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Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly.

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Presentation on theme: "Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly."— Presentation transcript:

1 Loss of renal function and microvascular blood flow after suprarenal aortic clamping and reperfusion (SPACR) above the superior mesenteric artery is greatly augmented compared with SPACR above the renal arteries  Stuart I. Myers, MD, Li Wang, BS, Daniel J. Myers  Journal of Vascular Surgery  Volume 45, Issue 2, Pages (February 2007) DOI: /j.jvs Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

2 Fig 1 The effects of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal cortical blood flow. Laser Doppler probes were placed 2 mm into the cortex and blood flow was continuously monitored at basal time period and after 30 minutes of suprarenal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synsthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

3 Fig 2 The effects of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal medullary blood flow. Laser Doppler probes were placed 4 mm into the medulla and blood flow was continuously monitored at basal time period and after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

4 Fig 3 The effects of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal cortical nitric oxide release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump, and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero and after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

5 Fig 4 The effects of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal medullary nitric oxide release. Microdialysis probes were placed 4 mm into the medulla, connected to a syringe pump, and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared to sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

6 Fig 5 The effects of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal cortical prostaglandin E2(PGE2) release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump, and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared to sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

7 Fig 6 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal medullary prostaglandin E2(PGE2) release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and are expressed as mean ± SEM. (a, indicates significance at P < .05 compared to sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

8 Fig 7 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal cortical thromboxane B2 release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of suprarenal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; b, indicates significance at P < .05 compared with the IR group without drug treatment at P < .05) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

9 Fig 8 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal medullary thromboxane B2 release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump and perfused in vivo at 3 μL/min with lactated ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; b, indicates significance at P < .05 compared with the IR group without drug treatment; d, indicates significance at P < .05 compared with the L-NAME group at P < .05.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

10 Fig 9 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal cortical prostaglandin I2 (PGI2) (6-keto-PGF1α) release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump and perfused in vivo at 3 μL/min with lactated Ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of suprarenal aortic clamping, followed by 60 minutes of reperfusion, and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

11 Fig 10 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on renal medullary prostaglandin I2(PGI2)(6-keto-PGF1α) release. Microdialysis probes were placed 2 mm into the cortex, connected to a syringe pump and perfused in vivo at 3 μL/min with lactated ringer’s solution. Dialysate fluid was collected at basal time zero, after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger; n = 8). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

12 Fig 11 The effect of superior mesenteric artery (SMA) suprarenal aortic clamping and reperfusion (SRACR) and renal-SRACR on creatinine clearance (Cr Cl). Serum and urine were collected from separate groups of animals to measure serum creatinine, urine creatinine, and urine volume to calculate creatinine clearance. The serum and urine were collected at basal time zero and after 30 minutes of supra-renal aortic clamping, followed by 60 minutes of reperfusion and compared with sham operation. The ischemia–reperfusion (IR) groups (n = 8 each) were treated with carrier, indomethacin (intravenous cyclooxygenase-1 and cyclooxygenase-2 inhibitor, 10 mg/kg), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg, nitric oxide synthase inhibitor), L-arginine (400 mg/kg, nitric oxide precursor), or superoxide dismutase (SOD; 10,000 U/kg, oxygen-derived free radical scavenger). Data are reported as percentage change from basal time zero and expressed as mean ± SEM. (a, indicates significance at P < .05 compared with sham; e, indicates significance at P < .05 compared with the renal-SRACR group.) Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2007 The Society for Vascular Surgery Terms and Conditions

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