Comparison of Clamping Modalities in a Rabbit Model of Normothermic Renal Ischemia (original) (raw)
Related papers
Journal of Endourology, 2012
Purpose: To evaluate glomerular injury in the rat model during renal warm ischemia (WI), comparing artery and vein (AV) clamping with artery only (AO) clamping. Materials and Methods: Twenty-four adult male rats underwent 60 minutes of renal WI in the left kidney. The animals were divided into three groups: AV clamping, AO clamping, and Sham surgery. After 30 days, the animals were euthanized, and both kidneys were processed for paraffin embedding and stained with hematoxylin and eosin. Glomerular volume density (Vv[glom]), mean glomerular volume (MGV), and number of glomeruli per mm 3 (Nv[glom]) were evaluated in the renal cortex. Results: The Vv[glom] was reduced in the left kidney (ischemic) when compared with the right kidney in both AV and AO groups by 11.1% and 35.4%, respectively; however, the difference was significant only in the AV group. The Nv[glom] was reduced in the left kidney when compared with the right kidney in both AV and AO groups by 11.6% and 31.4%, respectively; nevertheless, the difference was significant only in the AV group. The MGV of left and right kidneys was the same in both Sham and AO groups and was diminished by 6.7% in the AV group-not significant. Conclusion: AV clamping causes a significant decrease in the number of glomeruli in the rat model, while AO clamping reduces the glomerular number, but not significantly. To minimize renal injury, AO clamping may be preferred over AV clamping when WI is necessary in patients with previously compromised renal function. Abbreviations Used AO ¼ artery only AV ¼ artery and vein MGV ¼ mean glomerular volume Nv[glom] ¼ number of glomeruli per mm3 LPN ¼ laparoscopic partial nephrectomy Vv[glom] ¼ glomerular volume density WI ¼ warm ischemia RENAL ARTERY CLAMPING REDUCES GLOMERULI IN RATS 1339 View publication stats View publication stats
Panminerva medica
The contraction/relaxation responses of thoracic aortal rings clamped with two clamping pressures to potassium chloride (KC1), noradrenaline and carbachol were studied using a scanning electron microscope (SEM) to ascertain endothelial lacerations. Clamp A had the tip pressure PA = 0.60 N/ram 2 and clamp B PB=5.16 N/mm 2. In 15 Wistar albino rats, weighing 328 _+ 19 g (mean _+ SD), the thoracic aorta was occluded for 15 rain and then three vascular rings (2 mm wide) were excised. The proximal unclamped ring served as a control. The aorta diameter was calculated from the circumference of distal rings 1.61 +_0.01 mm (n= 15, dmin = 1.51 mm, dm~×= 1.70 ram). The rings were challenged with cumulative additions of KC1 (10-80 mmol/1) to measure the contraction. Then cumulative relaxation on the administration of carbachol (0.01-100 gmol/1) as a response to noradrenaline precontraction (0.1 gmol/1) was determined. A significant loss (P < 0.05) of vascular relaxation in all clamped rings (clamped with Pa and PB clamping pressures) was seen. No significant differences (P > 0.05) were observed for contraction between clamped and control rings clamped with clamp A, however the rings clamped with clamp B showed significantly reduction of contraction (P< 0.05). No significant differences were seen from control rings between groups A and B (P>0.05), as well as from clamped rings between groups A and B (P > 0.05) for both the contraction and relaxation parts of the experiments. With SEM, great endothelial lacerations with complete disruption of the endothelial layer in the rings clamped with the clamp B were seen, but no disruption in rings clamped with clamp A. Therefore endothelial vascular layers are much more susceptible to pressure injuries than was previously believed. The clamped vessel wall injuries, particularly in endothelial layers, depend on the momentary peak clamping pressure (MPCP) as well as on the lower stationary clamping pressure (SCP). [Eur J Cardio-thorac Surg (1996) 10: 684-689]
Loss of endothelium-mediated vascular relaxation as a response to various clamping pressures
European Journal of Cardio-Thoracic Surgery, 1996
The contraction/relaxation responses of thoracic aortal rings clamped with two clamping pressures to potassium chloride (KC1), noradrenaline and carbachol were studied using a scanning electron microscope (SEM) to ascertain endothelial lacerations. Clamp A had the tip pressure PA = 0.60 N/ram 2 and clamp B PB=5.16 N/mm 2. In 15 Wistar albino rats, weighing 328 _+ 19 g (mean _+ SD), the thoracic aorta was occluded for 15 rain and then three vascular rings (2 mm wide) were excised. The proximal unclamped ring served as a control. The aorta diameter was calculated from the circumference of distal rings 1.61 +_0.01 mm (n= 15, dmin = 1.51 mm, dm~×= 1.70 ram). The rings were challenged with cumulative additions of KC1 (10-80 mmol/1) to measure the contraction. Then cumulative relaxation on the administration of carbachol (0.01-100 gmol/1) as a response to noradrenaline precontraction (0.1 gmol/1) was determined. A significant loss (P < 0.05) of vascular relaxation in all clamped rings (clamped with Pa and PB clamping pressures) was seen. No significant differences (P > 0.05) were observed for contraction between clamped and control rings clamped with clamp A, however the rings clamped with clamp B showed significantly reduction of contraction (P< 0.05). No significant differences were seen from control rings between groups A and B (P>0.05), as well as from clamped rings between groups A and B (P > 0.05) for both the contraction and relaxation parts of the experiments. With SEM, great endothelial lacerations with complete disruption of the endothelial layer in the rings clamped with the clamp B were seen, but no disruption in rings clamped with clamp A. Therefore endothelial vascular layers are much more susceptible to pressure injuries than was previously believed. The clamped vessel wall injuries, particularly in endothelial layers, depend on the momentary peak clamping pressure (MPCP) as well as on the lower stationary clamping pressure (SCP). [Eur J Cardio-thorac Surg (1996) 10: 684-689]
Surgery, 2008
Background. Arterial inflow occlusion is a well-known mechanism of renal injury during major vascular surgery. In contrast, renal injury from venous outflow obstruction is poorly understood. The goal of this study was to examine the injury pattern of renal venous outflow obstruction, compare this with the traditional model of arterial occlusion, and examine possible mechanisms. Methods. Male Fisher rats were used for the renal warm ischemia model. Twenty-five minutes of renal ischemia was induced by selectively occluding either the renal artery or vein. After 24 h of reperfusion, whole blood and kidney tissue were collected for further analysis. Results. Serum creatinine (SCr) concentrations taken 24 h after reperfusion were significantly greater in the venous occlusion group (V) when compared to the arterial group (A). While histology did not demonstrate significant differences in extent of necrosis between both groups, a stronger inflammatory response resulted from venous occlusion. Specifically, significantly greater MCP-1 mRNA and significantly greater MCP-1, TNF-a, and HO-1 protein levels were found in the venous group, while no differences in MIP-2, ICAM-1, and VCAM-1 mRNA expression existed between A and V. Further analysis demonstrated presence of increased cleaved caspase-3 protein in the artery group than in the venous group. Conclusions. Venous renal outflow obstruction results in more severe functional renal injury when compared to arterial inflow occlusion. Macrophage activation and neutrophilic infiltration appear to be exaggerated during venous occlusion. (Surgery
International braz j urol
Purpose: This study aimed to study morphological and renal structural changes in relation to different ischemic times and types of renal vascular pedicle clamping. Methods: Sixteen pigs were divided into two groups (n = 8): Group AV -unilateral clamping of the renal artery and vein and Group A -unilateral clamping of the renal artery only, both with the contralateral kidney used as control. Serial biopsies were performed at 0, 10, 20, 30, 40, 50, 60, 70, 80, and 90 minutes after clamping. Results: there is a correlation between the occurrence of renal damage as a function of time (p <0.001), with a higher frequency of Group A lesions for cellular alterations (vascular congestion and edema, interstitial infl ammatory infi ltrate, interstitial hemorrhage and cell degeneration), with the exception of in the formation of pigmented cylinders that were evidenced only in the AV Group. Conclusion: the number of lesions derived from ischemia is associated with the duration of the insult, there is a signifi cant difference between the types of clamping, and the AV Group presented a lower frequency of injuries than Group A. The safety time found for Group A was 10 minutes and for Group AV 20 minutes.
Glomerular loss after arteriovenous and arterial clamping for renal warm ischemia in a swine model
Acta Cirurgica Brasileira, 2016
To evaluate the glomerular loss after arteriovenous or arterial warm ischemia in a swine model. Twenty four pigs were divided into Group Sham (submitted to all surgical steps except the renal ischemia), Group AV (submitted to 30 minutes of warm ischemia by arteriovenous clamping of left kidney vessels), and Group A (submitted to 30 minutes of ischemia by arterial clamping). Right kidneys were used as controls. Weigh, volume, cortical volume, glomerular volumetric density (Vv[Glom]), volume-weighted glomerular volume (VWGV), and the total number of glomeruli were measured for each organ. Group AV showed a 24.5% reduction in its left kidney Vv[Glom] and a 25.4% reduction in the VWGV, when compared to the right kidney. Reductions were also observed when compared to kidneys of sham group. There was a reduction of 19.2% in the total number of glomeruli in AV kidneys. No difference was observed in any parameters analyzed on the left kidneys from group A. Renal warm ischemia of 30 minutes ...
Journal of Endourology, 2009
Introduction: Laparoscopic partial nephrectomy has emerged as a standard of care for small renal masses. Nevertheless, there remains concern over the potential for irreversible insult to the kidney as a result of exposure to warm ischemia. We aim to investigate the utility of selective segmental arterial clamping as a means to reduce the potential for ischemic damage to a solitary kidney during laparoscopic partial nephrectomy utilizing a porcine model. Materials and Methods: A total of 20 domestic swine were randomized into four equal groups. Each subject underwent laparoscopic radical nephrectomy to create the condition of a solitary kidney. On the contralateral side, a laparoscopic lower pole partial nephrectomy was performed, employing either selective or nonselective vascular clamping for either 60 or 90 minutes. Postoperatively, clinical status and serial serum studies were closely monitored for 1 week. Results: There were no intraoperative complications. The 90-minute nonselective clamping produced devastating effects, resulting in rapid deterioration into florid renal failure within 72 hours. The 60-minute nonselective clamping group experienced modest but significant rises in both blood urea nitrogen and creatinine. Both 60-and 90-minute selective clamping groups performed well, with no significant rises in creatinine over a 7-day period, and no instances of renal failure. Conclusions: Selective arterial clamping is a safe and feasible means of vascular control during laparoscopic partial nephrectomy. In the porcine model, selective clamping appears to improve functional outcomes during prolonged periods of warm ischemic insult. Prospective evaluation of the technique in humans is necessary to determine if selective arterial control confers long-term functional benefits in patients with limited renal reserve.
Experimental ischemic renal arterial necrosis with resolution
The American journal of pathology, 1970
WHILE RENAL ARTERIAL NEcRosis has been observed in a variety of clinical states-ie, malignant nephrosclerosis,"2 periarteritis nodosa,3,4 bilateral renal cortical necrosis and others,5 6 the mechanisms of production are not entirely clear. Experimentally, arterial necrosis has been produced by bacterial toxins,7 hypertension,>'2 hypersensitivity,'3 and in a variety of other ways including acute ischemia,'145 which is the subject of the present investigation. The present study was carried out as part of a project to compare the renal morphology and pathophysiology produced by renal ischemia with the changes in structure and function produced by acute tubular obstruction following intratubular precipitation of globin.'1617 Focal arterial and arteriolar necrosis was a uniform development in the rat following 75 minutes of bilateral complete renal arterial occlusion. The development and healing of these necrotic arteries was studied by light and electron microscopy. A remarkable susceptibility of arterial smooth muscle to hypoxia is emphasized by this work. It is possible that this susceptibility to ischemia following occlusion or spasm mav be of importance in the development of some forms of arterial necrosis not explained in other wavs. Methods Seventy-five white rats of the Sprague-Dawley strain, weighing 200-250 g were used. Under intraperitoneal Nembutal 50 mg/kg anesthesia, the renal arteries were isolated through two dorsal paraspinal incisions without damage to other hilar structures. A 4-0 Merscelene loop was placed around each renal artery excluding the vein, and this loop was pulled into a flanged segment of PE-150 polyethylene tubing, thus occluding each artery. The occlusion was maintained for 75 min.
Journal of Surgical Research, 2009
dence of renal failure due to renal ischemia. The effect of remote ischemic preconditioning (RIPC) in renal ischemia/reperfusion (IR) injury during a thoracoabdominal aortic aneurysm open repair approach was examined on an animal model. Materials and methods. Three groups of rats underwent the following operations respectively: (a) Sham operation in control group; (b) Renal IR injury produced by subphrenic aortic cross-clamping (45/45 min IR), in IR group; (c) The same renal IR injury following RIPC produced by a brief occlusion of the infrarenal aorta (15/15 min IR) in RIPC group. Levels of lactate, base excess, and malondialdehyde (MDA) were measured in selective blood samples from the left renal vein, while levels of MDA were measured in samples of kidney tissues.
Postconditioning in major vascular surgery: prevention of renal failure
Journal of Translational Medicine, 2015
Background: Postconditioning is a novel reperfusion technique to reduce ischemia-reperfusion injuries. The aim of the study was to investigate this method in an animal model of lower limb revascularization for purpose of preventing postoperative renal failure. Methods: Bilateral lower limb ischemia was induced in male Wistar rats for 3 hours by infrarenal aorta clamping under narcosis. Revascularization was allowed by declamping the aorta. Postconditioning (additional 10 sec reocclusion, 10 sec reperfusion in 6 cycles) was induced at the onset of revascularization. Myocyte injury and renal function changes were assessed 4, 24 and 72 hours postoperatively. Hemodynamic monitoring was performed by invasive arterial blood pressure registering and a kidney surface laser Doppler flowmeter. Results: Muscle viability studies showed no significant improvement with the use of postconditioning in terms of ischemic rhabdomyolysis (4 h: ischemia-reperfusion (IR) group: 42.93 ± 19.20% vs. postconditioned (PostC) group: 43.27 ± 27.13%). At the same time, renal functional laboratory tests and kidney myoglobin immunohistochemistry demonstrated significantly less expressed kidney injury in postconditioned animals (renal failure index: 4 h: IR: 2.37 ± 1.43 mM vs.