Disease relevance of Indo

• 1. The effect of amylin on gastric ulcers induced by oral administration of indomethacin (Indo, 20 mg kg-1 at a dosing volume of 5 ml) or ethanol 50% (EtOH, 1 ml/rat) was investigated in conscious rats [1].
• CONCLUSIONS: The long-lasting Indo-induced ileitis was accompanied by macroscopic ulceration and microcirculatory disturbances [2].
• The bradykinin antagonist, with or without Indo, was associated with significant hypotension relative to control [3].
• Four groups of rats were used: Control (CT, normotensive), LN (50 mg/kg/day, hypertensive), indomethacin (Indo-4 mg/kg/day, normotensive), and LN plus Indo (LN + Indo, partially prevented hypertension) [4].

High impact information on Indo

• Indo or FSK had no effect on FRCl% in control rats and Indo did not prevent inhibition of FRCl% by luminal PGE2 (1 microM) [5].
• Indo reduced excretion of the prostacyclin derivative 6-keto-PGF1 alpha and TXB2 and lowered whole kidney GFR and renal plasma flow, whereas UK lowered excretion of TXB2 only and did not change basal renal hemodynamics [6].
• Furosemide was infused i.v. at 0.25 mg kg(-1) h(-1) in anaesthetized rats, untreated or treated with intramedullary indomethacin (Indo) or Ado [7].
• The effects of exogenous Ang II on intrarenal circulation were determined in anaesthetised rats that were untreated or pretreated with indomethacin (Indo) or L-NAME [8].
• Ovariectomy abolished and estrogen replacement restored the inhibitory effects of Indo, NS-398, and SQ-29,548 [9].

Biological context of Indo

• Quin 2-AM and Indo 1-AM (2.5 microM) induced lipid peroxidation in the cells after 1 or 3 hr of treatment, respectively [10].
• Second, it examines the relative roles of: altered gastric myoelectrical activity (MEA) resulting from indomethacin (Indo) pretreatment, insulin-induced gastric peristalsis, and a combination of the two in the generation of mucosal lesions [11].
• CONCLUSION: The Indo-induced increase in leukocyte-endothelial cell interaction is blunted by Lac and Neo [12].
• Indo, both in the absence and presence of the antagonist, was associated with a progressive decrease in blood pressure compared with control [3].
• Massive bacterial translocation into the mesenteric lymph nodes, liver, and spleen following two injections of Indo was significantly attenuated by metronidazole [13].

Anatomical context of Indo

• To determine the roles of estrogen and constrictor prostanoids in vasopressin (VP)-induced contraction of female rat aorta, vascular reactivity to VP was determined in thoracic aortas of intact, ovariectomized, and ovariectomized + estrogen-replaced female rats in the presence of indomethacin (Indo), NS-398, SQ-29,548, or vehicle control [9].
• Increased peroxidase activity -index of tissue neutrophil infiltration- in the distal ileum of LPS-treated rats was decreased by alpha-MSH and this effect was reversed by pretreatment with Indo [14].
• We investigated the potential toxic effects of Indo on ileal mucosa and the role of phosphatidylcholine (PC) [15].
• BACKGROUND: Indomethacin (Indo) exerts local toxic effects on small intestinal mucosa, possibly in association with hydrophobic bile salts [15].
• Compared with LPS alone, LPS with Indo significantly impaired gastric microcirculation and systemic hemodynamics [16].

Associations of Indo with chemical compounds

• Outer medullary [PGE2] in HC rats was 9 to 10 times greater than control and could be normalized by Indo [5].
• Those factors were the following: 1) the prostanoid indomethacin (Indo); 2) the Ca2+-dependent K+ (K(Ca)) channel, iberiotoxin (IbTX); 3) the ATP-regulated K+ (K(ATP)) channel glibenclamide (Glib); 4) the K(Ca)-regulating epoxygenase pathway miconazole (Mic); and 5) the adenosine receptor 8-sulfophenyltheophylline (8-SPT) [17].
• Indo and NS-398 significantly attenuated maximal responses to VP in intact female rats to a similar extent [3,176 +/- 179 (P < 0.0001) and 3,258 +/- 152 mg (P < 0.0001), respectively] [9].
• Indomethacin (Indo), inhibitor of cyclo-oxygenase and benoxaprofen (Ben), inhibitor of cyclo-oxygenase and lipoxygenase, caused an enhancement of the onset of rejection and an early cessation of blood flow in allografts [18].
• In the presence of L-NNA or Indo, ACh-induced dilation was not significantly inhibited in young or old SFA; however, double blockade with L-NNA + Indo inhibited ACh-induced dilation in young SFA such that the response to ACh was no longer greater than old SFA [19].

Regulatory relationships of Indo

• Pretreatment with Indo did not significantly increase the ulcer index induced by EtOH but counteracted the ability of amylin to prevent the ulcer formation [1].

Other interactions of Indo

• Treatment with SOD, catalase, or deferoxamine significantly (P less than 0.05) reduced 51Cr-EDTA leakage during the intragastric perfusion with Indo and during the subsequent exposure to HCl [20].
• Cort decreased TDR and CDP while Indo did not [21].
• To determine the mechanism(s) by which aging affected dilator responses to flow and ACh, dilation was assessed in the presence of Nomega-nitro-L-arginine (L-NNA; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), and L-NNA + Indo [19].
• From these observations, it is considered that microcirculatory disturbances, especially leukocyte accumulation and 5-lipoxygenase products, possibly leukotriene B4, may be involved in the development of Indo-induced intestinal ulcer [22].
• Central microinjection or infusion of an arginine vasopressin (AVP) V1-receptor antagonist within the brain of the conscious, unrestrained, and febrile rat inhibited or abolished the antipyretic effects of peripherally administered indomethacin (Indo) [23].

Analytical, diagnostic and therapeutic context of Indo

• All three compounds exhibited antiinflammatory activity in male Sprague-Dawley rats at an equivalent Indo dose of 10 mg/kg following oral administration of the drugs in 2% CMC solution [24].
• Four days later animals received a single intraperitoneal injection of either 0.9% saline, 0.5 ml/kg (SO, n = 10; BDL, n = 10), or indomethacin, 5 mg/kg (SO + Indo, n = 10; BDL + Indo, n = 10), and renal function was reassessed [25].
• Two daily subcutaneous injections of Indo produced a more extensive and chronic inflammation that lasted in an active form in more than 75% of the rats for at least two weeks [13].
• Central microinjection of a V2-receptor antagonist did not significantly effect Indo-induced antipyresis compared with paired saline controls [23].
• L-NNA significantly reduced flow-induced dilations (from 38 +/- 11 to 17 +/- 9 micron at 14 mmHg Pdiff), whereas in the additional presence of Indo, flow elicited constriction of venules decreasing basal diameter (by 21 +/- 8 micron at Pdiff 12 mmHg) [26].

References