Comparison of lidocaine and lidocaine-xylazine for distal paravertebral anesthesia in dairy cattle.

OBJECTIVE: To determine the time of onset and duration of action of distal paravertebral blocks (DPB) in dairy cattle using lidocaine and lidocaine plus xylazine (LX). ANIMALS: 10 healthy adult Holstein cows. METHODS: Unilateral DPB were performed in 6 cows at L1, L2, and L4. They received 2 treatments (lidocaine and LX) in a blinded random crossover design. Due to treatment failure, 4 additional cows were enrolled. The lidocaine treatment received 1,800 mg (90 mL) of lidocaine, and treatment LX received 1,784 mg (89.2 mL) of lidocaine and 16 mg (0.8 mL) of xylazine. Anesthesia was assessed by response (rapid movements of the tail, directed movements of the feet, or turning of the head towards the site of the needle pricks) to 6 approximately 1-cm deep needle pricks to the paralumbar fossa with a 22-gauge hypodermic needle. The time of onset, duration of action, maximum sedation score, and average heart rate (HR) were compared between treatments. RESULTS: Duration of anesthesia was significantly prolonged after DPB in cows treated with LX (251.6 ± 96.94 minutes) compared to lidocaine (105.8 ± 35.9 minutes; P = .01). Treatment with LX was associated with significantly lower average heart rate (56 ± 3 beats/min) compared to cows treated with lidocaine (59 ± 3 beats/min; P = .045). The LX treatment was associated with mild sedation but was not significant (P = .063). CLINICAL RELEVANCE: The addition of xylazine to a lidocaine DPB provides a longer duration of anesthesia, is inexpensive and practical, and can be implemented with ease.

Somatostatin signaling and the regulation of growth and metabolism in fish.

The study of the somatostatins (SS) signaling system in fish has provided important information about the structure, function, and evolution of SSs and their receptors. The SS signaling system elicits widespread biological actions via multiple hormone variants, numerous receptor subtypes, and a variety of signal transduction pathways. SSs alter growth via both direct and indirect actions, including inhibiting growth hormone release at the pituitary, decreasing hepatic GH sensitivity, and lowering plasma IGF-I levels. Metabolism also is significantly influenced by SSs. SSs stimulate the breakdown of energy stores and influences digestion, food intake, nutrient absorption, and food conversion both directly and through the modulation of other hormonal systems. The study of fish, which display a diversity of habitat types and life history forms, reveals that the SS signaling system helps regulate energy partitioning and integrate metabolism with growth and other biological processes.

Somatostatin inhibits basal and growth hormone-stimulated hepatic insulin-like growth factor-I production.

Growth of vertebrates is controlled by the growth hormone (GH)-insulin-like growth factor-I (IGF-I) system, and somatostatins (SSs) have been shown to inhibit growth by reducing the release of growth hormone (GH) from the pituitary. In this study, we used rainbow trout to assess the effects of SSs on the production of IGF-I. Somatostatin-14 (SS-14-I) implantation for 15 days significantly reduced steady-state levels of IGF-I mRNA in liver and lowered IGF-I concentration in plasma compared to control animals. The direct effects of SSs were examined on hepatocytes incubated in vitro. SS-14-I inhibited basal and GH-stimulated IGF-I mRNA expression. SS-14-I inhibition of GH-stimulated IGF-I expression was concentration- and time-dependent; the ED(50) was ca. 40 ng/ml and the maximum response was observed after 6h. All SS isofoms tested, including the N-terminally extended form of SS-14-I, SS-28-I, and the [Tyr(7), Gly(10)]-substituted forms of SS, SS-14-II, SS-25-II and SS-28-II, inhibited GH-stimulated IGF-I mRNA expression. The inhibitory effects of SS-14-I on steady-state levels of IGF-I mRNA resulted from reduced IGF-I mRNA transcription and not from altered mRNA stability. SS-14-I also reduced basal and GH-stimulated release of IGF-I into culture medium. These results indicate that SSs regulate growth in an extrapituitary manner by reducing hepatic IGF-I biosynthesis and secretion.