Shuhei Matsumoto

Increased incidence of emergency airway management after combined anterior-posterior cervical spine surgery.

Among some kinds of cervical spine surgeries, combined anterior-posterior cervical spine surgery (CAP-CS surgery) requires prolonged operative time and highly invasive procedure. This study was performed to determine whether CAP-CS surgery was associated with increased risk of emergency airway management compared with other cervical spine surgeries (O-CS surgeries). The records of the patients who underwent cervical spine surgery between July 2001 and March 2003 at our institution were reviewed retrospectively, and we determined whether the CAP-CS surgery was associated with an increased risk of emergency airway management in comparison with O-CS surgeries, using the logistic regression analysis. A total of 165 were eligible for inclusion in the study. A total of 127, 20, 11, 5, and 2 patients suffered from cervical myelopathy, traumatic cervical spinal cord injury, atlantoaxial dislocation, cervical spinal tumors, and cervical pyogenic spondylitis, respectively. The operative approaches were CAP-CS surgery, anterior surgery, posterior surgery, and atlantoaxial surgery in 10, 56, 88, and 11 patients, respectively. Thus, the operative approaches were CAP-CS surgery in 10 patients and O-CS surgeries in 155 patients. Postoperative emergency airway management was required in 7 of the 10 patients (70%) who underwent CAP-CS surgery, and 2 of the 155 patients (1%) who underwent O-CS surgeries. The increased risk of postoperative emergency airway management imposed by CAP-CS surgery was 178.5 by an odds ratio, with a 95% confidence interval of 25.6 to 1246. The results show that CAP-CS surgery provides a major risk factor for postoperative emergency airway management.

High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: role of mitochondrial KATP channels

BackgroundThe current study was carried out to determine whether fasudil hydrochloride (fasudil), a Rho-kinase inhibitor, has myocardial postconditioning (PostC) activity under hyperglycemia as well as normoglycemia, and if so, whether the effects could be mediated by mitochondrial ATP-sensitive potassium (m-KATP) channels.MethodsMale Sprague-Dawley rats were anesthetized with sodium pentobarbital. After opening the chest, all rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received low-dose (0.15 mg/kg) or high-dose (0.5 mg/kg) fasudil or diazoxide, an m-KATP channel opener, at 10 mg/kg, just before reperfusion under normoglycemic or hyperglycemic conditions. In another group, rats received 5-hydroxydecanoic acid (5HD), an m-KATP channel blocker, at 10 mg/kg, before high-dose fasudil. Myocardial infarct size was expressed as a percentage of area at risk (AAR).ResultsUnder normoglycemia, low-dose and high-dose fasudil and diazoxide reduced myocardial infarct size (23 ± 8%, 21 ± 9% and 21 ± 10% of AAR, respectively) compared with that in the control (42 ± 7%). Under hyperglycemia, low-dose fasudil (40 ± 11%) and diazoxide (44 ± 14%) could not exert this beneficial effect, but high-dose fasudil reduced myocardial infarct size in the same manner as under normoglycemia (21 ± 13%). 5HD prevented fasudil-induced reduction of myocardial infarct size (42 ± 13%).ConclusionFasudil induces PostC against myocardial infarction via activation of m-KATP channels in the rat. Although hyperglycemia attenuates the PostC, high-dose fasudil can restore cardioprotection.

Roles of Cyclooxygenase 2 in Sevoflurane- and Olprinone-Induced Early Phase of Preconditioning and Postconditioning Against Myocardial Infarction in Rat Hearts

Purpose: 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. Methods: Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. After opening the chest, all rats underwent 30-minute occlusion of left anterior descending coronary artery followed by 2-hour reperfusion, and the infarct size was measured after the reperfusion. The rats were randomly assigned to groups with pre- and postischemic exposure to sevoflurane and administration of olprinone with or without a selective COX-2 inhibitor, NS-398. Results: The infarct size in the control group was 42% ± 6% of the area at risk. Infarct size was significantly reduced by pre- and postischemic administration of sevoflurane (16% ± 7% and 17% ± 6%, respectively), as well as by olprinone (14% ± 4% and 15% ± 10%, respectively). NS-398 prevented the protective effects of both pre- and postischemic exposure to sevoflurane (35% ± 8% and 42% ± 10%, respectively), whereas the protective effect of both pre- and postischemic administration of olprinone was not influenced by NS-398 (12% ± 5% and 19% ± 7%, respectively). Conclusions: Cyclooxygenase 2 could be a critical mediator of sevoflurane-induced but not olprinone-induced E-PreC or PostC in rat hearts.

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

BackgroundThe 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).MethodsWistar 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.ResultsUnder 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.ConclusionMilrinone 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.

Preadministration of low-dose ketamine reduces tourniquet pain in healthy volunteers

We evaluated whether preadministration of low-dose ketamine could attenuate tourniquet pain and arterial pressure increase using high tourniquet pressure in ten healthy awake volunteers. Ketamine, 0.1 mg·kg−1, or normal saline was given intravenously in a double-blind fashion before tourniquet inflation with a pressure of 400 mmHg at the thigh. Visual analog scale (VAS) scores and systolic blood pressure (SBP) were measured at 5-min intervals. Ketamine significantly reduced VAS scores compared to saline just after tourniquet inflation [90 (64–100) mm, median (range), with saline versus 66 (50–81) mm with ketamine, P < 0.01] and at 30 min [92 (61–100) mm with saline versus 70 (50–100) mm with ketamine, P < 0.03), and significantly prolonged tourniquet time (28 ± 6 min with saline, mean ± SD, versus 37 ± 7 min with ketamine, P < 0.01). SBP (120 ± 9 mmHg) significantly increased before tourniquet deflation (133 ± 16 mmHg) in the saline trial, but not in the ketamine trial. The results show that preadministration of low-dose ketamine attenuates tourniquet pain and arterial pressure increase during high-pressure tourniquet application and prolongs tourniquet time in healthy volunteers.

Anesthetic management of a patient with a double inferior vena cava and pulmonary alveolar proteinosis who underwent bilateral living-donor lobar lung transplantation

A 43-year-old woman with pulmonary fibrosis secondary to pulmonary alveolar proteinosis was scheduled to undergo lung transplantation. Before the lung transplantation, she had undergone multiple whole-lung lavage procedures on extracorporeal circulation (ECC), which had caused scarring of the right femoral subcutaneous tissues. Preoperative examination revealed a double inferior vena cava (IVC) with interiliac communication, and the left IVC ended at the left renal vein. Surgical exposure of the right femoral vessels was performed immediately after anesthetic induction for emergent vascular access to establish an ECC. Cardiopulmonary collapse did not occur and the ECC was not required until lung resection. The lung transplantation was completed uneventfully. Congenital IVC anomaly is rare, but may make cannulation through the femoral vein difficult. Scarring of the subcutaneous tissue could result in a difficult “percutaneous” approach to the vessels. Evaluation of the vascular anatomy related to the establishment of an ECC is important before lung transplantation.

Intestinal fatty acid-binding protein level as a predictor of 28-day mortality and bowel ischemia in patients with septic shock: A preliminary study

Purpose: We sought to evaluate the levels of intestinal fatty acid‐binding protein (I‐FABP), a biomarker of enterocyte injury, as a predictor of 28‐day mortality and bowel ischemia in septic shock patients. Material and methods: In this preliminary prospective observational study, 57 adult septic shock patients under mechanical ventilation were enrolled. Serum I‐FABP levels and prognostic biomarkers were recorded upon intensive care unit (ICU) admission. Results: The overall 28‐day mortality rate of participants was 23% (13/57). Non‐survivors displayed significantly higher lactate (p = 0.009), I‐FABP (p = 0.012), and N‐terminal pro‐B‐type natriuretic peptide (p = 0.039) levels compared to survivors. Only I‐FABP was associated with 28‐day mortality (odds ratio, 1.036; 95% confidence interval, 1.003–1.069; p = 0.031) in a multiple logistic regression analysis adjusted for the Acute Physiology and Chronic Health Evaluation II score. When divided into low and high I‐FABP groups based on the optimum cut‐off value of 19.0 ng/mL for predicting 28‐day mortality, high‐I‐FABP patients had a significantly higher incidence of non‐occlusive mesenteric ischemia (NOMI) (2% [1/43] vs 29% [4/14]; p = 0.011). Conclusions: I‐FABP level at ICU admission can serve as a predictor of 28‐day mortality in septic shock patients and is associated with the incidence of NOMI. HighlightsWe studied intestinal fatty acid‐binding protein and mortality in septic shock.I‐FABP level was a predictor of 28‐day mortality in septic shock patients.Predictive ability of ICU baseline I‐FABP in septic shock patients was evaluated.