The Impact of Perioperative Factors on Changes in Diastolic Function after Kidney Transplantation: A Retrospective Analysis

PURPOSE: Cardiac changes in end-stage renal disease are the most common causes of death after kidney transplantation (KT). Chronic kidney disease presents a major risk factor for the development and progression of diastolic dysfunction. The purpose of this study was to identify the association between changes in left ventricular (LV) diastolic function and perioperative clinical factors in patients with preserved ejection fraction following KT. MATERIALS AND METHODS: We reviewed 115 patients who underwent KT between January 2011 and December 2015 with both preand post-transplant echocardiograms; patients with LV systolic dysfunction were excluded. LV diastolic function was measured using the ratio of early transmitral flow velocity to early diastolic velocity of the mitral annulus (E/e′). RESULTS: Patients with normal pre-operative LV systolic function (n=97) showed improvement in E/e′ after KT (11.9±4.4 to 10.5±3.8, p=0.023). Additionally, post-KT estimated glomerular filtration ratio was associated with changes in E/e′ (odds ratio, −0.056; 95% confidence interval, −0.014 to −0.007; p=0.026). Among patients with preexisting diastolic dysfunction (20/97 patients), the amount of intraoperative fluid administration was related to E/e′ changes (odds ratio, 0.003; 95% confidence interval, 0.000 to 0.005; p=0.029). CONCLUSION: KT is associated with improved diastolic function. Post-KT renal function was significantly related to changes in LV diastolic function. The amount of intraoperative fluid was a risk factor for worsening diastolic function after KT in patients with preexisting diastolic dysfunction.

“Spray-as-you-go” medical technique for awake intubation using a combination of an epidural catheter and the OptiScope in a patient with Ludwig's angina: A case report

A 73-year-old woman presented to the emergency department with submandibular pain and swelling. The patient was diagnosed to have Ludwig's angina, and she was planned to undergo urgent incision and drainage under general anesthesia. However, her physical examination revealed severe diffuse swelling extending from the bilateral submandibular spaces to the submental space and further down to the neck. As our view was blocked by the patient's neck swelling, we did not perform a regional anesthesia of the airway or a transtracheal block. Several non-invasive alternatives were considered. The “spray-as-you-go” technique was chosen, and it was performed using the OptiScope®. However, the OptiScope did not have a working channel or syringe adaptor for the administration of the local anesthetic solution. To solve this problem, we combined the OptiScope with a 27-G tunneled epidural catheter (100 cm) for the administration of lidocaine and this combination made the awake intubation successful.

Reduction of Food Intake by Fenofibrate is Associated with Cholecystokinin Release in Long-Evans Tokushima Rats

Fenofibrate is a selective peroxisome proliferator-activated receptor alpha (PPARalpha) activator and is prescribed to treat hyperlipidemia. The mechanism through which PPARalpha agonists reduce food intake, body weight, and adiposity remains unclear. One explanation for the reduction of food intake is that fenofibrate promotes fatty acid oxidation and increases the production of ketone bodies upon a standard experimental dose of the drug (100~300 mg/kg/day). We observed that low-dose treatment of fenofibrate (30 mg/kg/day), which does not cause significant changes in ketone body synthesis, reduced food intake in Long-Evans Tokushima (LETO) rats. LETO rats are the physiologically normal controls for Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are obese and cholecystokinin (CCK)-A receptor deficient. We hypothesized that the reduced food intake by fenofibrate-treated LETO rats may be associated with CCK production. To investigate the anorexic effects of fenofibrate in vivo and to determine whether CCK production may be involved, we examined the amount of food intake and CCK production. Fenofibrate-treated OLETF rats did not significantly change their food intake while LETO rats decreased their food intake. Treatment of fenofibrate increased CCK synthesis in the duodenal epithelial cells of both LETO and OLETF rats. The absence of a change in the food intake of OLETF rats, despite the increase in CCK production, may be explained by the absence of CCK-A receptors. Contrary to the OLETF rats, LETO rats, which have normal CCK receptors, presented a decrease in food intake and an increase in CCK production. These results suggest that reduced food intake by fenofibrate treatment may be associated with CCK production.

Overexpression of AMPKalpha1 Ameliorates Fatty Liver in Hyperlipidemic Diabetic Rats

5'-AMP-activated protein kinase (AMPK) is a heterotrimeric complex consisting of a catalytic (alpha) and two regulatory (beta and gamma) subunits. Two isoforms are known for catalytic subunit (alpha1, alpha2) and are encoded by different genes. To assess the metabolic effects of AMPKalpha1, we examined the effects of overexpression of adenoviral-mediated AMPKalpha1 in hyperlipidemic type 2 diabetic rats. The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an established animal model of type 2 diabetes that exhibits chronic and slowly progressive hyperglycemia and hyperlipidemia. Thirty five-week-old overt type 2 diabetic rats (n=10) were administered intravenously with Ad.AMPKalpha1. AMPK activity was measured by phosphorylation of acetyl CoA carboxlyase (ACC). To investigate the changes of gene expression related glucose and lipid metabolism, quantitative real-time PCR was performed with liver tissues. Overexpression of AMPKalpha1 showed that blood glucose concentration was decreased but that glucose tolerance was not completely recovered on 7th day after treatment. Plasma triglyceride concentration was decreased slightly, and hepatic triglyceride content was markedly reduced by decreasing expression of hepatic lipogenic genes. Overexpression of AMPKalpha1 markedly improved hepatic steatosis and it may have effective role for improving hepatic lipid metabolism in hyperlipidemic state.