Atraumatic Microvascular Clamp Research Articles

Evaluation of the effect of enriched hydrogen saline solution on distant organ (lung) damage in skeletal muscle ischemia reperfusion in rats.

Ischemia-reperfusion (IR) injury is a major concern that frequently occurs during vascular surgeries. Hydrogen-rich saline (HRS) solution exhibits antioxidant and anti-inflammatory properties. This study aimed to examine the effects of HRS applied before ischemia in the lungs of rats using a lower extremity IR model. After approval was obtained from the ethics committee, 18 male Wistar albino rats weighing 250-280 g were randomly divided into three groups: control (C), IR and IR-HRS. In the IR and IR-HRS groups, an atraumatic microvascular clamp was used to clamp the infrarenal abdominal aorta, and skeletal muscle ischemia was induced. After 120 min, the clamp was removed, and reperfusion was achieved for 120 min. In the IR-HRS group, HRS was administered intraperitoneally 30 min before the procedure. Lung tissue samples were examined under a light microscope and stained with hematoxylin-eosin (H&E). Malondialdehyde (MDA) levels, total sulfhydryl (SH) levels, and histopathological parameters were evaluated in the tissue samples. MDA and total SH levels were significantly higher in the IR group than in the control group (p < 0.0001 and p = 0.001, respectively). MDA and total SH levels were significantly lower in the IR-HRS group than in the IR group (p < 0.0001 and p = 0.013, respectively). A histopathological examination revealed that neutrophil infiltration/aggregation, alveolar wall thickness, and total lung injury score were significantly higher in the IR group than in the control group (p < 0.0001, p = 0.001, and p < 0.0001, respectively). Similarly, alveolar wall thickness and total lung injury scores were significantly higher in the IR-HRS group than in the control group (p = 0.009 and p = 0.004, respectively). A statistically significant decrease was observed in neutrophil infiltration/aggregation and total lung injury scores in the IR-HRS group compared to those in the IR group (p = 0.023 and p = 0.022, respectively). HRS at a dose of 20 mg/kg, administered intraperitoneally 30 min before ischemia in rats, reduced lipid peroxidation and oxidative stress, while also reducing IR damage in lung histopathology. We believe that HRS administered to rats prior to IR exerts a lung-protective effect.

Assessment of the Effects of Quercetin on Lung Injury After Hind Limb Ischemia Reperfusion in Rats

Background: Quercetin has antioxidant and anti-inflammatory effects. Although there are previous animal experi-ments investigating Quercetin’s effect on ischemia reperfusion (IR) injury in the literature, studies involving effect of lower extremity IR on remote organ are rare.Materials and Methods: 18 male Wistar Albino rats were randomly divided into 3 groups, 6 in each group as; Cont-rol (C), Ischemia-reperfusion (IR), IR-Quercetin, (IR-Q). Their weights were between 200-250 g. 30 minutes before the procedure20 mg/kgQuercetin was administered via intraperitoneal route. In the IR groups, infrarenal abdomi-nal aorta was clamped by an atraumatic microvascular clamp. After 120 minutes of ischemia and reperfusion was achieved for another 120 minutes. When reperfusion period ended, tissue samples were taken from the lungs. Malondialdehyde (MDA) level, superoxide dismutase (SOD) and catalase (CAT) enzyme activity and histopathological parameters were compared.Results: We found the MDA level in the IR group higher than the control group (p&amp;lt;0.0001). Lower MDA level was found in the IR-Q group compared tothe IR group (p=0.012). SOD and CAT enzyme activity in the IR group was notably lower in the control group (p&amp;lt;0.0001, p&amp;lt;0.001, respectively). Higher SOD and CAT enzyme activities were found in the IR-Q group compared to the IR group (p=0.012, p&amp;lt;0.001, respectively). Neutrophil infiltra-tion/aggregation, alveolar wall thickness and total lung injury score were notably higher in IR group than in C group (p=0.001, p=0.002, p&amp;lt;0.0001, respectively). In addition, a statistically significant decrease was observed in the Quercetin treated group in neutrophil infiltration/aggregation, alveolar wall thickness and total lung injury score compared to the IR group (p=0.023, p=0.022, p=0.002, respectively).Conclusions: We determined that intraperitoneally administered Quercetin at a dose of 20 mg/kg30 minutes before ischemia in rats reduces lipid peroxidation, oxidative stress and reduces the damage caused by IR in lung histo-pathology.Study findings suggest that Quercetin has a lung protective effect when administered before IR.

Mir-221, mir-190b, mir-363-3p, mir-200c are involved in rat liver ischaemia-reperfusion injury through oxidative stress, apoptosis and endoplasmic reticulum stress.

In this study, it was aimed to investigate the relationship between expression levels of micro-RNAs, endoplasmic reticulum (ER) stress, apoptosis and oxidative stress markers in hepatic ischaemia-reperfusion (IR) injury. Sixteen rats were randomised into two groups: Sham and IR groups. In the IR group, portal vein and hepatic artery were totally clamped with an atraumatic microvascular clamp and 60minutes later unclamped and finally IR model was accomplished (60minutes ischaemia and 60minutes reperfusion). After sacrification, serum insulin-like growth factor-1 (IGF-1), tumour necrosis factor-α (TNF-α), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue samples were evaluated histopathologically. The expression levels of IR1-alpha, Perk, Catalase, Gpx-1, Caspase-3, Bcl-2 genes and miR-33a, miR-221, miR-190b, miR-363-3p, miR-200c, miR-223, miR-133b were measured by quantitative real-time polymerase chain reaction method. Biochemical parameters of the IR group showed significantly higher changes compared with the Sham group (P<.01). Histological tissue damage was significantly prominent in the IR group. ER stress, oxidative stress and apoptosis gene expression levels were significantly higher in the IR group (P<.01). Expression levels of miR-221, miR-190b, miR-363-3p and miR-200c were increased in the IR group compared with the Sham group. No significant difference was found between the two groups in terms of miR-33a, miR-133b and miR-223 expression levels (P>.05). There is a strong need to enlighten the physiopathological and molecular mechanisms of liver IR injury and to find more specific biomarkers for IR damage, and miR-221, miR-190b, miR-363-3p and miR-200c maybe used as potential biomarkers of hepatic IR injury.

Primary anastomosis in difficult cases of type “C” esophageal atresia: The atraumatic microvascular clamp technique of minimal tension with good outcome

BackgroundSurgical maneuvers for esophageal anastomosis in difficult cases of Gross type “C” esophageal atresia (EA) are challenging. The methods of early primary anastomosis are technically difficult and staged surgeries expose the child to repeated general anesthesia with problems of nursing care. We describe a simple method of partial disconnection of the lower esophagus from the fistula followed by approximation by an atraumatic microvascular clamp. The suitability of this method and its outcomes are discussed. MethodsIt was a prospective observational study that included 32 patients of type “C” EA between January 2014 and December 2016. Babies with birth weight more than 2 kg without cyanotic heart defects and requirement of intensive care were included. An early primary anastomosis using this technique was tried in all. A cervical esophagostomy with feeding gastrostomy was done where it was not possible. Analysis of the gap and post operative outcomes i.e. gastroesophageal reflux (GER), stricture, tracheomalacia, dysmotility, recurrence and survival were analyzed. ResultsThe mean gap between esophageal ends was 4.3 cm. Primary anastomosis was possible in 26 (81.25%). Minor and major leak occurred in 3 (11.54%) and 1 (3.85%) patients respectively. Survival was 84.62% (22/26). All mortalities were early post operative. During mean follow up of 23.73 months (till December 2019), GER decreased from 63.64% (14/22) to 13.64% (3/22), partial stricture was seen in 18.18% (4/22), tracheomalacia in 36.36% (8/22) and dysmotility in 77.27% (17/22). There was no recurrence of fistula. Complications with this method did not show any significant difference as mentioned with other methods. ConclusionThis technique seems to be physiologically suitable as it enables anastomosis with minimal trauma to the esophageal ends. It is easy, reproducible and produces favorable outcomes comparable with other methods for difficult cases of type “C” esophageal atresia (EA).

The Effect of Cerium Oxide on Lung Tissue in Lower Extremity Ischemia Reperfusion Injury in Sevoflurane Administered Rats.

IntroductionWe aimed to investigate the effects of cerium oxide, applied before the sevoflurane anesthesia, on lung tissue in rats with lower extremity ischemia-reperfusion (IR).Materials and MethodsA total of 30 rats were randomly divided into five groups as; control (C), IR, cerium oxide-IR (CO-IR), IR-sevoflurane (IRS), and cerium oxide-IR-sevoflurane (CO-IRS). In the CO-IR group, 30 minutes after the injection of cerium oxide (0.5 mg/kg, intraperitoneal (i.p)), an atraumatic microvascular clamp was placed on the infrarenal abdominal aorta for 120 minutes. Then, the clamp was removed and reperfused for 120 minutes. Sevoflurane was applied in 100% oxygen at a rate of 2.3% at 4 L/min during IR. The blood samples were taken for biochemical analysis and the lung tissue samples were taken for histological analysis.ResultsNeutrophil infiltration/aggregation was significantly higher in the IR group than in the C and CO-IRS groups. The alveolar wall thickness and total lung injury scores were significantly higher in the IR group than in the C, IRS, CO-IR and CO-IRS groups.DiscussionWe determined that the administration of 0.5 mg/kg dose of cerium oxide with sevoflurane reduces the oxidative stress and corrects IR-related damage in lung tissue. Our results show that the administration of cerium oxide before IR and the administration of sevoflurane during IR have a protective effect in rats.

Targeted Parathyroidectomy—Use of the Atraumatic Microvascular Clamp

Targeted Parathyroidectomy—Use of the Atraumatic Microvascular Clamp

Effect of picroside II on hind limb ischemia reperfusion injury in rats

IntroductionMany structural and functional damages are observed in cells and tissues after reperfusion of previously viable ischemic tissues. Acute ischemia reperfusion (I/R) injury of lower extremities occurs especially when a temporary cross-clamp is applied to the abdominal aorta during aortic surgery. Research regarding the treatment of I/R injury has been increasing day-by-day. In this study, we aimed to investigate the effect of picroside II on skeletal muscle of rats experiencing simulated I/R.Materials and methodsTwenty-four male Wistar albino rats weighing between 210 and 300 g were used in this study. Rats were randomly divided into 4 groups of 6 rats each (control, I/R, control + picroside II, and I/R + picroside II). The infrarenal section of the abdominal aorta was occluded with an atraumatic microvascular clamp in I/R group. The clamp was removed after 120 minutes and reperfusion was provided for a further 120 minutes. Picroside II (10 mg kg−1) was administered intraperitoneally to the animals in control + picroside II and I/R + picroside II groups. At the end of the study, skeletal muscle tissue was obtained for the determination of total oxidant status (TOS) and total antioxidant status (TAS) levels. Apoptosis was evaluated by TUNEL experiment.ResultsTOS levels were significantly higher in I/R group than that of control and I/R + picroside II groups (P=0.014, P=0.005, respectively). TAS levels were significantly higher in I/R group than that of control and I/R + picroside II groups (P=0.007 P=0.005, respectively). TUNEL assay revealed that picroside II reduced cell necrosis.ConclusionThe results of this study demonstrated that picroside II plays a critical role to prevent I/R injury. Even though our results were found to be satisfactory, it should be encouraging to those who want to conduct future research on this topic.

Effect of picroside II on erythrocyte deformability and lipid peroxidation in rats subjected to hind limb ischemia reperfusion injury.

BackgroundIschemia reperfusion injury (I/R) in hind limb is a frequent and important clinical phenomenon. Many structural and functional damages are observed in cells and tissues in these kinds of injuries. In this study, we aimed to evaluate the effect of picroside II on lipid peroxidation and erythrocyte deformability during I/R in rats.MethodsRats were randomly divided into four groups – each containing six animals (sham, I/R, sham + picroside II, and I/R + picroside II). The infrarenal section of the abdominal aorta was occluded with an atraumatic microvascular clamp in I/R groups. The clamp was removed after 120 minutes and reperfusion was provided for a further 120 minutes. Picroside II (10 mg·kg−1) was administered intraperitoneally to the animals in the appropriate groups (sham + picroside II, I/R + picroside II groups). All rats were euthanized by intraperitoneal administration of ketamine (100 mg·kg−1) and taking blood from the abdominal aorta. Erythrocytes were extracted from heparinized complete blood samples. Buffer (PT) and then erythrocytes (PE) were passed through the filtration system and the changes in pressure were measured to investigate the role of serum malondialdehyde and nitric oxide (NO) in lipid peroxidation and erythrocyte deformability index.ResultsDeformability index was significantly increased in the I/R group compared to groups sham, sham + picroside-II, and I/R + picroside-II (P<0.0001, P<0.0001, and P=0.007). Malondialdehyde (MDA) and NO levels were evaluated. MDA level and NO activity were also higher in the I/R group than in the other groups. Picroside II treatment before hind limb I/R prevented these changes.ConclusionThese results support that deformability of erythrocytes is decreased in I/R injury and picroside II plays a critical role to prevent these alterations. Further experimental and clinical studies are needed to evaluate and clarify the molecular mechanisms of action and clinical importance of these findings.

Effect of IL-18 binding protein on hepatic ischemia-reperfusion injury induced by infrarenal aortic occlusion.

PurposeSevere local and systemic tissue damage called ischemia/reperfusion (IR) injury occurs during the period of reperfusion. Free oxygen radicals and proinflammatory cytokines are responsible for reperfusion injury. IL-18 binding protein (IL-18BP) is a natural inhibitor of IL-18. The balance between IL-18 and IL-18BP has an important role in the inflammatory setting. The present study aimed to investigate whether IL-18BP had a protective role in remote organ hepatic IR injury.MethodsWistar-Albino rats were divided into three groups that contained seven rats. Group I (sham): Laparotomy and infrarenal abdominal aorta (AA) dissection were done but no clamping was done. Group II (I/R): The infrarenal AA was clamped by atraumatic microvascular clamp for 30 minutes and then was exposed to 90 minutes of reperfusion. Group III (IR + IL-18BP): 75 µg/kg of IL-18BP in 0.9% saline (1 mL) was administered 30 minutes before infrarenal AA dissection and clamping; 30 minutes of ischemia was applied and then was exposed to 90 minutes of reperfusion.ResultsSerum AST, ALT, and LDH levels were remarkably higher in IR group and returned to normal levels in treatment group. The proinflammatory cytokine levels had decreased in treatment group, and was statistically significant compared with the IR group. Serum levels of total oxidant status and oxidative stress index decreased and levels of total antioxidant status increased by IL-18BP.ConclusionThis study suggested that IL-18BP has antioxidant, anti-inflammatory and hepatoprotective effects in cases of IR with infrarenal AA induced liver oxidative damage.

The investigation of the effect of endothelial damage of rat aorta occlusion with microvascular clamp: an experimental study

Background: In this study, we investigated the potential effect of the endothelial damage by occluding the rat aorta through atraumatic microvascular clamp application. Methods: Fifteen 3-4 month old Wistar Albino type female rats weighted 300-400 g were anesthetized and the abdominal aorta was explored with median laparotomy. Distal segment of the abdominal aorta was clamped with a microvascular clamp. After almost 10 minutes, occluded segment with microvascular clamp was excised and defined as the clamp group. The incision lengthened proximally and thoracic aorta was explored. The samples of the thoracic aorta segment were defined as the control group. These two sampling groups were prepared for scanning electron microscopy. The analysis is performed by a single blind method and results were analyzed statistically. Results: No endothelial damage was observed in the samples of the control group. In microvascular clamp group, there was type 1 damage in 10 samples (66.7%), type 2 damage in four samples (26.6%) and type 3 damage in one sample (6.6%). The difference between microvascular clamp and control group was statistically significant in terms of endothelial damage (p

The antioxidant effect of melatonin in lung injury after aortic occlusion?reperfusion

Acute aortic occlusion with subsequent ischemia-reperfusion of the lower extremities is well known to predispose to lung injury. Melatonin (MEL), a pineal hormone, is a free radical scavenger and an antioxidant. The purpose of this study was to assess the putative protective role of MEL in lung ischemia-reperfusion injury induced by aortic occlusion-reperfusion. Thirty-two rats were randomly allocated to four groups as follows: SHAM (Sham Laparotomy), SHAM+MEL, Aortic Ischemia Reperfusion (AIR) and AIR+MEL. Twenty mg/kg live weight MEL was given intraperitoneally 1 h prior to the experiment. An atraumatic microvascular clamp was placed across the infrarenal abdominal aorta (IAA) just after its origin from the aorta for 30 min. The microvascular clamp on IAA was removed and reperfused for 12 h. Lung tissues were assessed for malondialdehyde (MDA) level and myeloperoxidase (MPO) activity. MDA level and MPO activity, indicating the extent of lipid peroxidation and neutrophil infiltration of lung, respectively, significantly increased in AIR group when compared to SHAM and SHAM+MEL groups (P<0.05). Treating rat with MEL significantly decreased MDA levels as well as MPO activity in AIR+MEL group when compared to AIR group (P<0.05). In this study, exogenously administered MEL reduced lung injury after aortic occlusion reperfusion.

SELENIUM PRETREATMENT PREVENTS BACTERIAL TRANSLOCATION IN RAT INTESTINAL ISCHEMIA/REPERFUSION MODEL

Protective role of selenium against free radical damage was first demonstrated in the heart and this effect was further questioned in other systems. In the present study, the effects of exogenously administered selenium on intestinal fine morphology, lipid peroxidation, and bacterial translocation (BT) in experimental intestinal ischemia/reperfusion (I/R) model were examined. Thirty-two male Wistar rats weighing 250–300 g were randomized into four groups. Sham group ( n=8) underwent laparotomy only. In the I/R group ( n=8), laparotomy was performed and the superior mesenteric artery was occluded using an atraumatic microvascular clamp for 30 min. In corresponding selenium-treated groups ( n=8 each), sodium selenate was given 0.2 mg kg −1 day −1 intraperitoneally (i.p.) for 3 consecutive days, prior to surgery for either laparotomy only or with I/R. Twenty-four hours later, tissue samples from liver, spleen, and mesenteric lymph nodes were obtained under sterile conditions for microbiological analysis and further evaluation of I/R-induced intestinal injury. Ileum samples were fixed in 10% formaldehyde for histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, and liver was significantly higher than other groups ( P<0.05). Selenium supplementation prevented I/R-induced BT and significantly reduced the I/R-induced intestinal injury ( P<0.05). Tissue MDA levels from the ileum specimens of selenium-treated rats were significantly lower than that of the I/R group ( P<0.05). Our results provide evidence that the relationship between BT and lipid peroxidation in intestinal tissue is crucial. Selenium pretreatment reduces lipid peroxidation which contributes to the maintenance of intestinal mucosal integrity.