ObjectiveAlthough many studies have been performed, no consensus exists as to the ideal entry for laparoscopic gynecologic surgery. We sought out to compare the safety of direct trocar insertion with that of the Veress needle entry technique in gynecologic laparoscopic surgery.DesignSystematic review with meta-analysis.SettingWe searched Medline, ClinicalTrials.Gov, PubMed, Cochrane CENTRAL, SCOPUS, and Web of Science from their inception through 31 July 2021 for relevant studies. We included only controlled trials and ultimately seven trials were included in our meta-analysis.ParticipantsInclusion criteria included women undergoing gynecological laparoscopic surgery.InterventionThe intervention of direct trocar insertion technique compared with Veress needle entry technique.Main outcome measuresWe compared five different outcomes associated with the efficacy and complications of laparoscopic entry.ResultsThe pooled analysis showed that Veress needle entry was associated with a significant increase in the incidences of extraperitoneal insufflation (RR=0.177, 95% Cl (0.094 to 0.333), p<0.001), omental injury (RR=0.418, 95% Cl (0.195 to 0.896), p<0.001), failed entry (RR=0.173, 95% Cl (0.102 to 0.292), p<0.001), and trocar site infection (RR=0.404, 95% Cl (0.180 to 0.909), p<0.029). There was no significant difference between the two groups regarding the visceral injury (RR=0.562, 95% Cl (0.047 to 6.676), p<0.648).ConclusionsWhen excluding all data apart from gynecologic surgery, the Veress needle entry technique may have an increased incidence of some, but not all complications of laparoscopic entry. It may also have a higher incidence of failed entry compared with direct entry techniques. Care should be taken in extrapolating these general results to specific surgeon experience levels.Trial registration numberCRD42021273726
Marfan syndrome (MFS) is an autosomal dominant inherited disease that affects the connective tissue of large vessels throughout the human body. MFS is caused by mutations in the FBN1 gene which encodes for fibrillin‐1, a major component of extracellular microfibrils and acts as a scaffolding protein for elastin deposition, and allows for the formation of elastic fibers in the extracellular matrix of large arteries. The loss of aortic wall structural integrity leads to cardiovascular manifestations of MFS, which include the dilation of the aortic root that can lead to dissection and rupture. Previous studies have shown that the activity of endothelial nitric oxide (eNOS) has decreased in the aortic wall leading to endothelial dysfunction in MFS mice. However, we have been able to show that despite an obvious decrease in eNOS activity, the basal NO level in the aortic tissue is significantly higher in MFS mice aorta. Therefore, we aim to further determine the role that inducible nitric oxide synthase (iNOS) may play in MFS aneurysm pathogenesis by creating a MFS mouse lacking iNOS expression. In this study, wild type C75BL/6, MFS (FBN +/−) and MFS mice lacking iNOS expression (FBN+/−, iNOS−/−) were subjected to high resolution, high frequency ultrasound imaging at the age of 3 and 6 months to evaluate various cardiac and aortic parameters including aortic diameter, pulse wave velocity, cardiac ejection fraction & stroke volume, left ventricular wall thickness and mass and mitral valve early and atrial velocities (E/A) ratio. Our data shows that aortic root diameters at the aortic annulus and sinus of Valsalva, aortic pulse wave velocity, and mitral valve early velocity were greater in 3‐month old MFS mice when compared to control and MFS mice lacking iNOS expression, indicating a significant increase in aortic wall stiffness in MFS mice aorta. At 6 months of age, mitral valve early and atrial velocities and E/A ration were significantly decreased in MFS mice compared to controls and MFS mice lacking iNOS expression. In addition, measurements for aortic annulus diameter, ejection fraction, fractional shortening were markedly increased in 6‐month old MFS mice as compared to control and MFS mice lacking iNOS expression. These findings indicate that inhibition of iNOS may have some protective effects in the cardiovascular system in MFS mice, and therefore, providing valuable information about the potential therapeutic value of iNOS inhibition on cardiac and aortic function and structure in the mouse model of MFS associated aortic aneurysm.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Alzheimer's disease (AD) is characterized with the progressive loss of cognitive abilities that typically presents in the elderly population, therefore most research has focused primarily on the brain. Hypertension, obesity and atherosclerosis are often comorbidities that present with AD patients. Per the American Heart Association, by 2035 nearly half of the US population will suffer from some type of vascular disease. Despite that, peripheral vascular dysfunction within the progression of AD has not been studied in detail. Apolipoprotein‐ɛ (ApoE) is a lipid‐binding protein that is a major factor in cholesterol metabolism in the brain and periphery. ApoE is polymorphic and the expression of the ApoE4 allele is associated with late onset AD. Conversely, the ApoE3 allele has been shown to likely prevent neurodegeneration, suggesting a protective role for ApoE3 protein in the brain. In this study we investigated the functional (vasoconstriction & vasodilation) and structural (elastin fiber organization and elasticity) properties of the aorta in 18‐month old mice expressing human ApoE4 or ApoE3, and wild type C57BL/6 mice using wire myography and conventional histological staining. Our data shows that phenylephrine‐induced contraction and acetylcholine‐induced vasodilation is not different among experimental groups. However, elastin fiber fragmentation and disorganization were observed within the aortic wall in ApoE4 mice as compared to age‐ and sex‐matched ApoE3 and C57BL/6 mice. Furthermore, the stretch‐induced wall stress and reversibility of elasticity were significantly reduced in aortic segments isolated from ApoE4 mice indicating an increase in aortic wall stiffness in ApoE4 mice. These data present the first evidence that neurodegenerative pathology in ApoE4 mice is associated with pathologic changes in the aortic wall that leads to increased vascular wall stiffness and reduced elasticity. This will establish a new direction aimed at studying the relationship between observed brain pathology in AD and abnormal changes in peripheral vascular function and structure that occur in a relevant mouse model for the disease.Support or Funding InformationThis study is supported by funding from Midwestern University Alzheimer's Advisory Committee.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Marfan syndrome (MFS) is a connective tissue disorder that causes complications throughout the body. However, the cardiovascular effects of MFS, specifically aortic aneurysms, are the leading cause of morbidity and mortality in patients. Both the transforming growth factor beta (TGF‐β) and angiotensin II type I receptor (AT1R) signaling pathways are known to contribute to the progression of MFS aneurysms. Recently, our laboratory reported that low‐intensity mild exercise could improve aortic function and structure in the mouse model of MFS. Losartan, an AT1R blocker, has been shown to slow down the progression of MFS aneurysms in both the mouse model and human patients. In this study, we have explored the potential of a combinational therapy of exercise and losartan in a well‐established mouse model of MFS associated aortic aneurysm in order to determine if there are additive protective and delaying effects on the progression of aortic aneurysm in the mouse model. Treatment consisted of 0.6 g/L (full dose) or 0.3 g/L (half dose) of losartan in drinking water combined with a 55% VO2 max exercise regimen (8 m/min, 30 min/day, 5 days/week). Mice were divided into experimental groups: control, MFS, MFS + exercise, MFS + 0.6 g/L losartan, MFS + 0.3 g/L losartan, MFS + exercise + 0.6 g/L losartan, and MFS + exercise + 0.3 g/L losartan. The biophysical properties of the aorta, such as the aortic diameter and pulse wave velocity (PWV), were determined by high resolution high frequency ultrasound imaging system (Vevo2100, FUJIFILM VisualSonics) in 3‐month‐old MFS and control mice. Aortic diameter measurements of the sinus of Valsalva were significantly higher in 3‐month‐old MFS mice as compared to control. However, losartan treatment, mild exercise, or combination of both had no effects on aortic root growth in MFS mice. In addition, measurements of the aortic annulus and sinotubular junction were not significantly different among experimental groups. MFS mice exhibited higher PWV as compared to control mice, indicating increased stiffness of aortic wall in these mice. Combination of mild aerobic exercise with full and half dose of losartan seems to have some effects on the aortic wall by decreasing the aortic diameter, although no statistical significant differences were observed among the treated and non‐treated groups. This study presents the effects of combination of mild exercise and losartan during the early stage of aneurysm progression in MFS mice. With the continuation of the longitudinal study at 6 and 9 months of age and as the aneurysm progresses, we will be able to continue our evaluation of aortic and cardiac function and structure in MFS mice subjected to exercise only, losartan only, or the combinational therapy. This study provides additional information on the most effective therapeutic approach to delay the progression of aneurysm in MFS.Support or Funding InformationThis study is supported by funding from The Marfan Foundation.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Apolipoprotein E (APOE) is a multifunctional protein with three isoforms (e2, e3, and e4) that correspond with diverse functional and pathological manifestations. Most notably, the e4 allele has been associated with an increased risk of cardiovascular disease, and is considered a prominent risk factor for the development of late onset Alzheimer disease (AD). AD is a progressive neurodegenerative disease and the leading cause of dementia. Although research in AD has been ongoing, the pathogenesis of the disease remains elusive. The discovery of cerebral vascular abnormalities in AD patients and the association of ApoE e4 (APOE4) with cardiovascular disease has led to the hypothesis that the condition may initially arise from peripheral vascular dysfunction. However, little is known about the pathological consequences associated with the apolipoprotein isoforms in major peripheral arteries, such as the aorta.In this study, we aimed to characterize the functional (vasoconstriction and vasodilation) and structural (aortic wall elasticity and integrity) characteristics of the thoracic aorta in wild type C57BL/6, targeted replacement APOE3, and targeted replacement APOE4 mice, at 12 and 18 months of age, using small chamber myography. In order to determine early changes that may be associated with vascular abnormalities noted at older ages, we aimed to evaluate cardiac and aortic function and structure including aortic root diameter, aortic stiffness, and cardiac parameters in young mice of all experimental groups using high‐resolution, high‐frequency ultrasound imaging. Our data showed a significant increase in phenylephrine (PE)‐induced contraction in aortic segments isolated from 12 and 18‐month old APOE4 mice as compared to APOE3 mice. There was no evident difference in acetylcholine‐induced relaxation between experimental groups at 12 or 18 months of age. However, the rupture point was significantly reduced in aortic segments isolated from APOE4 mice when compared to wild type mice, indicating a decrease in aortic wall integrity in APOE4 mice. Aortic root diameter at the sinotubular junction was significantly increased in APOE4 mice when compared to APOE3 mice, but was not significant at the regions of aortic anulus or sinus of Valsalva. Pulse wave velocity, a reliable index of aortic wall stiffness, was comparable amongst genotypes at 3 months of age. Cardiac stroke volume was significantly increased in APOE4 mice when compared to wild type, and there was a decreasing trend in left ventricular mass between wildtype, APOE3, and APOE4 mice. This study provides the first preliminary evidence of peripheral vascular dysfunction in the well‐established mouse model of AD (APOE).Support or Funding InformationThis study was funded by a Midwestern University graduate fund.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.