Effect of local bleomycin sulfate application on seroma formation in a rat mastectomy and axillary lymph node dissection model.

Seroma formation is one of the most common complications following breast cancer surgery. It may lead to delay of adjuvant therapies and increasement of therapy costs. Bleomycin sulfate is a sclerosing antibiotic with antineoplastic efficacy. It is locally used in the treatment of pleural effusion. The present study aimed to investigate seroma-reducing effect of local bleomycin application after mastectomy. Sixteen female Wistar Albino rats were used in this study. The rats were divided into two equal groups. Under general anesthesia all rats underwent unilateral mastectomy as definition by Harada. Serum physiologic was applied to animals in Group 1 (control group) and bleomycin to Group 2. Mastectomized localization was explored on the 10th day postoperatively. Seroma and tissue samples were obtained from axilla and thoracic wall for histopathological examination. The amount of seroma was significantly lower in the bleomycin group as compared to the control group (P=0.002). Fibrosis, PNL infiltration and the number of fibroblasts were significantly higher in the bleomycin group. No difference was identified between the groups in terms of angiogenesis, edema, congestion, and monocyte, lymphocyte and macrophage infiltration. Local bleomycin sulfate application might be a therapeutic option in patients with seroma formation, as well as in the patients with malignant pleural effusion. Nonetheless, further studies that compare the efficacy and adverse effects (benefit-to-harm ratio) of bleomycin sulfate are needed.

Effects of local phenytoin on seroma formation after mastectomy and axillary lymph node dissection: an experimental study on mice.

BACKGROUND: Seroma formation is the most common complication after breast cancer surgery. It is an important complication since it prolongs therapy duration, increases cost, and negatively affects patient psychology. Currently, there is no widely accepted method that prevents seroma formation. We tried to investigate impact of local phenytoin application on seroma formation following an experimental mastectomy model created in rats. METHODS: Two groups including eight rats in each were randomized. Saline injection was applied in the first group, whereas 1% phenytoin was locally used in the second group. Ten days after the surgery, seroma formation and wound-healing processes were evaluated using histopathological and biochemical examinations. RESULTS: Phenytoin significantly decreased seroma formation. Fibrosis was significantly increased and angiogenesis was significantly reduced in the phenytoin group (P < 0.05). Increased levels of macrophage and lymphocyte infiltration was detected in the control group (P < 0.05). No difference was detected between the groups in terms of necrosis, edema, congestion, and PNL (Polymorphonuclear leucocyte) and fibroblast infiltration. CONCLUSIONS: Seroma formation-reducing effect of phenytoin might have occurred over its anti-inflammatory, anti-angiogenetic, and fibrosis augmenting effects.

Investigation of the mechanism of nicotine-induced relaxation on the sheep sphincter of Oddi.

Possible mechanisms for nicotine-induced relaxation were investigated in the isolated sheep's sphincter of Oddi. Sheep's sphincter of Oddi rings were mounted in tissue bath with modified Krebs-Henseleit solution and aerated with 95% oxygen and 5% carbon dioxide. Tension was measured with isometric force transducers, and muscle relaxation was expressed as percent decrease of precontraction induced by carbachol. Nicotine (1 x 10(-5) to 3 x 10(-3) mol/L) produced concentration-dependent relaxation on sphincter of Oddi precontracted by carbachol (10(-6) mol/L). Nicotine-induced relaxation was 72.8 +/- 4.2% of precontraction with carbachol (10(-6) mol/L) (mean pD2 value, 3.76 +/- 0.05 mol/L). Nicotine-induced relaxation was not affected by N(w)-nitro L-arginine methyl ester (L-NAME) (3 x 10(-5) mol/L), methylene blue (10(-5) mol/L), indomethacin (10(-5) mol/L), hexamethonium (10(-5) mol/L), glibenclamide (10(-5) mol/L), 4-aminopyridine (10(-3) mol/L), tetraethylammonium (3 x 10(-4) mol/L), clotrimazole (10(-6) mol/L), 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) (10(-6) mol/L), and anthracene-9-carboxylate (9-AC) (10(-6) mol/L), but potentiated by bupivacain (10(-5) mol/L). A calcium-antagonizing effect of nicotine was not observed. The results suggest that nicotine-induced relaxation of the sheep's sphincter of Oddi is not mediated by the release of prostaglandins, nitric oxide (NO), or a related substance; by the activation of potassium channels or chloride channels; or by the stimulation of nicotinic cholinoceptors. Potentiation of the nicotine-induced relaxation by bupivacain indicates that blockade of sodium channels may play a role in this relaxation.