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91.
Treatment with sodium-channel-blocking agents is accompanied by a high incidence of gastrointestinal side effects. We therefore studied the influence of two sodium channel blockers, mexiletine and flecanaide, on gastric and jejunal myoelectrical activity of unanesthetized rats. Bipolar electrodes were implanted chronically on the serosal surface of the antrum or the jejunum of male rats (weight: 250-350 g). Electrical activity was recorded on a Polygraph starting on day 5 after the operation After 1 h of baseline recordings, either vehicle or an active drug was given randomly. Recordings were continued for 4 h after drug administration. Vehicle did not induce changes in slow-wave frequency. In contrast, gastric slow-wave activity significantly decreased after the administration of both mexiletine and flecanaide. Jejunal myoelectrical activity was only slightly affected by sodium channel blockade. The disruption of gastric myoelectrical activity may contribute to the side effects observed during chronic treatment with class I antiarrhythmic drugs. 相似文献
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Transcatheter occlusion of the patent ductus arteriosus in infants: Experimental testing of a new Amplatzer device 下载免费PDF全文
Objectives: This study assessed the feasibility and efficacy of implanting a new miniaturized nitinol device to occlude the patent ductus arteriosus (PDA) in a newborn porcine model. Background: Transcatheter device closure is the standard of care for PDA in older children and adults. Currently available technology is not designed for the newborn infant. Methods: The Amplatzer Duct Occluder II 0.5 is a new transcatheter Nitinol device without fabric designed to close the PDA with small aortic and pulmonary artery structures. The device was implanted in 8 infant pigs (average weight 2,400 g) after balloon dilation of PDA (average diameter 2.7 mm, average length 5.8 mm) with immediate, ~ 7, ~ 30, and ~ 90 day follow‐up by echocardiography, angiography, and final pathological examination. Half were implanted arterial, and half venous. Results: The device was successfully implanted in all animals. There was complete occlusion of the PDA in all cases without obstruction of the pulmonary arteries or aorta. There was complete late endothelialization without thrombus. The only complication was transection of a femoral artery accessed by cutdown. Conclusions: The success of this animal study confirms safety and feasibility of the Amplatzer Duct Occluder II 0.5 (now known as the ADO II AS) for use when the aorta and pulmonary arteries are small. Consideration can be given to transcatheter closure of the PDA in preterm and other small infants with this device. © 2011 Wiley Periodicals, Inc. 相似文献
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Marta Lishnevsky Lena C. Young Steven J. Woods Steven D. Groshong Randall J. Basaraba John M. Gilchrist David M. Higgins Mercedes Gonzalez-Juarrero Todd A. Bass William A. Muller Alan R. Schenkel 《Experimental and molecular pathology》2014
Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1) deficient mice in the FVB/n strain exhibit fatal chronic pulmonary fibrotic disease. The illness occurs in the absence of a detectable pro-inflammatory event. PECAM-1 is vital to the stability of vascular permeability, leukocyte extravasation, clotting of platelets, and clearance of apoptotic cells. We show here that the spontaneous development of fibrotic disease in PECAM-1 deficient FVB/n mice is characterized by early loss of vascular integrity in pulmonary capillaries, resulting in spontaneous microbleeds. Hemosiderin-positive macrophages were found in interstitial spaces and bronchoalveolar lavage (BAL) fluid in relatively healthy animals. We also observed a gradually increasing presence of hemosiderin-positive macrophages and fibrin deposition in the advanced stages of disease, corresponding to the accumulation of collagen, IL-10 expression, and myofibroblasts expressing alpha smooth muscle actin (SMA). Together with the growing evidence that pulmonary microbleeds and coagulation play an active part in human pulmonary fibrosis, this data further supports our hypothesis that PECAM-1 expression is necessary for vascular barrier function control and regulation of homeostasis specifically, in the pulmonary environment. 相似文献
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Theken KN Schuck RN Edin ML Tran B Ellis K Bass A Lih FB Tomer KB Poloyac SM Wu MC Hinderliter AL Zeldin DC Stouffer GA Lee CR 《Atherosclerosis》2012,222(2):530-536
ObjectivePreclinical and genetic epidemiologic studies suggest that modulating cytochrome P450 (CYP)-mediated arachidonic acid metabolism may have therapeutic utility in the management of coronary artery disease (CAD). However, predictors of inter-individual variation in CYP-derived eicosanoid metabolites in CAD patients have not been evaluated to date. Therefore, the primary objective was to identify clinical factors that influence CYP epoxygenase, soluble epoxide hydrolase (sEH), and CYP ω-hydroxylase metabolism in patients with established CAD.MethodsPlasma levels of epoxyeicosatrienoic acids (EETs), dihydroxyeicosatrienoic acids (DHETs), and 20-hydroxyeicosatetraenoic acid (20-HETE) were quantified by HPLC–MS/MS in a population of patients with stable, angiographically confirmed CAD (N = 82) and healthy volunteers from the local community (N = 36). Predictors of CYP epoxygenase, sEH, and CYP ω-hydroxylase metabolic function were evaluated by regression.ResultsObesity was significantly associated with low plasma EET levels and 14,15-EET:14,15-DHET ratios. Age, diabetes, and cigarette smoking also were significantly associated with CYP epoxygenase and sEH metabolic activity, while only renin-angiotensin system inhibitor use was associated with CYP ω-hydroxylase metabolic activity. Compared to healthy volunteers, both obese and non-obese CAD patients had significantly higher plasma EETs (P < 0.01) and epoxide:diol ratios (P < 0.01), whereas no difference in 20-HETE levels was observed (P = NS).ConclusionsCollectively, these findings suggest that CYP-mediated eicosanoid metabolism is dysregulated in certain subsets of CAD patients, and demonstrate that biomarkers of CYP epoxygenase and sEH, but not CYP ω-hydroxylase, metabolism are altered in stable CAD patients relative to healthy individuals. Future studies are necessary to determine the therapeutic utility of modulating these pathways in patients with CAD. 相似文献
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