Anesthetic management of a patient undergoing liver transplantation who had previous coronary artery bypass grafting using an in situ right gastroepiploic artery.

We describe successful anesthetic management during living-donor liver transplantation in a 63-year-old man with previous coronary artery bypass grafting (CABG) that employed an in situ right gastroepiploic artery (RGEA). Anesthesia was maintained with 1.5% isoflurane in air/oxygen and fentanyl. A five-lead electrocardiogram, transesophageal echocardiogram, and pacing pulmonary artery catheter evaluated cardiac function. A pacing wire was inserted through the catheter to prepare for intraoperative severe bradyarrhythmia. Olprinone and nicorandil were continuously infused to prevent decrease in coronary arterial blood flow and the collapse of cardiac function. Avoiding disruption of circulation to coronary arteries through injury or spasm of the RGEA graft and preparing for cardiac insufficiency during liver transplantation of a patient with previous CABG using an in situ RGEA is critical

Correlations between APACHE IIScore and Plasma Levels of Cytokines in Postsurgical Patients

This study was designed to assess whether plasma cytokines correlated with the clinical status of postsurgical patients. Plasma levels of cytokines in 72 patients admitted to the intensive care unit were measured using an Enzyme Linked Immuno Solubent Assay. The clinical status was evaluated with the Acute Physiology Age and Chronic Health Evaluation (APACHE) 11 scoring system. There were significant correlations between the APACHE 11 score and the plasma levels of Tumor Necrosis Factor(TNF)α and interleukin(IL)-1 β.But IL-8 and IL-6 did not correlate with the APACHE II score. Three patients died within postoperative 20 days. The plasma levels of TNF α,IL-1,β,IL-8 and IL-6 were significantly higher in nonsurvivors than in survivors. There was no significant difference in the APACHE II score and the plasma levels of IL-1β,IL-8 and IL-6 between the survivors with Systemic Inflammatory Response Syndrome (SIRS) and those without SIRS. The survivors without SIRS had a higher concentration of TNFα than those with SIRS. The results indicate that TNF α and IL-1 β correlate well with the severity of illness in the postsurgical patients, whereas IL-8 and IL-6 does not

Hyperglycemia raises the threshold of levosimendan- but not milrinone-induced postconditioning in rat hearts

<p>Abstract</p> <p>Background</p> <p>The authors examined whether milrinone and levosimendan could exert cardiac postconditioning effects in rats under normoglycemia and hyperglycemia, and whether the effects could be mediated by mitochondrial permeability transition pore (mPTP).</p> <p>Methods</p> <p>Wistar rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received milrinone or levosimendan just before reperfusion under normoglycemic or hyperglycemic conditions with or without atractyloside, an mPTP opener.</p> <p>Results</p> <p>Under normoglycemia, both 30 μg/kg milrinone (29 ± 12%) and 10 μg/kg levosimendan (33 ± 13%) reduced infarct size compared with that in the control (58 ± 7%). Under hyperglycemia, milrinone (34 ± 13%) reduced infarct size at the same dose as under normoglycemia. In contrast, neither 10 nor 30 μg/kg levosimendan protected hyperglycemic hearts, and only 100 μg/kg levosimendan (32 ± 9%) reduced infarct size compared with that in the hyperglycemic control (58 ± 13%). All of these cardioprotective effects under normoglycemia and hyperglycemia are abolished by atractyloside.</p> <p>Conclusion</p> <p>Milrinone and levosimendan exert postconditioning effects via inhibition of mPTP opening. Hyperglycemia raises the threshold of levosimendan-induced postconditioning, while milrinone-induced postconditioning is not influenced by hyperglycemia.</p

Extent of sympathectomy affects postoperative compensatory sweating and satisfaction in patients with palmar hyperhidrosis

Purpose: Endoscopic thoracic sympathectomy (ETS) for the treatment of palmar hyperhidrosis is generally performed at one or two levels ranging between T2 and T4; however, compensatory sweating (CS) is an occasional bothersome side effect. The aim of our study was to evaluate the association between the extent of ETS and the degree of postoperative CS and palmar sweating, as well as patient satisfaction. Methods: The participants represented a consecutive series of 76 patients who underwent bilateral ETS for palmar hyperhidrosis at level T2 and/or T3. Patients were interviewed by postal questionnaires to assess their self-reported degree of postoperative palmar sweating and CS and their outcome satisfaction. Of the 53 patients who replied to the postal questionnaire, 25 underwent bilateral ETS at one level (group A), and 27 underwent bilateral ETS at two levels (group B). One patient who underwent asymmetrical sympathectomy was excluded. Results: The degree of postoperative palmar sweating was significantly lower in group B than in group A. The severity of CS was significantly higher in group B than in group A. The severity of CS was significantly inversely correlated with the degree of patient satisfaction. However, the degree of postoperative palmar sweating was not correlated with the degree of patient satisfaction. Conclusions: Compared to ETS at two levels, single-level ETS of T2 or T3 reduces postoperative palmar sweating to a milder degree, and causes CS to a less severe degree. The severity of CS is inversely correlated with the degree of patient satisfaction

Hemodynamic and Catecholamine Responses to Tracheal Intubation during Inhalation of Isoflurane or Sevoflurane

This study was designed to evaluate the hemodynamic and catecholamine responses to the inhalation of isoflurane and sevoflurane during anesthetic induction and to tracheal intubation in 46 adult patients who received elective surgery, Anesthesia was induced with thiamylal and vecuronium, followed by 3-min ventilation with 60% N2O (final control group ; n = 13), 60% N2O-3% isoflurane (final isoflurane group ; n = 15), or 60% N2O-4.5% sevoflurane (sevoflurane group ; n = 16) in oxygen, and the trachea was then intubated. Isoflurane inhalation caused significant increases in heart rate and plasma norepinephrine, but attenuated the pressor response to tracheal intubation. Sevoflurane inhalation caused a decrease in systolic arterial pressure with an unchanged heart rate, and attenuated the pressor and tachycardia response to tracheal intubation to a greater extent than that observed in the control and isoflurane group. Plasma norepinephrine did not show any change in the sevoflurane group. Isoflurane induction increased the sympathoadrenal activity, resulting in marked tachycardia, but attenuated the pressor response to tracheal intubation. Sevoflurane caused milder hemodynamic change during inhalation and tracheal intubation, and was accompanied by stable plasma catecholamine levels, indicating a suppression of sympathoadrenal activity

High concentrations of landiolol, a beta(1)-adrenoceptor antagonist, stimulate smooth muscle contraction of the rat trachea through the Rho-kinase pathway.

PURPOSE: Gradually progressing contraction of airway smooth muscle is suggested to be due to the Rho-kinase signaling pathway. In our preliminary study in rat tracheas, landiolol, a beta(1)-adrenoceptor antagonist, at high doses caused gradually progressing contraction, and this contraction reached a plateau after 20 min. Therefore, this study was carried out to clarify whether landiolol could stimulate the Rho-kinase pathway or the phosphatidylinositol (PI) response in the rat trachea. METHODS: Seventy-eight male Wistar rats weighing 250-350 g were used for the experiments. Their tracheas were cut into 3-mm-wide ring segments or 1-mm-wide slices. Measurements of isometric tension and [(3)H] inositol monophosphate (IP(1)) production were conducted, using these tracheal rings or slices. Data values are expressed as means +/- SD, and statistical significance (P < 0.05) was determined using analysis of variance (ANOVA). RESULTS: Landiolol (700 microM)-induced contraction was completely inhibited by fasudil at 30 microM, while the landiolol-induced contraction was not inhibited by 4-diphenylacetoxy-N-methyl-piperidine methobromide (4-DAMP), ketanserin, or nicardipine. Landiolol did not stimulate IP(1) production. CONCLUSION: These results suggest that high concentrations of landiolol could cause airway smooth muscle contraction through the Rho-kinase pathway, but not through the PI response coupled with muscarinic M(3) receptors, 5-HT receptors or the activation of L-type Ca(2+) channels

Roles of cyclooxygenase 2 in sevoflurane- and olprinone-induced early phase of preconditioning and postconditioning against myocardial infarction in rat hearts.

It is known that selective cyclooxygenase 2(COX-2) inhibitors increase mortality in patients with previous myocardial infarction, and it has been suggested that COX-2 plays an important role in cardioprotection against ischemia. The current study was carried out to determine whether COX-2 is involved in the mechanisms of sevoflurane- and olprinone-induced early-phase preconditioning (E-PreC) and postconditioning (PostC) in rat hearts