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This study was performed to evaluate the effect of topical and intravenous heparin on thrombosis and patency in the microvascular anastomosis of the traumatized veins. Nine white rabbits weighing about 2kg were used. After exposure of both femoral veins, the veins were crushed by the jaws of smooth needle holder in order to create a thrombosis model. Transectional incision was made in the vein. The animals were then divided into 3 groups based on the administration method of heparin: 1) Experimental Group I, topical irrigation of lumen with heparin saline solution (n=6); 2) Experimental Group 2, topical irrigation of lumen with heparin saline solution and intravenous injection of heparin (0.75 mg/kg) via the marginal ear vein for 3 days; 3) Control Group, topical irrigation of lumen with saline solution (n=6). The patency was evaluated with empty-and-refill test and thrombus formation was judged by surgical microscope. The results were as follows: 1. Thirty minutes after microvascular anastomosis, the patency fall Experimental Groups was better than Control group. However, there was no significant difference among groups. 2. Three days after anastomosis, the patency of all Experimental Groups was much more improved than that of Control Group (P<0.05). There was no significant difference between Experimental Group 1 and 2. 3. Three days after anastomosis, the amount of thrombus in all Experimental Groups was much less than that of Control Group (P<0.05). 4. In histologic findings a lot of luminal thrombus were observed around sutured area in Control Groups. Few luminal thrombus was observed in all Experimental Groups. Mild necrosis in the vessel wall was observed around sutured area in all specimens. These results indicate that topical irrigation of heparin may improve the patency and inhibit the formation thrombus in the microvascular anastomosis of the traumatized veins.
Animals ; Ear ; Femoral Vein ; Heparin* ; Injections, Intravenous ; Jaw ; Necrosis ; Needles ; Phenobarbital ; Rabbits ; Sodium Chloride ; Thrombosis* ; Veins

10.Influence of glucocorticoids on cholinergic stimulation-induced catecholamine secretion from the rat adrenal medulla.

Dong Yoon LIM ; Jae Joon LEE ; Oh Seong GWEON

The Korean Journal of Physiology and Pharmacology 1998;2(2):173-184

The present study was undertaken to examine the influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100 micrometer) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K+ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100 micrometer for 2 min), McN-A-343 (a muscarinic receptor agonist, 100 micrometer for 4 min), Bay-K-8644 (a calcium channel activator, 10 micrometer for 4 min) and cyclopiazonic acid (a releaser of intracellular Ca2+ 10 micrometer for 4 min). Similarly, the preperfusion of hydrocortisone (30 micrometer) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, Ca2+ channel activation and the release of intracellular Ca2+. Furthermore, even in the presence of betamethasone (30micrometer), CA secretion evoked by ACh, excess K+, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Acetylcholine ; Adrenal Glands ; Adrenal Medulla* ; Animals ; Betamethasone ; Calcium ; Calcium Channels ; Catecholamines ; Chromaffin Cells ; Dexamethasone ; Dimethylphenylpiperazinium Iodide ; Glucocorticoids* ; Hydrocortisone ; Perfusion ; Rats* ; Receptors, Muscarinic ; Receptors, Nicotinic ; Veins

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9.Effects of topical and intravenous heparin on thrombosis of microvascular anastomoses.

10.Influence of glucocorticoids on cholinergic stimulation-induced catecholamine secretion from the rat adrenal medulla.

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