Artery Ligation Research Articles

Abstract 16200: Chronic Central Nervous System Actions of Leptin Protect Against Myocardial Ischemia/reperfusion Injury

While myocardial reperfusion is the most effective therapy to reduce mortality after myocardial infarction, it can paradoxically exacerbate ischemic injury. We recently showed that leptin, via its actions on the central nervous system (CNS), improved left ventricular function in a model of heart failure induced by permanent ligation of the left anterior coronary artery (LAD). To investigate whether leptin also protects the heart against ischemia/reperfusion (I/R) injury via its actions in the CNS, we instrumented female Wistar rats (15 weeks of age) with an intracerebroventricular (ICV) cannula into the lateral ventricle, and after 7 days of recovery and baseline assessment of cardiac function by echocardiography (VisualSonics VEVO-3100®), myocardial I/R was induced by temporary LAD ligation (60 min). Vehicle (saline, 0.5 μL/hr, n=6) or leptin (15 μg/day, n=7) were infused ICV for 28 consecutive days starting 20 min after reperfusion using osmotic minipump connected to the ICV cannula. Echocardiographic assessment of cardiac function was performed every week and at the end of the 4 th week of treatment, the heart was collected and processed for protein analysis and histological evaluation of infarct size and collagen deposition. Compared to vehicle treatment, chronic ICV leptin infusion significantly reduced infarcted area (21±2 vs. 37±4 %), septal collagen deposition (2.2±0.2 vs. 4.0±0.7 %), and markedly attenuated systolic dysfunction as evidenced by increased ejection fraction 4 weeks post I/R (59±1 vs. 30±2%), stroke volume (296±19 vs. 159±8 μL) and cardiac output (108±5 vs.63±4 μL/min). ICV leptin infusion also prevented the increase in left atrium to aorta diameter ratio (1.5±0.1 vs. 2±0.1 mm), an index of cardiac congestion. In addition, we found a 2-fold increase in the ratio of phospho-acetyl-CoA carboxylase (p-ACC) to total ACC protein expression, a marker of fatty acid oxidation, in hearts of leptin-treated rats compared with vehicle infusion. These results indicate that leptin exerts powerful beneficial CNS-mediated effects on the heart that improve systolic function and protect the myocardium against I/R injury. Our results also suggest that these beneficial actions may involve improved myocardial bioenergetics.

Abstract 12907: Treatment of Anomalous Left Coronary Artery From the Pulmonary Artery in a 60-year-old Patient With Primary Re-implantation

Anomalous left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital heart defect accounting for 0.26% - 0.46% of congenital anomalies. Most (85%) cases are diagnosed in the first month of life with only 18-25% of patients reaching adulthood. Patients diagnosed in adulthood typically have collaterals from the right coronary artery (RCA) which provide blood flow to the left coronary artery (LCA) system. They can present with heart failure, mitral insufficiency, arrhythmias, and/or sudden cardiac death. An otherwise healthy 60 y/o female presented to an outside hospital after a witnessed cardiac arrest when leaving the gym. Bystander CPR was started, and she received 2 shocks from an automated external defibrillator for ventricular tachycardia/ventricular fibrillation (VT/VF) with return of spontaneous circulation and taken to the local ED. A CTPE showed no acute PE and a possible ALCAPA. She was transferred to our institution for further assessment by adult congenital cardiology. TTE was performed on arrival which showed a global cardiomyopathy with color flow in the myocardium consistent with extensive collateralization. CT coronary artery was performed which confirmed ALCAPA anatomy without significant CAD. The case was discussed with CT surgery, interventional cardiology and adult congenital cardiology. The decision was made for a right and left heart catheterization and cardiac MRI to plan for possible surgery. Angiography showed a large RCA with extensive collaterals filling the left coronary system and no significant disease. RHC showed a normal cardiac output with a large left to right shunt and moderate pulmonary hypertension. MRI showed a mild diffuse subendocardial ischemia with high viability of the entire left ventricle and a pulmonary to systemic flow ratio (Qp:Qs) of 2.1. The decision was made to go ahead with primary re-implantation of the LCA to the aorta, the preferred method. Ligation of the anomalous coronary artery and coronary artery bypass grafting can also be used. She was taken for surgery and tolerated the procedure well. Follow up echo is pending, but she has had no further VT/VF episodes. This case demonstrates successful re-implantation of an ALCAPA in a symptomatic adult.

Abstract 15013: Ischemic Mitral Regurgitation is Associated With Impaired Transforming Growth Factor/Bone Morphogenic Protein Signaling and Increased CD45+ Cell Presence in the Mitral Valve Interstitial Cell Population

Introduction: Ischemic mitral regurgitation (IMR) develops in a fraction of patients in response to left ventricular (LV) remodeling after ischemia. IMR independently predicts adverse events and doubles mortality. While largely driven by LV distortion, the susceptibility of the mitral valve (MV) to undergo remodeling may play a role in determining whether MR develops. We hypothesized that impaired cellular response in MV cells may contribute to MR development by inducing maladaptive tissue remodeling. Methods: Dorsett hybrid sheep (n=32) were subjected to ligation of the circumflex coronary artery to induce myocardial infarction (MI). Development of MR was reported by echocardiography. MV leaflets and isolated MV interstitial cells (MVIC) were collected at baseline (Control), 4-, and 8-weeks post MI. RNAseq (150 paired end reads, 20 million reads/sample) was performed on MV leaflets from all groups. MVICs were treated with for 24h with 10ng/ml TGFβ1 of 50ng/ml BMP4. Results: Gene set enrichment analysis using pre-defined gene sets from the Gene Ontology project, considering genes with significant changes (p<0.05) between MV with/without MR showed enrichment of cardiac contraction biological processes. TGFβ/BMP-dependent SMAD7 was the main hub in the protein-protein-interaction network of the top contributing genes to the enriched pathways in MR. In vitro, collagen matrix-contracting ability of MR MVICs was higher than non-MR MI MVICs. MVICs from MI sheep were less responsive to BMP4 pro-osteogenic stimulation (as reflected by blunted increased in ID2, osteopontin and osteocalcin mRNA) than control. MVICs from sheep with MR had a diminished COL1A1 mRNA response to TGFβ1 and enhanced pro-chondrogenic RUNX2 and SOX9 mRNA response to BMP4 vs. non-MR MVICs. Baseline CD45 expression was detectable only in MR MVICs. Upon TGFβ1 stimulation, CD45 expression was detected in all groups. Immunostaining confirmed increased presence of CD45+ cells in IMR MV interstitium. Conclusions: MVs from sheep developing MR had altered TGFβ/BMP response, which may be partially mediated by increased CD45+ fibrocyte presence. Pharmacological strategies aimed to modulate TGFβ/BMP signaling after MI may protect from pathological MV remodeling leading to IMR.

Abstract 15735: Neonatal Cardiac Regeneration Depends on IGF1R-signaling

Introduction: In contrast to other adult tissues myocardium cannot be sufficiently regenerated following significant myocardial infarction (MI). Efficient cardiac regeneration was demonstrated in neonatal mouse myocardial injury models. Similar observations were reported in other neonatal mammals including newborn human babies suffering from MI. The mechanisms of neonatal mammalian cardiac regeneration remain unclear. Here we show the crucial role of IGF1R which was unraveled in a time-course transcriptome analysis of neonatal mouse hearts. Methods: IGF1R was specifically knocked-down (KD) in cardiomyocytes of wildtype postnatal day one (P1) mice using adeno-associated virus (rAAV9) delivered shRNAmirs. KD of Renilla served as control (REN-CTRL). 5x10 13 viral genomes per kg bodyweight were injected intrathoracally. Three batches of rAAV9 with different shRNAmirs were used for the IGF1R-KD groups. Viral transduction was confirmed by bioluminescence imaging on luciferase containing rAAV9 copies and by immunofluorescence staining of rAAV9 delivered GFP reporter. KD efficiency was confirmed in vitro using a retrovirus system and in vivo. On P2 mice underwent either left anterior descending artery (LAD) ligation for induction of MI or SHAM surgery. Cardiac function was subsequently assessed by echocardiography 1 day post injury (dpi) and 21 dpi. Thereafter, hearts were harvested and left ventricular fibrosis was analyzed histologically. Results: LAD ligation resulted in significant MI in both, IGF1R-KD and REN-CTRL, LAD groups as proven by a markedly reduced ejection fraction (EF) 1 dpi. Importantly, 21 dpi IGF1R-KD and REN-CTRL SHAM groups displayed normal cardiac function proving no effect on neonatal cardiac growth and development of only KD of IGF1R without LAD ligation. In contrast, LAD ligation IGF1R-KD mice presented significantly reduced EF 21dpi compared to the other 3 groups. Histological analysis revealed significant fibrosis in the IGF1R-KD LAD hearts compared to the other 3 groups. Conclusions: Whereas IGF1R-KD or control rAAV9 does not alter physiological cardiac development, KD of IGF1R markedly impairs neonatal cardiac regeneration in neonatal mice after MI suggesting a crucial role in neonatal cardiac regeneration.

Abstract 17169: Endothelium-Specific Reduction in Mitochondrial ROS Induces Coronary Angiogenesis in Ischemic Myocardium via Activation of PI3k/Akt/ERG, ERK1/2, and Jag-1 Signaling

Introduction: Global reduction in reactive oxygen species (ROS) failed to improve outcomes in cardiovascular disease patients. Recent reports suggest that subcellular, rather than global ROS, play a crucial role in endothelial cell (EC) health. To that end, we generated a novel transgenic mouse model that overexpresses mitochondrial antioxidant MnSOD in EC-specific manner (MnSODVE-OE). Hypothesis: We hypothesized that decreased EC mitochondrial-ROS will improve post-myocardial infarction (MI) cardiac function by inducing coronary angiogenesis in ischemic myocardium. Methods: MnSODVE mice were assigned to Tet-ON (control) or Tet-OFF (MnSODVE-OE) group. To turn off the transgene, Tetracycline (Tet) (2mg/kg) was added to the drinking water (Tet-ON), while Tet-OFF mice did not receive Tet. Both groups underwent left anterior descending coronary artery (LAD) ligation surgery to mimic acute MI. Echocardiography was done 28 days after LAD ligation. Capillaries, arteriole density, and proliferating ECs were measured in heart sections using anti-CD31, anti-αSMA, and anti-PCNA immunofluorescence. Western blot, proteomic and phosphoproteomic analyses of mouse heart ECs isolated from MnSODVE (Tet-ON and Tet-OFF) animals were performed to study modulation of signaling cascades. Results: MnSODVE-OE mice demonstrated improved cardiac function (EF and FS increased by 16±7.87% and 21.73±10.31%, respectively, p <0.01), increase in capillary and arteriole densities by 4.13±4.10-fold, p<0.05 and 5.48±3.51-fold, p<0.001, respectively, and in EC proliferation by 1.46±0.80-fold, p <0.01, suggesting de novo coronary angiogenesis. Western blots showed activation of Akt (80.46±3.95% increase in p-Akt/ t-Akt ratio, p<0.05) and ERK1/2 (21.05±4.45% increase in p-ERK/ t-ERK 1/2 ratio, p<0.05). Proteome and phosphoproteome analyses showed upregulation of mitochondrial complex I biogenesis, RNA metabolism, and upregulation of Notch-related proteins ERG and Jag-1 (p<0.05). Student’s t-test was used for data analyses. Conclusions: Taken together, these results suggest that decreased mito-ROS in ECs improves post-MI cardiac function by inducing coronary angiogenesis through activation of PI3k/Akt/ERG, ERK1/2, and Jag-1 signaling.

Vascular protective effect of aspirin and rivaroxaban upon endothelial denudation of the mouse carotid artery

While in recent trials the dual pathway inhibition with aspirin plus rivaroxaban has shown to be efficacious in patients with atherosclerotic cardiovascular disease, little is known about the effects of this combination treatment on thrombus formation and vascular remodelling upon vascular damage. The aim of this study was to examine the effects of aspirin and/or rivaroxaban on injury-induced murine arterial thrombus formation in vivo and in vitro, vessel-wall remodelling, and platelet-leukocyte aggregates. Temporary ligation of the carotid artery of C57BL/6 mice, fed a western type diet, led to endothelial denudation and sub-occlusive thrombus formation. At the site of ligation, the vessel wall stiffened and the intima-media thickened. Aspirin treatment antagonized vascular stiffening and rivaroxaban treatment led to a positive trend towards reduced stiffening. Local intima-media thickening was antagonized by both aspirin or rivaroxaban treatment. Platelet-leukocyte aggregates and the number of platelets per leukocyte were reduced in aspirin and/or rivaroxaban treatment groups. Furthermore, rivaroxaban restricted thrombus growth and height in vitro. In sum, this study shows vascular protective effects of aspirin and rivaroxaban, upon vascular injury of the mouse artery.

Curcumin-loaded extracellular vesicles endowed with heart targeting properties facilitate treatment of myocardial infarction

Abstract Background Myocardial infarction (MI) is a public health problem and a leading cause of death worldwide. Due to insufficient current treatments, it is essential to develop effective alternatives for MI treatment. Curcumin is known to exhibit a variety of protective effects on the cardiovascular system such as MI, hypertension, and diabetic cardiomyopathy. However, due to its low solubility/stability and quick systemic elimination, curcumin has limited bioavailability. Extracellular vesicles (EVs) have lately emerged as a promising drug delivery vehicles by overcoming drug delivery hurdles. However, strategies are needed for delivery of EVs into the heart avoiding accumulation of other organs. Purpose The aim of this study is to investigate whether curcumin-loaded EVs functionalized with cardiac targeting peptide (CTP) may function as efficient heart-targeted delivery vehicles of curcumin, and further identify the molecular mechanisms underlying curcumin-mediated therapeutic effects in the MI. Methods EVs functionalized to express CTP (CTP-EVs) were isolated from culture medium of HEK293 cells transfected with mCherry-CD81–10 plasmid and CTP-LAMP2 plasmid by differential centrifugation, and then loaded with curcumin by coincubation, named CTP-EVs-Cur. The effect of CTP-EVs-Cur were evaluated H9C2 cardiomyocytes and mouse MI model. For the in vivo experiments, CTP-EVs-Cur (approximately 8–10 × 109 particles) were administered by intravenous injection into the tail vein and mice were subjected to the left anterior descending (LAD) artery ligation with a 6–0 silk suture. Results CTP-EVs were safely and successfully delivered curcumin to H9C2 cardiomyocytes and mouse hearts (4-fold; P<0.05), and CTP-EVs-Cur have a protective effect against MI in vitro and in vivo models. After validating potential utility of CTP-EVs-Cur in MI treatment, we investigated the mechanism of curcumin-mediated recovery effects after MI. In H2O2 treated-cardiomyocytes, curcumin significantly reduced apoptosis by regulating the PTEN/AKT pathway following upregulation of miR-144-3p expression. Furthermore, mice injected with CTP-EVs-Cur reduced infarct size and apoptosis with the regulation of miR-144-3p/PTEN/Akt pathway. Conclusion These findings suggest highly stable/effective ability of CTP-EVs for heart-targeted delivery and the novel mechanism of curcumin-mediated cardioprotective effects after MI, therefore, CTP-EVs-Cur are potentially powerful therapeutic strategy for MI treatment. Funding Acknowledgement Type of funding source: None

Systemic mesenchymal stem cell-derived exosomes reduce myocardial infarct size: characterization with MRI in a porcine model

Abstract Background Mesenchymal stem cells (MSCs) have been shown to exert cardiac protection and repair via their secretome with the active component(s) identified as exosomes. Purpose To determine whether MSC-derived exosomes administered systemically by the convenient method of intravenous (IV) bolus injection reduce infarct size and improve cardiac function in an established porcine model of myocardial infarction (MI). Methods A total of 20 pigs underwent experimental MI by permanent ligation of the left circumflex coronary artery (LCX). Ten pigs (exosome treated) received twice daily IV injection of exosomes (1000ug protein equivalent) for 7 days. The remaining 10 pigs received vehicle control injections. Cardiac structure and function were measured by MRI which was performed at baseline (pre-MI) and repeated on days 7 and 28 post-MI. Infarct size was also confirmed post-mortem. Blood samples were drawn over first 7 days for measurement of hs Troponin T. The study followed the principles of laboratory animal care and was approved by our institution's IACUC. Results All LCX ligations resulted in permanent ischaemia with MI as evidenced by pallor of the myocardium, ECG changes including ST segment elevation and increases in plasma hs Troponin T. Exosomes administered IV for 7 days resulted in clear reduction (30–40%) of infarct size measured at both 7 (p<0.05) and 28 days (p<0.01) post-MI, despite near identical release of hs Troponin T. Together with reduced infarct size, exosome treatment reduced transmurality and lessened wall thinning (p<0.01) in the infarct zone. Exosome treated pigs showed relative preservation of LV function with significant amelioration of falls in fractional wall thickening (p<0.01) compared with control. However, global measures of LV function were less protected by exosome treatment. It is possible that greater preservation of global LV function may have been attenuated by increased cardiac fibrosis, as T1 values showed significant increase in the exosome pigs compared to control particularly in the infarct related segments. Conclusion Taken together, our results show clear effects of IV exosomes administered over 7 days to reduce infarct size with relatively preserved cardiac function compared to control treated infarct pigs. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): STaR Award (AM Richards), National Medical Research Council, Singapore. IAF-ICP, National Research Foundation, Singapore (RC Lai and SK Lim).

CXCR7 in cardiomyocytes prevents cardiac dysfunction after myocardial infarction

Abstract Background Beta blockers and angiotensin II receptor blockers take effect through G protein-coupled receptors (GPCRs) and their protective roles in heart failure are partially attributable to beta-arrestin biased agonism. CXCR7, a chemokine receptor, is beta-arrestin biased receptor and one of the most expressing GPCRs in the heart. CXCL12 is a common ligand of CXCR4 and CXCR7 and is known to ameliorate myocardial infarction (MI), reportedly through CXCR4 dependent mechanisms. However, the role of another receptor, CXCR7 and its downstream target including beta-arrestin is not fully elucidated in MI. Purpose The aim of this study is to uncover the role of CXCR7 in cardiomyocytes after MI. Methods First, we quantified CXCR7 mRNA expressions in neonate rat cardiomyocytes (NRCM) in a dish by qRT-PCR. NRCMs were treated with CXCR7 agonist: TC14012 and phosphorylation of extracellular signal regulated kinase (ERK) was measured as readout of the downstream of CXCR7, with immunoblotting. Second, MI was induced by left anterior descending artery (LAD) ligation in male 12-week-old mice. We explored spatial expressions of CXCR7 by qRT-PCR in infarct, peri-infarct and remote zones of wild-type MI mice. Finally, we developed cardiomyocyte-specific CXCR7 knockout mice (cKO) by the Cre/loxP system and analyzed CXCR7 expression in cKO by qRT-PCR. LAD ligation was also performed in cKO and littermate controls (Ctl). Heart weight (HW) was measured and systolic function was examined by echocardiography 4 weeks after ligation. Phosphorylated ERK was evaluated with immunoblotting one-day after ligation. Results First, we found that CXCR7 expression was significantly higher in NRCM than neonatal rat fibroblasts (NRFB) and ERK was phosphorylated by CXCR7 stimulation in NRCM. Second, CXCR7 expression was higher in infarct and peri-infarct zones than remote zones. Finally, cardiomyocyte-specific knockout of CXCR7 resulted in 78±21% reduction of CXCR7 expression in the whole heart. HW and left ventricular area was significantly greater (HW: Ctl 190.7±18.4, cKO 220.3±26.4 mg) and fractional area change of left ventricle was significantly lower in cKO than those in Ctl 4 weeks after MI (LV FAC: Ctl 20.6±4.9%, cKO 13.9±5.4%), indicating that loss of CXCR7 in cardiomyocytes caused left ventricle enlargement and systolic dysfunction. One day after MI of Ctl heart, ERK was more phosphorylated in peri-infarct zone than remote zone. However, this ERK phosphorylation in peri-infarct zone was reduced in cKO MI heart. Conclusion We revealed that CXCR7 is expressed in cardiomyocytes and deletion of this chemokine receptor in cardiomyocytes resulted in ventricle enlargement and systolic dysfunction possibly through ERK phosphorylation in peri-infarct zone. Therefore, CXCR7 in cardiomyocytes could prevent cardiac dysfunction after myocardial infarction, which may be another pathway of CXCL12 dependent-protective effect. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): JSPS KAKENHI

Dr. W. B. Dorsett, (from St. Louis to the Americas) - Ligation of the Uterine Arteries for the Cure of Fibroid Tumors and Checking Haemorrhage. (New-Jork Med. Journ., 1894, 3 / xi, p. 567). Ligation of uterine arteries for the healing of fibroids and stopping bleeding

Dr. Dorsett disputes with others the honor of the first application of the named method, referring to the production of this operation in 1889, about which he informed the medical society in St. Louis 17 / V 1890 and that was published by him in St. Louis Courrier of Medecine in the same year.

Novel oxygen saturation imaging endoscopy to assess anastomotic integrity in a porcine ischemia model

BackgroundEstablishing anastomotic integrity is crucial for avoiding anastomotic complications in colorectal surgery. This study aimed to evaluate the safety and feasibility of assessing anastomotic integrity using novel oxygen saturation imaging endoscopy in a porcine ischemia model.MethodsIn three pigs, a new endoscope system was used to check the mechanical completeness of the anastomosis and capture the tissue oxygen saturation (StO2) images. This technology can derive the StO2 images from the differences in the absorption coefficient in the visible light region between oxy- and deoxy-hemoglobin. Bowel perfusion at the proximal rectum was assessed before and after the anastomosis, and 1 min and 30 min after the ligation of the cranial rectal artery (CRA).ResultsThe completeness of the anastomoses was confirmed by the absence of air leakage. Intraluminal oxygen saturation imaging was successfully performed in all animals. There was no significant difference in the StO2 level before and after the anastomosis (52.6 ± 2.0 vs. 52.0 ± 2.6; p = 0.76, respectively). The StO2 level of the intestine on the oral side of the anastomosis one minute after the CRA ligation was significantly lower than immediately after the anastomosis (15.9 ± 6.0 vs. 52.0 ± 2.6; p = 0.006, respectively). There was no significant difference in the StO2 level between 1 min after and 30 min after the CRA ligation (15.9 ± 6.0 vs. 12.1 ± 5.3; p = 0.41, respectively).ConclusionNovel oxygen saturation imaging endoscopy was safe and feasible to assess the anastomotic integrity in the experimental model.

The Surgical Approach to Hysterectomy in a Patient with Mullerian Duct Anomaly

Study Objective To present the key surgical steps to complete hysterectomy safely in the presence of uterine anomalies. Design An educational video reviewing Mullerian duct anomalies, their associated anatomic malformations, and the steps to safely complete laparoscopic hysterectomy in a patient with these anomalies. Setting Minimally Invasive Gynecology division at a tertiary care hospital. Patients or Participants N/A Interventions A 45-year-old female undergoing robotic-assisted laparoscopic hysterectomy with presence of Mullerian duct anomaly including proximal vaginal septum with two cervices. Surgical intervention including the robotic localization and resection the proximal vaginal septum. Key points of surgical safety are reviewed including complete bilateral ureterolysis and ligation of the uterine arteries at their origin. Measurements and Main Results N/A Conclusion Minimally invasive approaches can be ideal for use in a patient with a noted Mullerian duct anomaly. Identification of dual collecting ducts or additional renal anomalies is vital to complete hysterectomy safely in these patients, specifically if a uterine anomaly is not recognized prior to surgical intervention.

Obliterated Cul-De-Sac in Endometriosis: Retrograde Dissection of Rectum

Study Objective To demonstrate a retrograde dissection technique for safe management of the obliterated cul-de-sac during hysterectomy in stage IV endometriosis. Design A case report. Setting Academic tertiary care hospital. Patients or Participants 50-year-old G3P3 with chronic pelvic pain and abnormal uterine bleeding requiring blood transfusion who failed medical management and was referred to our clinic for definitive surgical management. Her surgical history is significant for three prior cesarean sections and tubal ligation. Pelvic ultrasound notable for fundal fibroid, left ovary with 8 cm cystic mass and left hematosalpinx. Interventions Patient placed in dorsal lithotomy in Trendelenburg position with uterine manipulator in place. Patient underwent robotic-assisted laparoscopic hysterectomy, bilateral salpingectomy and left oophorectomy with lysis of adhesions and bilateral ureterolysis. Measurements and Main Results The obliterated cul-de-sac can pose risk for injury to rectum, ureters and hypogastric nerves during hysterectomy. Here, we present a technique to safely dissect rectum from the obliterated cul-de-sac. First, we show bilateral ureterolysis and ligation of uterine artery at the origin to decrease risk of ureteral injury and for early control of blood supply. We show mobilization of the sigmoid colon starting above the pelvic brim. We then show a technique to perform dissection of the rectum starting at the rectovaginal septum medial to the uterosacral ligaments. The dissection is carried from deep to superficial until the rectosigmoid was completely mobilized. The remainder of hysterectomy and resection of side wall endometriosis was thus completed without any complications. Final pathology was consistent with 18cm endometrioma and uterine leiomyoma. Conclusion The retrograde technique to dissect the obliterated cul de sac in stage IV endometriosis is a safe surgical approach to restore normal anatomy in advanced endometriosis. These steps will help surgeon access correct surgical planes to minimize risk of injury and blood loss.

Laparoscopic Ureterolysis in the Setting of Endometriosis

Study Objective This video presentation will review the medial and lateral approaches to ureter identification and illustrate surgical techniques to perform a laparoscopic ureterolysis in cases of endometriosis and retroperitoneal fibrosis. Design Stepwise demonstration of advanced laparoscopic surgical techniques with narrated video footage. Setting Ureteral identification is crucial in the setting of advanced endometriosis when performing a laparoscopic hysterectomy. Retroperitoneal fibrosis as a result of endometriosis can make ureterolysis challenging. Associated risks can include ureteral transection with improper identification in the retroperitoneum, unrecognized or delayed thermal injury to the ureter due to aggressive electrocautery use or incomplete resection of endometriosis surrounding the ureter. Patients or Participants Two patients with endometriosis requiring ureterolysis who underwent laparoscopic hysterectomy. Interventions Identification of the ureter and laparoscopic ureterolysis can be safely performed in the setting of endometriosis with several key strategies: 1. Use of the medial and lateral approaches to ureter identification, which may be facilitated by the placement of a preoperative ureteral stent when dense retroperitoneal fibrosis is present 2. Minimizing risk of thermal injury by use of directed blunt dissection with the “open and spread” and “hook” techniques 3. Use of reliable anatomic landmarks such as the medial umbilical ligament and development of the paravesical and pararectal spaces to aid in retroperitoneal dissection 4. Meticulous attention to hemostasis to include control of both small vessels in retroperitoneal aerolar tissue and ligation of the uterine artery at the origin to maintain adequate visualization Measurements and Main Results N/A Conclusion In patients with advanced endometriosis, ureterolysis is often necessary given extensive retroperitoneal fibrosis and inherent risk of ureteral injury. An intimate knowledge of anatomic landmarks, directed blunt and sharp dissection techniques, judicious use of cautery and careful hemostasis may allow for safe and effective completion of a laparoscopic ureterolysis in complex cases.

Electroacupuncture on the Scalp over the Motor Cortex Ameliorates Behavioral Deficits Following Neonatal Hypoxia-Ischemia in Rats via the Activation of Neural Stem Cells.

Electroacupuncture (EA) therapy via alternating current stimulation on the scalp over the motor cortex is used for the treatment of brain disorders. Perinatal hypoxia-ischemia (HI), a brain injury in newborns, leads to long-term neurologic complications. Here, we investigated whether EA could promote functional improvements and neurogenesis in a neonatal HI rat model. A neonatal HI rat model was induced by permanent ligation of the left carotid artery in postnatal day 7 pups. EA for neonatal HI rats was performed at 2 Hz (1, 3, or 5 mA; 20 min) from 4–6 weeks after birth. HI rats undergoing EA had improved motor and memory function, with the greatest improvement after 3 mA EA. The corpus callosum was significantly thicker and showed a significant increase in proliferating astrocytes in the 3 mA EA group. We observed proliferating cells and a greater number of newly developed neurons and astrocytes in the subventricular zone and dentate gyrus of the 3 mA EA group than in those of the HI group. These results suggest that EA promotes functional improvements following neonatal HI assault via the proliferation and differentiation of neural stem cells. This effect was the strongest after 3 mA EA, suggesting that this is the optimal treatment dose.

Plasmatic Membrane Expression of Adhesion Molecules in Human Cardiac Progenitor/Stem Cells Might Explain Their Superior Cell Engraftment after Cell Transplantation.

Human bone marrow mesenchymal stem cells (BM-MSCs) and cardiac progenitor/stem cells (CPCs) have been extensively studied as a potential therapeutic treatment for myocardial infarction (MI). Previous reports suggest that lower doses of CPCs are needed to improve cardiac function relative to their bone marrow counterparts. Here, we confirmed this observations and investigated the surface protein expression profile that might explain this effect. Myocardial infarction was performed in nude rats by permanent ligation of the left coronary artery. Cardiac function and infarct size before and after cell transplantation were evaluated by echocardiography and morphometry, respectively. The CPC and BM-MSC receptome were analyzed by proteomic analysis of biotin-labeled surface proteins. Rats transplanted with CPCs showed a greater improvement in cardiac function after MI than those transplanted with BM-MSCs, and this was associated with a smaller infarct size. Analysis of the receptome of CPCs and BM-MSCs showed that gene ontology biological processes and KEGG pathways associated with adhesion mechanisms were upregulated in CPCs compared with BM-MSCs. Moreover, the membrane protein interactome in CPCs showed a strong relationship with biological processes related to cell adhesion whereas the BM-MSCs interactome was more related to immune regulation processes. We conclude that the stronger capacity of CPCs over BM-MSCs to engraft in the infarcted area is likely linked to a more pronounced cell adhesion expression program.

High ligation of the inferior mesenteric artery with nerve-sparing in laparoscopic surgery for advanced colorectal cancer.

High ligation of the inferior mesenteric artery with nerve-sparing in laparoscopic surgery for advanced colorectal cancer.

VP65.05: Obstetrical outcome after B‐lynch sutures and ligation of uterine arteries: a case report

VP65.05: Obstetrical outcome after B‐lynch sutures and ligation of uterine arteries: a case report

Surgical hemostasis for obstetric hemorrhage: experimental and clinical studies

The article presents a review of the literature on the problems of treatment of obstetric bleeding in the light of historical development and modern opportunities. Currently existing options for surgical hemostasis: ligation of pelvic vessels, ligation of internal iliac arteries, embolization of uterine arteries and compression sutures on the uterus are considered from the perspective of experimental work and clinical research. The paper reflects the opinions of domestic and foreign scientists, which were a vector for further study and experiments.

Short- and long-term outcomes of rectal cancer patients with high or improved low ligation of the inferior mesenteric artery

The ligation site of the inferior mesenteric artery (IMA) during laparoscopic radical resection for rectal cancer has been controversial. Consecutive patients (n = 205) with rectal cancer who underwent laparoscopic-assisted low anterior resection from January 2009 to December 2015 were retrospectively analyzed. The patients were divided into high ligation (n = 126) and improved low ligation groups (n = 79). A total of 205 rectal cancer patients underwent laparoscopic assisted anterior resection: 126 patients in the high ligation group and 79 patients in the improved low ligation group. The improved low ligation group was better than the high ligation group in terms of postoperative flatus time and postoperative defecation time. There were no differences between the groups in terms of blood loss, operation time, total number of lymph nodes, anastomotic leakage, postoperative time to first liquid diet and postoperative hospital stay. There were also no differences in 5-year overall survival (OS). Compared to high ligation, the improved low ligation ensures the extent of lymph node dissection, and promotes the early recovery of postoperative gastrointestinal function, but does not increase the operation time, bleeding risk, or anastomotic leakage. A ligation site of the IMA in laparoscopic rectal cancer surgery may not influence oncological outcomes.