuring insulin resistance. Conjugated estrogen (0.625 mg/d) and medroxyprogesterone acetate (5 mg/d) were given to 15 postmenopausal women with insulin resistance. After 3 mo of HRT, the M value (total glucose consumption) increased 28% (p < 0.001), low-density lipoprotein (LDL) cholesterol decreased 12.9% (p < 0.044), high-density lipoprotein (HDL) cholesterol increased 17% (p < 0.009), total cholesterol decreased 9.1% (p < 0.016), and serum insulin decreased 33% (p < 0.022) compared to baseline values before HRT was started. No significant changes in glucose, C-peptide, and triglyceride levels were observed. Whereas there were no differences regarding glucose, total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels between the insulin-resistant (n = 15) and non-insulin-resistantwomen (n = 24) (p > 0.05), there were significant differences in M value, insulin, and C-peptide levels between these groups (p < 0.05). We believe that HRT with this combination may protect postmenopausal women from coronary artery disease (CAD) through its beneficial effects on insulin resistance, hyperinsulinemia, and lipid levels, which are considered to be important factors in CAD pathogenesis.

Ketamine 0.5-0.75 mg/kg is more rapid than meperidine (25 mg) for the reduction of postoperative shivering, but the side effect profile may limit its usefulness.

Electrical and pharmacologic stimulation of the efferent cholinergic antiinflammatory pathway suppress the systemic inflammatory response and can prevent lethal endotoxemia. Neostigmine, a cholinergic agent, has not been tested to determine if it can prevent histopathologic organ injury in endotoxemia. In the present study, the effects of neostigmine treatment on the histopathologic organ injury inflicted by Escherichia coli endotoxin in a mouse model of septic shock was investigated. Endotoxemia in mice caused weight loss and increased spleen, liver, and lung weight. When the organs were examined for histopathologic injury, endotoxemia increased interstitial inflammation in the lungs, liver injury, and organ injury in general terms; neostigmine, at a dose of 0.1 mg/kg, failed to attenuate these effects. Although the simultaneous administration of neostigmine at a dose of 0.3 mg/kg and endotoxin decreased interstitial inflammation in the lungs, vacuolar degeneration in the liver, and total liver injury, mortality was increased with this dose in the presence of endotoxemia. We conclude that neostigmine at a dose of 0.1 mg/kg was not protective against histopathologic organ injury in mice with endotoxemia, and a higher dose (0.3 mg/kg) was not tolerated probably owing to nonspecific parasympathetic action including cardiovascular effects. Further studies are required to determine the contribution of sites in the cholinergic antiinflammatory pathway.