PubMed · 3839322
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M S Bornman, D du Plessis, D J Jacobs, R C Franz. 1985-06-29. Elevated thromboxane B2 levels during erection.. https://pubmed.ncbi.nlm.nih.gov/3839322/
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BACKGROUND: Recent study suggested that endothelial progenitor cells (EPCs), a novel therapeutic approach for endothelial dysfunction, present limited antithrombogenic potentials. However, few attempts have been done to improve the antithrombogenic potentials of EPCs. Our previous study proved that in vitro shear stress contributes to the increase in t-PA production by human EPCs. Here, we further investigated whether in vitro shear stress contributes to the secretion of antithrombogenic substances including plasminogen activator inhibitor-1 (PAI-1) and prostaglandin I(2) (PGI(2)) by human EPCs. METHODS: The peripheral blood mononuclear cells of healthy subjects were induced into EPCs. Then the human EPCs were treated with four levels of shear stress including stationary condition low media and high flow shear stress. The production of PAI-1 and 6-keto-prostaglandin F1(1alpha)(6-Keto-PGF(1alpha)) by human EPCs with shear stress treatment were measured. RESULTS: In vitro medium and high flow shear stress inhibited PAI-1 secretion by human EPCs, but low flow shear stress had no effect on PAI-1 secretion by human EPCs. All levels of shear stress significantly increased 6-Keto-PGF(1alpha )production by human EPCs in a dose-dependent manner. CONCLUSIONS: The present study demonstrates that in vitro shear stress can promote PGI(2 )secretion and inhibit PAI-1 secretion by human EPCs, which improves the antithrombogenic potentials of human EPCs.
Sensory neuron activation reduces water-immersion restraint stress (WIR)-induced gastric mucosal injury by inhibiting neutrophil activation through increase in endothelial production of prostacyclin. This study was designed to examine whether lafutidine, which is an H(2)-receptor antagonist and activates sensory neurons, inhibits neutrophil activation, thereby reducing WIR-induced gastric mucosal injury. Lafutidine enhanced WIR-induced increases in gastric tissue levels of calcitonin gene-related peptide (CGRP) and 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, whereas famotidine, another H(2)-receptor antagonist, did not. Such lafutidine-induced increases in gastric tissue levels of 6-keto-PGF(1alpha) were reversed by pretreatment with capsazepine, an inhibitor of sensory neuron activation, CGRP(8-37), a CGRP antagonist, and indomethacin. Lafutidine inhibited acid-induced exacerbation of gastric mucosal injury in animals subjected to WIR by inhibiting neutrophil activation, whereas famotidine did not. Lafutidine synergistically increased CGRP release from isolated rat dorsal root ganglion neurons in the presence of anandamide, but famotidine did not. These observations suggest that lafutidine might reduce WIR-induced gastric mucosal injury not only by inhibiting acid secretion but also by inhibiting neutrophil activation through enhancement of sensory neuron activation.
Recent studies have shown that the activated endocannabinoid system participates in the increase in IHR (intrahepatic resistance) in cirrhosis. The increased hepatic production of vasoconstrictive eicosanoids is involved in the effect of endocannabinoids on the hepatic microcirculation in cirrhosis; however, the mechanisms of these effects are still unknown. The aim of the present study was to investigate the effects of chronic CB(1) (cannabinoid 1) receptor blockade in the hepatic microcirculation of CBL (common bile-duct-ligated) cirrhotic rats. After 1 week of treatment with AM251, a specific CB(1) receptor antagonist, IHR, SMA (superior mesenteric artery) blood flow and hepatic production of eicosanoids [TXB(2) (thromboxane B(2)), 6-keto PGF(1alpha) (prostaglandin F(1alpha)) and Cys-LTs (cysteinyl leukotrienes)] were measured. Additionally, the protein levels of hepatic COX (cyclo-oxygenase) isoforms, 5-LOX (5-lipoxygenase), CB(1) receptor, TGF-beta(1) (transforming growth factor beta(1)), cPLA(2) [cytosolic PLA(2) (phospholipase A(2))], sPLA(2) (secreted PLA(2)) and collagen deposition were also measured. In AM251-treated cirrhotic rats, a decrease in portal venous pressure was associated with the decrease in IHR and SMA blood flow. Additionally, the protein levels of hepatic CB(1) receptor, TGF-beta(1), cPLA(2) and hepatic collagen deposition, and the hepatic levels of 5-LOX and COX-2 and the corresponding production of TXB(2) and Cys-LTs in perfusates, were significantly decreased after 1 week of AM251 treatment in cirrhotic rats. Furthermore, acute infusion of AM251 resulted in a decrease in SMA blood flow and an increase in SMA resistance in CBL rats. In conclusion, the chronic effects of AM251 treatment on the intrahepatic microcirculation were, at least partly, mediated by the inhibition of hepatic TGF-beta(1) activity, which was associated with decreased hepatic collagen deposition and the activated PLA(2)/eicosanoid cascade in cirrhotic livers.