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K.a. Balasubramanian - One of the best experts on this subject based on the ideXlab platform.
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Surgical Stress-induced alterations in retinoid metabolism in the small intestine: role of oxygen free radicals
Archives of biochemistry and biophysics, 2005Co-Authors: Ramamoorthy Prabhu, Simmy Thomas, K.a. BalasubramanianAbstract:Oxidative Stress in the small intestine can result in altered cell proliferation, migration, and differentiation of villus-crypt cells. Retinoid metabolism is recognized as an important mediator of cellular differentiation in the intestine. This study examined the effect of oxidative Stress in retinoid metabolism in a Surgical Stress model. Surgical Stress was performed by handling the intestine as done during laparotomy. Villus-crypt cells were isolated at different time periods and various retinoid concentrations in the cell homogenate and the retinoic acid forming enzymes were quantitated using HPLC. Surgical Stress resulted in altered retinoid levels in various cell populations in the small intestine at 1 and 12 h. The activity of alkaline phosphatase and retinal oxidase was also altered at these time points and all these changes were prevented by inhibiting superoxide generation using xanthine oxidase inhibitor, allopurinol. These studies suggest that alterations seen in enterocytes during Surgical Stress may be mediated by changes in retinoid metabolism.
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Intestinal Mitochondrial Dysfunction in Surgical Stress
The Journal of surgical research, 2001Co-Authors: Anup Ramachandran, Susama Patra, K.a. BalasubramanianAbstract:Abstract Background. Surgical Stress is associated with altered intestinal function. Our earlier study using a rat model indicated that oxidative Stress plays an important role in this process. Since mitochondria are crucial to cellular function and survival and are both a target as well as a source of reactive oxygen species, the present study looks at the changes in enterocyte mitochondria during Surgical Stress. Methods. Surgical Stress was induced by opening the abdominal wall and handling the intestine as done during laparotomy. Mitochondria were prepared from the isolated enterocytes at different time periods after Surgical Stress. The effect of Surgical Stress on enterocyte mitochondrial ultrastructure, respiration, anti-oxidant enzyme activity, thiol redox status, calcium flux, permeability, and matrix enzymes was then studied. Results. Surgical Stress resulted in alterations in mitochondrial respiration and thiol redox status. It was also associated with altered mitochondrial matrix enzyme activity, decreased superoxide dismutase activity, induction of mitochondrial permeability transition, and swelling, as well as impairment of mitochondrial calcium flux. These alterations were seen at a maximum of 60 min following Surgical Stress and were reversed by 24 h. Conclusions. Laparotomy and mild intestinal handling itself results in enterocyte mitochondrial damage. Since mitochondria are important cellular organelles, this damage can probably lead to compromised intestinal function.
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Nitric oxide prevents intestinal mitochondrial dysfunction induced by Surgical Stress.
The British journal of surgery, 2001Co-Authors: S. Thomas, R. Anup, P. Susama, K.a. BalasubramanianAbstract:Background: The intestine is highly susceptible to free radical-induced damage and earlier work has shown that Surgical Stress induces generation of oxygen free radicals in enterocytes, resulting in intestinal damage along with changes in mitochondrial structure and function. Nitric oxide is an important mediator of gastrointestinal function and this study looked at the effect of nitric oxide on Surgical Stress-induced intestinal mitochondrial alterations. Methods: Controls and rats pretreated with the nitric oxide donor L-arginine were subjected to Surgical Stress by opening the abdominal wall and handling the intestine. Enterocytes were isolated, mitochondria prepared and the protection offered by L-arginine against damage due to Surgical Stress was determined. Protection to structural as well as functional aspects of mitochondria was examined. Results: Mild handling of the intestine affected the enterocyte mitochondrial structure as assessed by lipid composition and electron microscopy. Mitochondria were also functionally impaired with altered calcium flux and decreased respiratory control ratio. Pretreatment with the nitric oxide synthase substrate L-arginine prevented these damaging effects of Surgical Stress. Protection with arginine was abolished by the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester, indicating the role of nitric oxide. Conclusion: Surgical Stress in the small intestine can affect enterocyte mitochondrial structure and function. These damaging effects can be prevented by nitric oxide, an important modulator of cellular function.
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Role of xanthine oxidase in small bowel mucosal dysfunction after Surgical Stress.
The British journal of surgery, 2000Co-Authors: R. Anup, P. Susama, K.a. BalasubramanianAbstract:Background: The small intestine is highly susceptible to Surgical Stress even at remote locations. An earlier study using a rat model indicated that oxidative Stress plays an important role in this process. The enzyme xanthine oxidase is an important source of free radicals in the small intestine. The role of this enzyme in intestinal damage after Surgical Stress was examined. Methods: Rats pretreated with xanthine oxidase inhibitors were subjected to Surgical Stress by opening the abdomen and handling the intestine, as done during laparotomy. Enterocytes at various stages of differentiation were isolated and the protection offered by xanthine oxidase inhibitors against damage due to Surgical Stress was determined and compared with normal controls. Protection against ultrastructural changes to the mucosa, as well as mitochondrial function was examined. Results: Surgical Stress affected both the villus as well as crypt cells, causing increased superoxide generation, accompanied by increased activity of xanthine oxidase. Xanthine oxidase inhibitors ameliorated the increased superoxide generation, and protected against mitochondrial damage and ultrastructural changes in the intestine. Conclusion: Surgical Stress affects both the villus and crypt cell populations in the small intestine. The enzyme xanthine oxidase maybe an important mediator of Surgical Stress in the intestine.
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Protease Activation during Surgical Stress in the Rat Small Intestine
The Journal of surgical research, 2000Co-Authors: Anup Ramachandran, K.a. BalasubramanianAbstract:Abstract Background. Surgical Stress affects intestinal permeability and our earlier study using a rat model indicated that oxidative Stress plays an important role in this process. Proteases are important mediators of cellular damage and are known to be activated in oxidative Stress. This study looked at protease activity in enterocytes after Surgical Stress. Methods. Surgical Stress was induced by opening the abdominal wall and handling the intestine as done during laparotomy, in normal and xanthine oxidase-deficient rats. Enterocytes at various stages of differentiation were isolated and protease activity and protection offered by xanthine oxidase inhibitors were determined. Mitochondria and cytosol were prepared from total isolated enterocytes at different periods after Surgical Stress and protease activation was studied. Results. Surgical Stress induced activation of proteases in both the villus and crypt cells. Protease activation is seen in both mitochondria and cytosol, and similar to the other alterations in mucosal cells, protease activation was maximum 60 min after Stress, returning to normal by 24 h. Thiol compounds modulate protease activity in both mitochondria and cytosol and the activation is not seen in xanthine oxidase-deficient animals. Conclusions. Surgical Stress induces activation of proteases in villus and crypt cells of the small intestine. Both mitochondrial and cytosolic proteases are activated and free radicals generated by xanthine oxidase may mediate protease activation after Surgical Stress in the intestine.
R. Anup - One of the best experts on this subject based on the ideXlab platform.
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Nitric oxide prevents intestinal mitochondrial dysfunction induced by Surgical Stress.
The British journal of surgery, 2001Co-Authors: S. Thomas, R. Anup, P. Susama, K.a. BalasubramanianAbstract:Background: The intestine is highly susceptible to free radical-induced damage and earlier work has shown that Surgical Stress induces generation of oxygen free radicals in enterocytes, resulting in intestinal damage along with changes in mitochondrial structure and function. Nitric oxide is an important mediator of gastrointestinal function and this study looked at the effect of nitric oxide on Surgical Stress-induced intestinal mitochondrial alterations. Methods: Controls and rats pretreated with the nitric oxide donor L-arginine were subjected to Surgical Stress by opening the abdominal wall and handling the intestine. Enterocytes were isolated, mitochondria prepared and the protection offered by L-arginine against damage due to Surgical Stress was determined. Protection to structural as well as functional aspects of mitochondria was examined. Results: Mild handling of the intestine affected the enterocyte mitochondrial structure as assessed by lipid composition and electron microscopy. Mitochondria were also functionally impaired with altered calcium flux and decreased respiratory control ratio. Pretreatment with the nitric oxide synthase substrate L-arginine prevented these damaging effects of Surgical Stress. Protection with arginine was abolished by the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester, indicating the role of nitric oxide. Conclusion: Surgical Stress in the small intestine can affect enterocyte mitochondrial structure and function. These damaging effects can be prevented by nitric oxide, an important modulator of cellular function.
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Role of xanthine oxidase in small bowel mucosal dysfunction after Surgical Stress.
The British journal of surgery, 2000Co-Authors: R. Anup, P. Susama, K.a. BalasubramanianAbstract:Background: The small intestine is highly susceptible to Surgical Stress even at remote locations. An earlier study using a rat model indicated that oxidative Stress plays an important role in this process. The enzyme xanthine oxidase is an important source of free radicals in the small intestine. The role of this enzyme in intestinal damage after Surgical Stress was examined. Methods: Rats pretreated with xanthine oxidase inhibitors were subjected to Surgical Stress by opening the abdomen and handling the intestine, as done during laparotomy. Enterocytes at various stages of differentiation were isolated and the protection offered by xanthine oxidase inhibitors against damage due to Surgical Stress was determined and compared with normal controls. Protection against ultrastructural changes to the mucosa, as well as mitochondrial function was examined. Results: Surgical Stress affected both the villus as well as crypt cells, causing increased superoxide generation, accompanied by increased activity of xanthine oxidase. Xanthine oxidase inhibitors ameliorated the increased superoxide generation, and protected against mitochondrial damage and ultrastructural changes in the intestine. Conclusion: Surgical Stress affects both the villus and crypt cell populations in the small intestine. The enzyme xanthine oxidase maybe an important mediator of Surgical Stress in the intestine.
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Surgical Stress and the gastrointestinal tract
The Journal of surgical research, 2000Co-Authors: R. Anup, Kunisserry A BalasubramanianAbstract:Surgery on any part of the body results in a wide spectrum of alterations in normal body homeostasis. The gastrointestinal tract is extremely sensitive to Surgical Stress, even at remote locations. It is now evident that the G.I. tract also plays an important role in development of postoperative complications, such as the systemic immune response syndrome and multiple organ failure syndrome. The amount of information available on the cellular and subcellular changes occurring in the gastrointestinal tract after Surgical Stress is scant. These changes are important since they would act as initiators of tissue damage seen at a later stage, which in turn lead to postoperative complications. This review looks at the information available on the effect of Surgical Stress on the small intestine, the role of oxygen free radicals in this process, and the changes occurring at the cellular level.
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Surgical Stress Induces Phospholipid Degradation in the Intestinal Brush Border Membrane
The Journal of surgical research, 2000Co-Authors: Ramamoorthy Prabhu, R. Anup, Kunissery A. BalasubramanianAbstract:Background. Surgical Stress can lead to translocation of bacteria from the intestine into the systemic circulation. The intestinal brush border membrane (BBM) plays an important role in defense against such invasion by luminal bacteria and endotoxin. Our earlier work has shown the development of oxidative Stress in the intestine after Surgical Stress and since the BBM is sensitive to free radical attack, this study examined the effect of Surgical Stress on the structure and function of intestinal BBM. Methods. Intestinal BBM were isolated from control and after Surgical Stress and compared for structural and functional alterations. Surgical Stress was also carried out following pretreatment with the xanthine oxidase inhibitor allopurinol or the nitric oxide donor l-arginine, to study the protection offered by these compounds. Results. Surgical Stress affected intestinal BBM structure as well as function. A decrease in alkaline phosphatase activity and α-tocopherol content, accompanied by an increase in lipid peroxidation, was seen. Surgical Stress induced phospholipid degradation with generation of arachidonic acid. Functional impairment with a decrease in glucose transport ability was also seen. These changes are prevented by inhibition of xanthine oxidase by allopurinol pretreatment but not by NO. Conclusion. Surgical Stress in the small intestine causes structural and functional alterations in the BBM through oxidative Stress. This damage could affect gut barrier integrity and generation of arachidonic acid might mediate distal organ dysfunction.
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Surgical Stress and the small intestine: Role of oxygen free radicals
Surgery, 1999Co-Authors: R. Anup, V. Aparna, Anna B. Pulimood, K.a. BalasubramanianAbstract:Abstract Background: Any Surgical procedure can be associated with altered intestinal function. The mechanism involved in these changes at the cellular level during Surgical Stress has not been worked out. This study looked at the biochemical and functional alterations, along with ultrastructural changes, in the intestine during Surgical Stress in a simple rat model. Methods: Surgical Stress was induced by opening the abdominal wall and handling the intestine as during laparotomy. The effect of oxidative Stress on the enterocyte and altered intestinal permeability as well as the ultrastructural changes to the mucosa were studied. Results: Surgical Stress results in oxidative Stress on enterocytes, as evidenced by increased xanthine oxidase and decreased catalase activity along with altered thiol redox status. This was associated with increased intestinal permeability and widened intercellular spaces. These changes were prominent at 60 minutes after laparotomy and returned to normal by 24 hours. Conclusions: Mild intestinal handling is capable of inducing oxidative Stress in enterocytes; this could be one of the mechanisms by which intestinal mucosal alterations occur during Surgical Stress. (Surgery 1999;125:560-9.)
Alan David Kaye - One of the best experts on this subject based on the ideXlab platform.
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Metabolic and the Surgical Stress Response Considerations to Improve Postoperative Recovery
Current Pain and Headache Reports, 2019Co-Authors: Erik M. Helander, Michael P. Webb, Bethany Menard, Amit Prabhakar, John Helmstetter, Elyse M. Cornett, Richard D. Urman, Viet H. Nguyen, Alan David KayeAbstract:Purpose of Review Enhanced recovery pathways are a multimodal, multidisciplinary approach to patient care that aims to reduce the Surgical Stress response and maintain organ function resulting in faster recovery and improved outcomes. Recent Findings A PubMed literature search was performed for articles that included the terms of metabolic Surgical Stress response considerations to improve postoperative recovery. The Surgical Stress response occurs due to direct and indirect injuries during surgery. Direct Surgical injury can result from the dissection, retraction, resection, and/or manipulation of tissues, while indirect injury is secondary to events including hypotension, blood loss, and microvascular changes. Greater degrees of tissue injury will lead to higher levels of inflammatory mediator and cytokine release, which ultimately drives immunologic, metabolic, and hormonal processes in the body resulting in the Stress response. These processes lead to altered glucose metabolism, protein catabolism, and hormonal dysregulation among other things, all which can impede recovery and increase morbidity. Fluid therapy has a direct effect on intravascular volume and cardiac output with a resultant effect on oxygen and nutrient delivery, so a balance must be maintained without excessively loading the patient with water and salt. All in all, attenuation of the Surgical Stress response and maintaining organ and thus whole-body homeostasis through enhanced recovery protocols can speed recovery and reduce complications. Summary The present investigation summarizes the clinical application of enhanced recovery pathways, and we will highlight the key elements that characterize the metabolic Surgical Stress response and improved postoperative recovery.
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Metabolic and the Surgical Stress Response Considerations to Improve Postoperative Recovery.
Current pain and headache reports, 2019Co-Authors: Erik M. Helander, Michael P. Webb, Amit Prabhakar, John Helmstetter, Elyse M. Cornett, Richard D. Urman, Bethany L. Menard, Viet Nguyen, Alan David KayeAbstract:Purpose of Review Enhanced recovery pathways are a multimodal, multidisciplinary approach to patient care that aims to reduce the Surgical Stress response and maintain organ function resulting in faster recovery and improved outcomes.
Thomas Ledowski - One of the best experts on this subject based on the ideXlab platform.
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monitoring of intra operative nociception skin conductance and Surgical Stress index versus Stress hormone plasma levels
Anaesthesia, 2010Co-Authors: Thomas Ledowski, Elaine M Pascoe, B Ang, T Schmarbeck, Michael W Clarke, C Fuller, Vimal KapoorAbstract:'Surgical Stress Index' and the 'Number of Fluctuations in Skin Conductance.s⁻¹, use different methods to analyse sympathetic tone and so provide an estimate of peri-operative analgesia. The aim of our study was to investigate the relationship between these methods and Stress hormone plasma levels. In 20 patients scheduled for elective surgery, values of the two methods, mean arterial blood pressure, heart rate and blood samples (to measure plasma levels of adrenaline, noradrenaline, adrenocorticotrophic hormone and cortisol) were obtained at five time points. Changes in Surgical Stress Index and the Number of Fluctuations in Skin Conductance.s⁻¹ only partially reflected changes in plasma noradrenaline levels. Surgical Stress Index, heart rate and blood pressure, but not the 'Number of Fluctuations in Skin Conductance.s⁻¹ changed in response to changes in depth of analgesia by showing significant differences between before and after a bolus of fentanyl. However, the overall predictive ability of both methods was poor.
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monitoring of sympathetic tone to assess postoperative pain skin conductance vs Surgical Stress index
Anaesthesia, 2009Co-Authors: Thomas Ledowski, B Ang, T Schmarbeck, J RhodesAbstract:Summary The number of fluctuations in skin conductance per second has been described as a potential tool for monitoring postoperative pain. More recently, the Surgical Stress index has shown promising correlations with intra-operative painful stimuli. We compared both methods for their ability to assess postoperative pain, in 100 postoperative patients who were also asked to quantify their level of pain at different time points in the recovery room. The number of fluctuations per second and Surgical Stress index were significantly different between pain scoring ≤ 5/10 and > 5/10 on a numeric rating scale (mean (SE) number of fluctuations per second 0.12 (0.02) vs 0.21 (0.03), respectively; p = 0.017, and Surgical Stress index 57 (1.4) vs 64 (1.9) points, respectively; p = 0.001). Both number of fluctuations in skin conductance per second and Surgical Stress index identified timepoints with moderate to severe pain with only moderate sensitivity and specificity.
Erik M. Helander - One of the best experts on this subject based on the ideXlab platform.
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Metabolic and the Surgical Stress Response Considerations to Improve Postoperative Recovery
Current Pain and Headache Reports, 2019Co-Authors: Erik M. Helander, Michael P. Webb, Bethany Menard, Amit Prabhakar, John Helmstetter, Elyse M. Cornett, Richard D. Urman, Viet H. Nguyen, Alan David KayeAbstract:Purpose of Review Enhanced recovery pathways are a multimodal, multidisciplinary approach to patient care that aims to reduce the Surgical Stress response and maintain organ function resulting in faster recovery and improved outcomes. Recent Findings A PubMed literature search was performed for articles that included the terms of metabolic Surgical Stress response considerations to improve postoperative recovery. The Surgical Stress response occurs due to direct and indirect injuries during surgery. Direct Surgical injury can result from the dissection, retraction, resection, and/or manipulation of tissues, while indirect injury is secondary to events including hypotension, blood loss, and microvascular changes. Greater degrees of tissue injury will lead to higher levels of inflammatory mediator and cytokine release, which ultimately drives immunologic, metabolic, and hormonal processes in the body resulting in the Stress response. These processes lead to altered glucose metabolism, protein catabolism, and hormonal dysregulation among other things, all which can impede recovery and increase morbidity. Fluid therapy has a direct effect on intravascular volume and cardiac output with a resultant effect on oxygen and nutrient delivery, so a balance must be maintained without excessively loading the patient with water and salt. All in all, attenuation of the Surgical Stress response and maintaining organ and thus whole-body homeostasis through enhanced recovery protocols can speed recovery and reduce complications. Summary The present investigation summarizes the clinical application of enhanced recovery pathways, and we will highlight the key elements that characterize the metabolic Surgical Stress response and improved postoperative recovery.
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Metabolic and the Surgical Stress Response Considerations to Improve Postoperative Recovery.
Current pain and headache reports, 2019Co-Authors: Erik M. Helander, Michael P. Webb, Amit Prabhakar, John Helmstetter, Elyse M. Cornett, Richard D. Urman, Bethany L. Menard, Viet Nguyen, Alan David KayeAbstract:Purpose of Review Enhanced recovery pathways are a multimodal, multidisciplinary approach to patient care that aims to reduce the Surgical Stress response and maintain organ function resulting in faster recovery and improved outcomes.
