scholarly journals Acute renal venous obstruction is more detrimental to the kidney than arterial occlusion: implication for murine models of acute kidney injury

2012 ◽  
Vol 302 (5) ◽  
pp. F519-F525 ◽  
Author(s):  
Xiang Li ◽  
Manchang Liu ◽  
Djahida Bedja ◽  
Christopher Thoburn ◽  
Kathleen Gabrielson ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Renal Artery ◽  
Renal Vein ◽  
Renal Tubule ◽  
Ischemia Reperfusion ◽  
Arterial Blood Flow ◽  
Whole Body ◽  
Renal Vasculature ◽  
Renal Pedicle ◽  
Arterial Blood

In this study, we compared the traditional murine model with renal pedicle clamp with models that clamped the renal artery or vein alone as well as to a whole body ischemia-reperfusion injury (WBIRI) model. Male C57BL/6J mice underwent either clamping of the renal artery, vein, or both (whole pedicle) for 30 or 45 min followed by reperfusion, or 10 min of cardiac arrest followed by resuscitation up to 24 h. After 30 min of ischemia, the mice with renal vein clamping showed the mostly increased serum creatinine and the most severe renal tubule injury. After 45 min of ischemia, all mice with renal vasculature clamping had a comparable increase in serum creatinine but the renal tubule injury was most severe in renal artery-clamped mice. Renal arterial blood flow was most decreased in mice with a renal vein clamp compared with a renal artery or pedicle clamp. A 30-or 45-min renal ischemia time led to a significant increase in the protein level of interleukin-6, keratinocyte-derived chemokine (KC), and granular colony-stimulating factor in the ischemic kidney, but the KC was the highest in the renal pedicle-clamped kidney and the lowest in the renal vein-clamped kidney. Of note, 10 min of WBIRI led to kidney dysfunction and structural injury, although less than longer time clamping of isolated renal vasculature. Our data demonstrate important differences in ischemic AKI models. Understanding these differences is important in designing future experimental studies in mice as well as clinical trials in humans.

scholarly journals Inhibition of leukocyte L-selectin function with a monoclonal antibody attenuates reperfusion injury to the rabbit ear

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2322-2328 ◽  
Author(s):  
D Mihelcic ◽  
B Schleiffenbaum ◽  
TF Tedder ◽  
SR Sharar ◽  
JM Harlan ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Rabbit Ear ◽  
Adhesive Interactions

Abstract The leukocyte adhesion molecule L-selectin mediates neutrophil adhesive interactions with endothelial cells and is in part responsible for neutrophil rolling. We examined the role of L-selectin in ischemia- reperfusion injury of rabbit ears using a monoclonal antibody (MoAb) directed to a functional epitope of L-selectin. Arterial blood flow to the rabbit ear was occluded for six hours with ambient temperature at 23 degrees C to 24 degrees C. Rabbits were treated at reperfusion with saline (n = 8), the L-selectin function-blocking LAM1–3 MoAb (2 mg/kg), or the nonfunction-blocking LAM1–14 MoAb (2 mg/kg). Tissue injury was determined by measuring edema and necrosis. Edema in the LAM1–3 MoAb- treated group (peak = 25 +/- 4 mL) was significantly less (P < .05) than in saline-treated (peak = 40 +/- 8 mL) and LAM1–14 MoAb-treated (peak = 41 +/- 6 mL) groups. Tissue necrosis at 7 days was not observed in the LAM1–3 MoAb-treated group, whereas significant necrosis (P < .05) was seen in the saline- (8% +/- 3% necrosis) and LAM1–14 MoAb- treated (7% +/- 3% necrosis) group. We conclude that blocking L- selectin ameliorates necrosis and edema after ischemia and reperfusion in the rabbit ear, presumably by blocking neutrophil rolling.

"REFLEX" ANURIA IN THE DOG

1956 ◽  
Vol 34 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Sydney M. Friedman ◽  
Roland W. Radcliffe ◽  
J. E. H. Turpin ◽  
Constance L. Friedman
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Femoral Vein ◽  
Venous Catheter ◽  
Renal Vasoconstriction ◽  
Contralateral Kidney ◽  
Renal Pedicle ◽  
Ureteral Catheters ◽  
Surgical Manipulations ◽  
Reflex Anuria

The effects of various surgical manipulations on the function of the separate kidneys was studied in the dog. The application of a clamp to one renal artery produced vasoconstriction of varying severity in the contralateral kidney. The introduction of a venous catheter into the renal vein by passage upward from the femoral vein similarly caused renal vasoconstriction. The combination of manipulations involved in preparing the renal pedicle for later renal artery clamping with the passing of renal venous and ureteral catheters frequently produced oliguria or complete anuria. Since such nociceptive stimuli can cause renal vasoconstriction and, if sufficiently severe, antidiuresis, it is inferred that these mechanisms bear directly on the problem of traumatic anuria.

Diffusion of oxygen from arterial to venous segments of renal capillaries

1959 ◽  
Vol 196 (6) ◽  
pp. 1336-1339 ◽  
Author(s):  
Matthew N. Levy ◽  
Gerardo Sauceda
Keyword(s):  
Renal Artery ◽  
Oxygen Saturation ◽  
Renal Vein ◽  
Venous Blood ◽  
Renal Medulla ◽  
Appearance Time ◽  
Arterial Blood ◽  
Vasa Recta ◽  
Initial Appearance ◽  
Predominant Effect

Injections of three types of blood preparations were made into the renal arteries of dogs, namely, a) blood equilibrated with 95% O2, 5% CO2, b) arterial blood containing some methemoglobin-labeled erythrocytes and c) blood containing methemoglobinemic cells, but equilibrated with 95% O2, 5% CO2. The initial appearance time in the renal vein was 1.25 ± 0.97 second earlier for oxygen than for the methemoglobinemic red cells. When preparation c was introduced into the renal artery, a diphasic curve was consistently registered from the renal venous blood. The initial deflection was uniformly upright, indicating a preponderant effect due to increased oxygen saturation. This was followed by an inverted deflection, resulting from the predominant effect of methemoglobin. These findings are interpreted to indicate diffusion of some of the oxygen from arterial to venous limbs of capillary loops, probably the vasa recta located in the renal medulla.

Bronchial circulation in pulmonary artery occlusion and reperfusion

1990 ◽  
Vol 68 (1) ◽  
pp. 125-129 ◽  
Author(s):  
T. F. Kowalski ◽  
S. Guidotti ◽  
M. Deffebach ◽  
P. Kubilis ◽  
M. Bishop
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Arterial Blood Flow ◽  
Lung Edema ◽  
Base Line ◽  
Bronchial Circulation ◽  
Arterial Blood

Obstruction of pulmonary arterial blood flow results in minimal biochemical and/or morphological changes in the involved lung. If the lung is reperfused, a syndrome of leukopenia and lung edema occurs. We used the radiolabeled microsphere technique to measure the response of the bronchial circulation in rabbits to acute pulmonary artery occlusion (PAO) and to pulmonary artery reperfusion. We found that the bronchial blood flow (Qbr) decreased from a base line of 0.37 +/- 0.10 to 0.09 +/- 0.04 (SE) ml.min-1.g dry lung-1 (P less than or equal to 0.05) after 4 h of PAO. In a separate group of animals, Qbr 24 h after PAO remained low (0.20 +/- 0.07 ml.min-1.g dry lung-1, P = 0.06). Qbr during PAO was inversely correlated with the wet-to-dry ratio after reperfusion (r = -0.68, P = 0.06). Qbr did not change during 4 h of reperfusion. We speculate that a critical level of Qbr may be necessary during PAO to prevent ischemia/reperfusion injury from occurring.

The Intrarenal Release of Renin in the Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 81s-83s
Author(s):  
T. O. Morgan ◽  
J. Davis ◽  
A. Gillies
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Control Mechanism ◽  
Venous Blood ◽  
Local Formation ◽  
Efferent Arteriole ◽  
Arterial Blood

1. A technique was developed to measure renin concentration in nanolitre volumes of blood. 2. The renin concentration in renal venous blood was higher than in renal arterial blood. 3. The renin concentration in blood from the efferent arteriole was less than in blood from the renal artery and renal vein. 4. Renin enters the circulation distal to the efferent arteriole. 5. The release of renin into the interstitium would allow local formation of angiotensin and the system could act as an intrarenal control mechanism.

scholarly journals Inhibition of leukocyte L-selectin function with a monoclonal antibody attenuates reperfusion injury to the rabbit ear

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2322-2328
Author(s):  
D Mihelcic ◽  
B Schleiffenbaum ◽  
TF Tedder ◽  
SR Sharar ◽  
JM Harlan ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Rabbit Ear ◽  
Adhesive Interactions

The leukocyte adhesion molecule L-selectin mediates neutrophil adhesive interactions with endothelial cells and is in part responsible for neutrophil rolling. We examined the role of L-selectin in ischemia- reperfusion injury of rabbit ears using a monoclonal antibody (MoAb) directed to a functional epitope of L-selectin. Arterial blood flow to the rabbit ear was occluded for six hours with ambient temperature at 23 degrees C to 24 degrees C. Rabbits were treated at reperfusion with saline (n = 8), the L-selectin function-blocking LAM1–3 MoAb (2 mg/kg), or the nonfunction-blocking LAM1–14 MoAb (2 mg/kg). Tissue injury was determined by measuring edema and necrosis. Edema in the LAM1–3 MoAb- treated group (peak = 25 +/- 4 mL) was significantly less (P < .05) than in saline-treated (peak = 40 +/- 8 mL) and LAM1–14 MoAb-treated (peak = 41 +/- 6 mL) groups. Tissue necrosis at 7 days was not observed in the LAM1–3 MoAb-treated group, whereas significant necrosis (P < .05) was seen in the saline- (8% +/- 3% necrosis) and LAM1–14 MoAb- treated (7% +/- 3% necrosis) group. We conclude that blocking L- selectin ameliorates necrosis and edema after ischemia and reperfusion in the rabbit ear, presumably by blocking neutrophil rolling.

"REFLEX" ANURIA IN THE DOG

1956 ◽  
Vol 34 (1) ◽  
pp. 158-169
Author(s):  
Sydney M. Friedman ◽  
Roland W. Radcliffe ◽  
J. E. H. Turpin ◽  
Constance L. Friedman
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Femoral Vein ◽  
Venous Catheter ◽  
Renal Vasoconstriction ◽  
Contralateral Kidney ◽  
Renal Pedicle ◽  
Ureteral Catheters ◽  
Surgical Manipulations ◽  
Reflex Anuria

The effects of various surgical manipulations on the function of the separate kidneys was studied in the dog. The application of a clamp to one renal artery produced vasoconstriction of varying severity in the contralateral kidney. The introduction of a venous catheter into the renal vein by passage upward from the femoral vein similarly caused renal vasoconstriction. The combination of manipulations involved in preparing the renal pedicle for later renal artery clamping with the passing of renal venous and ureteral catheters frequently produced oliguria or complete anuria. Since such nociceptive stimuli can cause renal vasoconstriction and, if sufficiently severe, antidiuresis, it is inferred that these mechanisms bear directly on the problem of traumatic anuria.

scholarly journals An Unusual Course of Segmental Renal Artery Displays a Rare Case of Hilar Nutcracker Phenomenon

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Devendra A. Sawant ◽  
Thomas F. Moore
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Left Renal Vein ◽  
Left Kidney ◽  
Nutcracker Syndrome ◽  
Renal Vasculature ◽  
Renal Disorder ◽  
Nutcracker Phenomenon ◽  
Renal Hilum ◽  
Segmental Renal Artery

Nutcracker phenomenon or renal vein entrapment is classically seen as a compression of renal vein in between abdominal aorta and superior mesenteric artery with patients being asymptomatic or clinically manifested in the form of nutcracker syndrome as proteinuria, hematuria, flank pain, pelvic congestion in women, and varicocele in men. In this report, we are presenting a case of rare variant of nutcracker phenomenon along with brief review of anatomy, pathophysiology, public health, and clinical significance of nutcracker syndrome. On a routine dissection of an adult male cadaver, we noticed an unusual arrangement of the structures at the hilum of the left kidney showing entrapment of renal vein between left anterior inferior and posterior segmental renal arteries. The variation in the course of left anterior inferior segmental renal artery leads to compression of left renal vein at renal hilum. Therefore, we have named this rare abnormal anatomical entity as hilar nutcracker phenomenon. The structures in the right renal hilum are normal. The objective of this paper is to report an unusual but important variant of nutcracker phenomenon and also give collective knowledge of such anatomical variations in renal vasculature that will help in diagnosing and treating such rare renal disorder.

Abstract P034: Vasculature Remodeling In Two Models Of Reduced Renal Mass

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Ryan Adam ◽  
Amanda Marks ◽  
Victoria Nasci ◽  
Alison J Kriegel
Keyword(s):  
Blood Flow ◽  
Flow Direction ◽  
Arterial Blood Flow ◽  
Vascular Density ◽  
Molecular Pathways ◽  
Renal Vasculature ◽  
Flow Area ◽  
Axis Ratio ◽  
Arterial Blood ◽  
Remnant Kidney

Remnant kidney models of chronic kidney disease include the 1/3 nephrectomy (1/3Nx), and 5/6 nephrectomy rats. The 1/3Nx remnant kidney spontaneously atrophies with time, and the 5/6Nx hypertrophies. This disparate remodeling must occur with commensurate vascular changes, examination of which may reveal important molecular pathways and mechanisms underlying changes in renal function. The first step toward realizing this, and the aim of this study, was to characterize the renal vasculature from 1/3Nx, 5/6Nx, and sham Nx rats. Methods: The vasculature was examined in rats 10 weeks following surgery. To-date, these renal vasculatures have been quantified by (1) assessment of vascular density by analysis of bisected, renal vascular casts, and (2) renal blood flow doppler ultrasound. Data: Avg±SEM. Results: 1/3Nx remnant kidney atrophied and 5/6Nx hypertrophied (cross-sectional area: sham n=9; 241±7. 5/6Nx, n=9; 247±8. 1/3Nx, n=12; 132±11: mm 2 ). Despite this, kidney height (intact kidney long axis) to width (short axis) ratio was similar between the remnant models (5/6Nx; 0.8±0.04. 1/3Nx; 0.9±0.04). Sham kidney vascular density was significantly greater than that of 1/3Nx remnant kidneys, which exceeded that of 5/6Nx rats. Cortex vascular density was significantly different between all groups (sham; 95±2%. 1/3Nx; 57±9%. 5/6Nx; 25±11%). The statistical mode of the arterial blood flow distribution was not different between the groups, but mode venous flow was (sham; 100±6. 1/3Nx; 118±9. 5/6Nx; 136±8. Relative units.). Homogeneity of flow was quantified by expressing flow-direction boundaries as a percent of flow area. Sham flow was significantly more homogenous (1.8±0.2) than 1/3Nx (3.7±0.5), and 5/6Nx rats (3.9±0.3). Conclusion: These data demonstrate changes in vascular anatomy and function in both remnant kidney models. Interrogation of anatomical changes and molecular pathways may reveal novel treatment approaches.

Effects of statins on myocardial and coronary artery response to ischemia-reperfusion

2003 ◽  
Vol 81 (11) ◽  
pp. 1064-1071 ◽  
Author(s):  
Stephen V Rendig ◽  
J David Symons ◽  
Ezra A Amsterdam
Keyword(s):  
Coronary Artery ◽  
Ventricular Function ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Lv Function ◽  
Ischemic Region ◽  
Arterial Blood ◽  
Percent Recovery

This study tested the hypotheses that (i) lipophilic statins (atorvastatin and simvastatin) impair ventricular recovery from myocardial ischemia–reperfusion, owing to their greater myocyte permeability, compared with a hydrophilic statin (pravastatin), and (ii) statins enhance endothelium-dependent vasodilation of isolated coronary arteries from the ischemic region. Farm pigs consumed chow supplemented with atorvastatin (2.5 mg·kg–1·d–1; n = 6), pravastatin (10 (n = 3) or 20 (n = 2) mg·kg–1·d–1), simvastatin (5 mg·kg–1·d–1; n = 6), or no statin (control; n = 6) for 3 weeks. Animals were anesthetized and instrumented to measure regional (% segment shortening) and global (dP/dt max) left ventricular (LV) function during coronary artery occlusion (10 min) and reperfusion (30 min). Coronary resistance (i.d. = 119 ± 3 µm) and conductance (i.d. = 487 ± 11 µm) arteries were isolated from the ischemic region to measure receptor-dependent (acetylcholine (ACh)) and -independent (KCl) vasoconstriction, and endothelium-dependent (bradykinin (BK)) and -independent (sodium nitroprusside (SNP)) vasodilation. At 30 min reperfusion, neither percent recovery of regional ventricular function (atorvastatin, 24% ± 15%; pravastatin, 36% ± 13%; simvastatin, 29% ± 13%; control, 36% ± 13%) nor percent recovery of global LV cardiac function differed among groups. However, BK-induced vasorelaxation of coronary conductance vessels was greater (P < 0.05) in statins versus controls, and ACh-induced vasoconstriction was less in simvastatin-treated animals, suggesting the potential for enhanced coronary arterial blood flow to the jeopardized region. In conclusion, our data suggest that ischemia-induced myocardial stunning is similar among pigs treated for 3 weeks with atorvastatin, pravastatin, or simvastatin, even though statin treatment appears to augment endothelium-dependent vasodilation of conductance, but not resistance, vessels subjected to ischemia–reperfusion.Key words: ischemia, reperfusion, statins, vascocontriction–dilation, ventricular function.

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