Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the hepatic microvasculature and systemic arterial blood pressure were measured in anesthetized Sprague-Dawley rats receiving an i.v. infusion or topical application of compound 48/80, lodoxamide, or arterenol. Histochemical determination of the number of Falck-Hillarp positive (serotonin containing) mast cells also was performed on sections of liver at the light microscopic level. The infusion of arterenol (0.1 mg/kg) or Ringer's solution (control) provoked a vasopressor response within 25 sec in rats rendered hypotensive 5 min previously with compound 48/80. The duration of this response was brief with arterial pressure returning to the pre-injection (hypotensive) state within 3 min following arterenol or Ringer's administration. The injection of lodoxamide (a purported inhibitor of histamine release) inhibited compound 48/80-induced hypotension at all doses except 1 mg/kg. In vivo microscopy revealed that topical administration (0.1 microgram) significantly antagonized the microvascular responses elicited by compound 48/80. However, higher doses of lodoxamide (1.0-10 micrograms) when applied topically were found to be vasoactive. Given these results and the histochemical demonstration of an inhibition of compound 48/80-induced release of serotonin, it is suggested that: lodoxamide antagonizes the action of compound 48/80 by blocking the release of mast cell constituents, and neither compound 48/80 nor the released constituents appear to modify vascular responsiveness to arterenol or hypervolemia following the initiation of hypotension.
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PMID:Hepatic microvascular regulatory mechanisms. IV. Effect of lodoxamide tromethamine and arterenol-HCl on vascular responses evoked by compound 48/80. 615 10

An extensive blood loss activates generalized inflammatory response. Abdominal organs and especially intestines are very sensitive to the ischemia-reperfusion insults due to hemorrhagic shock (HS) and blood volume restoration. Previously obtained results suggest that studies on peritoneal lavage fluid (PLF) can contribute to elucidation of inflammatory processes in abdominal organs in HS. Histamine (H) levels, total cell, and mast cell (MC) numbers, and MC ultrastructure in the fluid lavaged from peritoneal cavity were compared in the following groups of rats: control (gr. 1), sham operation (gr. 2), untreated hemorrhagic shock (gr. 3), shock treated with blood volume restoration with lactated Ringer's solution (LR) (gr. 4), shock treated with platelet activating factor (PAF)-receptor antagonist Ginkgolide B (BN52021), and LR (gr. 5). A shock-related significant increase in total cell numbers, MC numbers, MC degranulation, and histamine levels in PLF were observed. The restoration of blood volume caused further elevation of the above phenomena (gr. 4) while BN52021 seemed to inhibit peritoneal MC mobilization and degranulation as well as to attenuate increase in peritoneal H level (gr. 5). The peritoneal cavity is a place of rapid and strong reaction to hemorrhage. Evaluation of peritoneal histamine levels might be helpful in the monitoring of shock dependent intra-abdominal processes. Peritoneal MC mobilization and degranulation, and increase in histamine level is inhibited by BN52021.
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PMID:BN52021 inhibits activation of peritoneal mast cells caused by hemorrhage and blood volume restoration. 1072 Dec 66

We examined the effect of NO on acid secretion in vitro using isolated preparations of Bullfrog stomach. The bullfrog fundic mucosa was bathed in unbuffered Ringer solution gassed with 100% O2 on the mucosal side and HCO3- Ringer's solution gassed with 95% O2/5% CO2 on the serosal side, and the acid secretion was measured at pH 5.0 using the pH-stat method and by adding 5 mM NaOH. Serosal addition of a NO donor NOR-3 (10(-5) approximately 10(-3) M: (+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexnamine) caused an increase of acid secretion in a dose-dependent manner, the effect lasting about 1 hr and reaching a maximal level of 2-fold the basal values. The acid stimulatory effect of NOR-3 was mimicked by another NO donor SNAP (10(-3) mol/L: S-nitroso-O-N-acetyl-penicillamine) and markedly and markedly inhibited by prior administration of cimetidine (10(-5) mol/L) as well as compound 48/80 (the mast cell degranulator). Likewise, the increased acid response to NOR-3 was significantly mitigatd by pretreatment with carboxy-PTIO (a NO scavenger) or superoxide dismutase (SOD), but not by indomethacin or methylene blue (a guanylyl cyclase inhibitor). Neoither L-NAME, L-arginine nor dibutyryl guanosine-3',5'-cyclic monophosphate (dbcGMP) has any effect on the basal acid secretion. Serosal addition of NOR-3 caused a significant increase in the luminal release of histamine, and this response was inhibited by pretreatment with either compound 48/80, carboxy-PTIO or SOD. These results suggest that the NO donor increases gastric acid secretion in the isolated frog stomach in vitro, and this action is mediated by endogenous histamine released from mast cells, the process being cGMP-independent but requiring the presence of superoxide radicals. In addition, it was speculated that the histamine releasing action of NO may be due to peroxynitrite produced by NO and superoxide radicals.
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PMID:Stimulation by nitric oxide of gastric acid secretion in bullfrog fundic mucosa in vitro. 1132 16