Disease relevance of Celiac Artery

• Gastric secretion was studied in rats (series A) with gastric fistula before, during and after the ischemia induced by clamping of celiac artery for 0.5 h followed by reperfusion in animals pretreated with vehicle (saline), omeprazole, a proton pump inhibitor, or ranitidine, a histamine (H(2)) receptor antagonist [1].
• The purpose of this study was to examine whether tetrahydrobiopterin (BH4), a cofactor of nitric oxide (NO) synthase, attenuates gastric ischemia-reperfusion injury induced by clamping of the celiac artery [2].

High impact information on Celiac Artery

• When this hyperemic response was inhibited by reducing celiac artery blood flow, ethanol caused lesions of similar degree as in animals not pretreated with 2 mol/L NaCl [3].
• Cats were subjected to gastric luminal perfusion with saline at pH = 1.0 and reduction of celiac artery blood flow for 90 min [4].
• Through the abdominal aorta, a catheter was advanced to the origin of the celiac artery for continuous regional arterial (CRA) pretreatment with isotonic saline (NP-S group) or superoxide dismutase/catalase (NP-SOD/CAT group) [5].
• Transport of 45Ca from the lumen to the venous effluent was studied in duodena of normal, vitamin D3-replete (+D) chicks perfused through the celiac artery with 130 pM 1,25(OH)2D3 or vehicle [6].
• The stomach was perfused via celiac artery with modified Krebs-Ringer solution containing 10 mM pargyline and 0.1% bovine serum albumin at a constant flow of 4 ml/min [7].

Anatomical context of Celiac Artery

• To evaluate the effect of bradykinin (BK) on rat islet alpha, beta, and delta cells, the rat pancreas was perfused in situ with BK (1 mumol/L) for 30 minutes via a cannula placed in the celiac artery [8].
• Under halothane anesthesia, the celiac artery or superior mesenteric artery in the rat was occluded for 60 min followed by reperfusion [9].
• Pulmonary artery and celiac artery ring segments were precontracted with phenylephrine, and cumulative concentration-relaxation curves to ACh were obtained before and after incubation of the rings with L-NAME or L-NMMA [10].
• The degree and duration of the flow increments were dose dependent; The celiac artery was more sensitive to the effect of PTH than the renal artery [11].

Associations of Celiac Artery with chemical compounds

• Under pentobarbital anesthesia, the celiac artery was clamped for 30 min and reperfused [12].
• L-NMMA, and to a lesser extent L-NAME, raised baseline tone more in pulmonary than celiac arteries [10].
• Pretreatment of pulmonary and celiac artery rings with meclofenamate did not alter this contractile effect [10].
• In the non-stimulated stomach, infusion of prostaglandin E2 or F2 alpha into the celiac artery resulted in a marked increase in mucosal blood flow and a sustained decrease, respectively [13].
• Differential effect of nitric oxide synthase inhibitors on acetylcholine-induced relaxation of rat pulmonary and celiac artery rings [10].

Gene context of Celiac Artery

• The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombesin-like immunoreactivity (BLI), somatostatin and gastrin from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer [14].
• In addition, cyclooxygenase products do not contribute to the direct contractile responses to L-NAME and L-NMMA in both the pulmonary and celiac artery rings but do modulate the ACh-induced relaxation of these vessels [10].
• The neurophysiological responses to 2-ml intragastric saline loads and 100-pmol celiac artery infusions of cholecystokinin (CCK) were obtained from 20 vagal afferent fibers in 14 rats [15].
• In the present experiments, insulin and glucagon were injected into the celiac artery of anesthetized rats to evaluate their effects on the secretion of amylase and trypsinogen by the pancreas [16].
• In isolated, vascularly perfused rabbit stomach, various concentrations (10-400 mM) of ethanol infused into the celiac artery increased the perfusion pressure and released endothelin-1 (ET-1) from the gastric vasculature in a concentration-dependent manner [17].

References