RESUMO
Background: Butyrate protects against ischemic injury to the small intestine by reducing inflammation and maintaining the structure of the intestinal barrier, but is expensive, short-lived, and cannot be administered easily due to its odor. Lactate, both economical and more palatable, can be converted into butyrate by the intestinal microbiome. This study aimed to assess in a rat model whether lactate perfusion can also protect against intestinal ischemia. Materials and Methods: Rat intestinal segments were loaded in an in vitro bowel perfusion device, and water absorption or secretion was assessed based on fluorescence of FITC-inulin, a fluorescent marker bound to a biologically inert sugar. Change in FITC concentration was used as a measure of ischemic injury, given the tendency of ischemic cells to retain water. Hematoxylin and eosin-stained sections at light level microscopy were examined to evaluate intestinal epithelium morphology. Comparisons between the data sets were paired Student t-tests or ANOVA with p < 0.05 performed on GraphPad. Results: Lactate administration resulted in a protective effect against intestinal ischemia of similar magnitude to that observed with butyrate. Both exhibited approximately 1.5 times the secretion exhibited by control sections (p = 0.03). Perfusion with lactate and methoxyacetate, a specific inhibitor of lactate-butyrate conversion, abolished this effect (p = 0.09). Antibiotic treatment also eliminated this effect, rendering lactate-perfused sections similar to control sections (p = 0.72). Perfusion with butyrate and methoxyacetate did not eliminate the observed increased secretion, which indicates that ischemic protection was mediated by microbial conversion of lactate to butyrate (p = 0.71). Conclusions: Lactate's protective effect against intestinal ischemia due to microbial conversion to butyrate suggests possible applications in the transplant setting for reducing ischemic injury and ameliorating intestinal preservation during transport.
RESUMO
OBJECTIVE: Hepatic arterial vasospasm has not been well recognized clinically as a post-liver transplant vascular complication because of the lack of sufficient data and diagnostic standards. The goal of this study was to provide new evidence and a diagnostic model for the clinical appreciation of hepatic arterial vasospasm and evaluate the role of ultrasonography in the diagnostic process. METHODS: Nine post-orthotopic liver transplant cases were retrospectively reviewed. Multiple clinical measurements were analyzed. Routine Doppler ultrasonography was performed within 24 hours, and additional ultrasonographic examinations were conducted as indicated. Each of the 9 patients was given a single 10 mg dose of nifedipine sublingually and monitored by ultrasonography when vasospasm was suspected on the basis of the Doppler ultrasonographic results. RESULTS: Doppler ultrasonography showed high-resistance hepatic arterial flow with absence of antegrade flow and even reversal of flow during diastole both extrahepatically and intrahepatically in all cases. Ten to 45 minutes after administration of the vasodilator, antegrade diastolic flow was observed along the course of the main hepatic artery and its intrahepatic branches with the resistive indices decreasing on average from 1.0 to 0.76. In addition, the peak systolic velocities increased from 57 cm/s before nifedipine administration to 77 cm/s after administration. CONCLUSIONS: High-resistance hepatic arterial flow (resistive index = 1) early after liver transplantation is indicative of hepatic arterial vasospasm if it responds to vasodilators. Doppler ultrasonography is a useful tool for the diagnosis of this vascular complication.
