Perioperative complications after full-thickness gastrointestinal surgery in cats with alimentary lymphoma.

OBJECTIVE: To determine perioperative risk factors for complications that occur before hospital discharge after gastrointestinal (GI) surgery in cats with alimentary lymphosarcoma (LSA). STUDY DESIGN: Case series. ANIMALS: Cats (n=70) with a histopathologically confirmed diagnosis of alimentary LSA that had full-thickness GI surgery. METHODS: Medical record data (February 1996-March 2009) from 3 academic referral centers were reviewed. Retrieved data included signalment, preoperative clinical signs and laboratory findings, perioperative medications administered, type and location of GI surgery performed and outcome until hospital discharge. RESULTS: In 38 surgeries, intestinal resection and anastomosis was performed. Gastrotomy and/or enterotomy was performed in 53 surgeries. A preoperative serum albumin concentration <2.5 g/dL was recorded for 11 cases. There was no clinical evidence of postoperative leakage from any biopsy or anastomosis site. Postoperative complications that occurred before hospital discharge included: anorexia or decreased appetite (n=8), hyperthermia (3), pancreatitis (1) and constipation (1). CONCLUSIONS: Cats with alimentary LSA do not appear to be at high risk of postoperative dehiscence after full-thickness GI surgery.

Role of calcitonin gene-related peptide in bone repair after cyclic fatigue loading.

BACKGROUND: Calcitonin gene related peptide (CGRP) is a neuropeptide that is abundant in the sensory neurons which innervate bone. The effects of CGRP on isolated bone cells have been widely studied, and CGRP is currently considered to be an osteoanabolic peptide that has effects on both osteoclasts and osteoblasts. However, relatively little is known about the physiological role of CGRP in-vivo in the skeletal responses to bone loading, particularly fatigue loading. METHODOLOGY/PRINCIPAL FINDINGS: We used the rat ulna end-loading model to induce fatigue damage in the ulna unilaterally during cyclic loading. We postulated that CGRP would influence skeletal responses to cyclic fatigue loading. Rats were fatigue loaded and groups of rats were infused systemically with 0.9% saline, CGRP, or the receptor antagonist, CGRP(8-37), for a 10 day study period. Ten days after fatigue loading, bone and serum CGRP concentrations, serum tartrate-resistant acid phosphatase 5b (TRAP5b) concentrations, and fatigue-induced skeletal responses were quantified. We found that cyclic fatigue loading led to increased CGRP concentrations in both loaded and contralateral ulnae. Administration of CGRP(8-37) was associated with increased targeted remodeling in the fatigue-loaded ulna. Administration of CGRP or CGRP(8-37) both increased reparative bone formation over the study period. Plasma concentration of TRAP5b was not significantly influenced by either CGRP or CGRP(8-37) administration. CONCLUSIONS: CGRP signaling modulates targeted remodeling of microdamage and reparative new bone formation after bone fatigue, and may be part of a neuronal signaling pathway which has regulatory effects on load-induced repair responses within the skeleton.

Systemic effects of ulna loading in male rats during functional adaptation.

Functional skeletal adaptation is thought to be a local phenomenon controlled by osteoctyes. However, the nervous system also may have regulatory effects on adaptation. The aim of this study was to determine the effects of loading of a single bone on adaptation of other appendicular long bones and whether these responses were neuronally regulated. Young male Sprague-Dawley rats were used. The right ulna was loaded to induce a modeling response. In other rats, a second regimen was used to induce bone fatigue with a mixed modeling/remodeling response; a proportion of rats from each group received brachial plexus anesthesia to induce temporary neuronal blocking during bone loading. Sham groups were included. Left and right long bones (ulna, humerus, tibia, and femur) from each rat were examined histologically 10 days after loading. In fatigue- and sham-loaded animals, blood plasma concentrations of TNF-α, RANKL, OPG, and TRAP5b were determined. We found that loading the right ulna induced an increase in bone formation in distant long bones that were not loaded and that this effect was neuronally regulated. Distant effects were most evident in the rats that received loading without bone fatigue. In the fatigue-loaded animals, neuronal blocking induced a significant decrease in plasma TRAP5b at 10 days. Histologically, bone resorption was increased in both loaded and contralateral ulnas in fatigue-loaded rats and was not significantly blocked by brachial plexus anesthesia. In young, growing male rats we conclude that ulna loading induced increased bone formation in multiple bones. Systemic adaptation effects were, at least in part, neuronally regulated.