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      Vascular relaxation of canine visceral arteries after ischemia by means of supraceliac aortic cross-clamping followed by reperfusion

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          Abstract

          Background

          The supraceliac aortic cross-clamping can be an option to save patients with hipovolemic shock due to abdominal trauma. However, this maneuver is associated with ischemia/reperfusion (I/R) injury strongly related to oxidative stress and reduction of nitric oxide bioavailability. Moreover, several studies demonstrated impairment in relaxation after I/R, but the time course of I/R necessary to induce vascular dysfunction is still controversial. We investigated whether 60 minutes of ischemia followed by 30 minutes of reperfusion do not change the relaxation of visceral arteries nor the plasma and renal levels of malondialdehyde (MDA) and nitrite plus nitrate (NOx).

          Methods

          Male mongrel dogs (n = 27) were randomly allocated in one of the three groups: sham (no clamping, n = 9), ischemia (supraceliac aortic cross-clamping for 60 minutes, n = 9), and I/R (60 minutes of ischemia followed by reperfusion for 30 minutes, n = 9). Relaxation of visceral arteries (celiac trunk, renal and superior mesenteric arteries) was studied in organ chambers. MDA and NOx concentrations were determined using a commercially available kit and an ozone-based chemiluminescence assay, respectively.

          Results

          Both acetylcholine and calcium ionophore caused relaxation in endothelium-intact rings and no statistical differences were observed among the three groups. Sodium nitroprusside promoted relaxation in endothelium-denuded rings, and there were no inter-group statistical differences. Both plasma and renal concentrations of MDA and NOx showed no significant difference among the groups.

          Conclusion

          Supraceliac aortic cross-clamping for 60 minutes alone and followed by 30 minutes of reperfusion did not impair relaxation of canine visceral arteries nor evoke biochemical alterations in plasma or renal tissue.

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          Most cited references26

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          The pathophysiology of aortic cross-clamping and unclamping.

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            The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia-reperfusion.

            The microcirculation undergoes a profound degree of endothelial dysfunction within minutes (i.e., 2.5 to 5 min) following reperfusion of ischaemic vasculature. This has been documented in the coronary and mesenteric microcirculation. The endothelial dysfunction is characterized by a loss in basal and agonist-mediated nitric oxide (NO) produced by the vascular endothelium. The loss of NO results in upregulation of cell adhesion molecules (CAMs) particularly P-selectin 10-20 min following reperfusion. Thus, CAM upregulation renders the endothelium sticky, and a marked degree of leukocyte adherence (particularly neutrophils) occurs 20 min following reperfusion. This enhanced involvement of neutrophils leads to neutrophil infiltration into the underlying tissue (e.g., myocardium) within 2-3 h of reperfusion. The infiltration of neutrophils leads to reperfusion injury (i.e., necrosis) which is significant at 3 h but becomes profound at 4.5 h following reperfusion. Cardiac necrosis can be significantly attenuated by treatment with NO, an organic NO donor, L-arginine, or specific blockers of CAMs given just prior to reperfusion. This approach is a promising one for a variety of types of reperfusion injury.
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              Emergency thoracotomy in thoracic trauma-a review.

              Thoracic trauma is one of the leading causes of death in all age groups and accounts for 25-50% of all traumatic injuries. While the majority of patients with thoracic trauma can be managed conservatively, a small but significant number requires emergency thoracotomy as part of their initial resuscitation. The procedure has been advocated for evacuation of pericardial tamponade, direct control of intrathoracic haemorrhage, control of massive air-embolism, open cardiac massage and cross-clamping of the descending aorta. Emergency thoracotomy can be defined as thoracotomy "occurring either immediately at the site of injury, or in the emergency department or operating room as an integral part of the initial resuscitation process". Following emergency thoracotomy, the overall survival rates for penetrating thoracic trauma are around 9-12% but have been reported to be as high as 38%. The survival rate for blunt trauma is approximately 1-2%. The decision to perform emergency thoracotomy involves careful evaluation of the scientific, ethical, social and economic issues. This article aims to provide a review of the current literature and to outline the pathophysiological features, technical manoeuvres and selective indications for emergency thoracotomy as a component of the initial resuscitation of trauma victims with thoracic injury.
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                Author and article information

                Journal
                Scand J Trauma Resusc Emerg Med
                Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
                BioMed Central
                1757-7241
                2010
                19 July 2010
                : 18
                : 41
                Affiliations
                [1 ]Department of Surgery and Anatomy, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil
                Article
                1757-7241-18-41
                10.1186/1757-7241-18-41
                2913934
                20642850
                c74fa6cb-13f7-41fe-ac0e-c7e7530433ee
                Copyright ©2010 Ciscato et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 May 2010
                : 19 July 2010
                Categories
                Original Research

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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