Renal Artery Ligation Research Articles

Laparoscopic-assisted nephrectomy with inferior vena cava tumor thrombectomy: Preliminary results

ObjectivesTo evaluate the feasibility and outcome of laparoscopic-assisted radical nephrectomy and inferior vena cava (IVC) tumor thrombectomy in patients with renal cell carcinoma and level I IVC tumor thrombus. MethodsThe clinical, operative, and pathologic data were retrospectively obtained from patients undergoing the above-mentioned procedure for renal tumors involving the IVC. This approach involved laparoscopic dissection of the kidney and renal vasculature/IVC. After renal artery ligation, an 8 to 12-cm incision was made from the tip of the 11th rib extending anteriorly toward the midline. Through this incision, a Satinsky vascular clamp was placed on the IVC in such a way as to include all the caval thrombus. The tumor thrombus was removed en bloc with the kidney and the cavotomy repaired with a running suture. ResultsFour obese patients underwent transperitoneal laparoscopic-assisted right nephrectomy with inferior vena cava (IVC) thrombectomy. The mean tumor size was 9 cm (range 6 to 13), with the thrombus extending 2 cm into the IVC in all cases. Patients had a mean body mass index of 32.8 (range 30.5 to 37.2) and a mean American Society of Anesthesiologists score of 2.8 (range 2 to 3). The mean operative time was 248 minutes (range 225 to 274). The mean estimated blood loss was 517 mL (range 250 to 900). No intraoperative or postoperative complications occurred. The mean hospital stay was 6.2 days (range 4 to 11, median 5). ConclusionsLaparoscopic-assisted nephrectomy and IVC thrombectomy is a difficult but feasible procedure. This approach allows a smaller incision than a typical open approach. Additional studies are needed to examine the advantages of this approach over a pure open approach.

Functional evaluation of normothermic ischemia and reperfusion injury in dog kidney by using MR perfusion-weighted imaging

目的 结合病理对照研究MR灌注成像评价犬肾缺血再灌注损伤后肾功能的变化.方法雄性家犬12只随机分成4组,分别结扎左侧肾动脉30、60、90和120 min,开放后再灌注损伤1 h.MR检查选择5个时间段,即动脉结扎前、动脉结扎后即刻、动脉开放前、动脉开放后即刻和再灌注损伤后,分别进行常规T2WI和(或)重T2WI(T2*WI)[包括:真实稳态进动快速成像(true-FISP),快速自旋回波(TSE),平面回波成像(EPI)]和T1WI,最后进行灌注加权成像(PWI)[采用反转恢复快速小角度激发(IR-turbo-FLASH)序列]检查.测量肾皮层(C)、外髓层(OM)和内髓层(IM)的信号强度值(SI),比较不同时间段肾脏各层之间的信号变化,并绘制信号强度与时间关系曲线(SI-T曲线).选择曲线峰值(P)、达峰时间(Tp)和曲线下面积(A)作半定量分析.结果动脉结扎后,在T2WI、T2*WI上左肾各层信号明显下降;动脉开放后,EPI各组中左肾OM和IM信号仍明显低于右肾.右肾各层SI-T曲线清晰显示三期增强方式,而左肾OM和IM均表现为单期增强,无明显的增强峰出现,且曲线下面积较右肾明显减低.结论PWI能较准确地评价缺血再灌注损伤后肾功能的变化。

1280: Comparison of Bursting Strength with Various Methods of Renal Artery Ligation

1280: Comparison of Bursting Strength with Various Methods of Renal Artery Ligation

Effects of a Selective Inhibitor of Inducible Nitric Oxide Synthase, ONO-1714, on Experimental Hemodialysis-Related Hypotension in Renal Dysfunctional Dogs

The effect of a selective inducible nitric oxide synthase inhibitor, ONO-1714 ((1S,5S,6R,7R)-7-chloro-3-imino-5-methyl-2-azabicyclo[4.1.0]heptane hydrochloride), on hemodialysis-related hypotension was investigated using a canine model of renal dysfunction. Renal dysfunction was induced in dogs by complete bilateral ligation of renal arteries. On performing hemodialysis with ultrafiltration, the blood pressure of the renal dysfunction dogs gradually decreased and persisted at reduced levels until completion. ONO-1714 ameliorated the hemodialysis-induced hypotension in the renal dysfunction dogs at a dose that did not influence blood pressure in non-hemodialysis dogs with normal renal function. The above findings indicated that ONO-1714 may elicit beneficial effects on hemodialysis-related hypotension.

Mesenteric vasoconstriction triggers nitric oxide overproduction in the superior mesenteric artery of portal hypertensive rats

Background & Aims: Vasoconstriction of the superior mesenteric artery (SMA) is the earliest hemodynamic event occurring after partial portal vein ligation (PVL). We tested the hypothesis that this early vasoconstriction of the SMA may initiate eNOS up-regulation in PVL. Methods: Portal hypertension with or without mesenteric vasoconstriction was induced by differentially calibrated stenosis of the portal vein (PVL-20G and PVL-18G, respectively). In a separate group of rats, mesenteric vasoconstriction was achieved by renal artery ligation. Sham-operated rats were used as controls. Effects of vasoconstriction of the SMA in PVL and RAL rats were evaluated by measuring perfusion pressure changes in isolated SMA beds in response to methoxamine, nitric oxide synthase activity, and eNOS protein expression. Mean arterial pressure, portal pressure, and SMA blood flow were measured by catheterization and Doppler flowmetry. SMA vascular resistance was calculated from arterial pressure, portal pressure, and SMA flow. Results: There was a significant increase in SMA vascular resistance in PVL-20G (2.33 ± 0.13 vs. 1.22 ± 0.03 mm Hg/% flow; P < 0.05) and RAL (2.32 ± 0.18 vs. 1.18 ± 0.02 mm Hg/% flow; P < 0.05) but not in PVL-18G, showing mesenteric vasoconstriction in both PVL-20G and RAL groups. The mesenteric vasculature of PVL-20G and RAL animals showed hyporeactivity to methoxamine ( P < 0.01). Whereas both PVL groups were portal hypertensive ( P < 0.01), RAL rats were not. The SMA hyporeactivity of PVL-20G and RAL rats was corrected by N G -monomethyl- l-arginine, and nitric oxide synthase enzyme activity was significantly higher in PVL-20G and RAL rats ( P < 0.05). Conclusions: Mesenteric arterial vasoconstriction plays a triggering role in up-regulation of eNOS catalytic activity in the SMA of portal hypertensive rats.

Ligation of an anatomic variant of renal vasculature during laparoscopic periaortic lymph node dissection: a cause of postoperative renal infarction

Background Minimally invasive surgical techniques are becoming more sophisticated as complex procedures are being incorporated into gynecologic oncology in routine and investigative settings. Case We present a case of an aberrant supernumerary right renal artery ligation during periaortic laparoscopic lymph node dissection for endometrial cancer. This injury resulted in infarction of the lower pole of the right kidney, with no late sequela. Conclusion The gynecologic oncologist should be aware of the possibility of aberrant renal vasculature, and special care should be taken to avoid accidental ligation of supernumerary renal arteries during dissection of the periaortic lymph nodes.

Model of robust induction of glomerulosclerosis in mice: Importance of genetic background

Increasing evidence suggests that genetic background plays an important role in the development of progressive glomerulosclerosis. The remnant kidney model (RKM) of progressive renal disease has been used extensively in rats. However, C57BL/6 mice are resistant to glomerulosclerosis with RKM induced by either pole amputation or renal artery ligation. A pole resection protocol, applied in 129/Sv mice, induced only mild glomerulosclerosis. We present here a highly reproducible, modified RKM approach to successfully establish a glomerulosclerosis model in mice. Male C57BL/6 (N = 17), 129/Sv (N = 20) and Swiss-Webster (N = 3) mice underwent RKM as follows: the lower branch of the left renal artery was ligated to produce about one third infarct; the upper pole of the left kidney (about one third kidney size) was removed by cautery and the right kidney was nephrectomized to induce a total 5/6 nephrectomy (Nx). In some C57BL/6 mice, 7/8 nephrectomy was induced by removing additional renal mass from the upper pole of the left kidney by cautery. Systolic blood pressure (BP) was measured in conscious mice using a tail-cuff blood pressure monitor and animals were sacrificed at 9, 12, 18, and 24 weeks after nephrectomy. Kidneys were harvested for morphologic analysis. BP in C57BL/6 mice increased slightly after 5/6 nephrectomy over time without significant difference compared to baseline blood pressure except at 8 weeks (blood pressure at week 0, 98 +/- 1 mm Hg; week 4, 105 +/- 2 mm Hg; week 8, 113 +/- 4 mm Hg; and week 12, 110 +/- 3 mm Hg). Blood presssure remained normal in C57BL/6 mice at 18 weeks after 7/8 nephrectomy (103 +/- 2 mm Hg). Blood pressure in 129/Sv mice increased significantly after 5/6 nephrectomy from 4 to 12 weeks (week 0, 112 +/- 3 mm Hg; week 4, 161 +/- 9 mm Hg; week 8, 166 +/- 5 mm Hg; and week 12, 176 +/- 5 mm Hg; P < 0.01 weeks 4, 8, and 12 vs. week 0 blood pressure). Urine protein excretion in C57BL/6 mice increased only at 4 weeks after 5/6 nephrectomy, and was back to normal at 8 and 12 weeks (week 0, 13.2 +/- 1.4 mg/24 hours; week 4, 20.5 +/- 1.8 mg/24 hours; week 8, 18.8 +/- 1.6 mg/24 hours; and week 12, 17.2 +/- 1.2 mg/24 hours, P < 0.05 week 4 vs. week 0). 129/Sv mice developed significant proteinuria 12 weeks after 5/6 nephrectomy compared to their baseline and to levels achieved in C57BL/6 mice (week 0, 17.2 +/- 1 mg/24 hours; week 4, 14.9 +/- 1.8 mg/24 hours; week 8, 23.8 +/- 6.7 mg/24 hours; and week 12, 36.3 +/- 6.6 mg/24 hours, P < 0.01 week 12 vs. week 0; P < 0.01 129/Sv vs. C57BL/6 at week 12). Mortality varied in response to nephrectomy injury in the different strains. Ten percent of C57BL/6 and 43% of 129/Sv died within 12 weeks after 5/6 nephrectomy. Although 50% of C57BL/6 mice died by 12 weeks after 7/8 nephrectomy, there was only mild glomerulosclerosis (<5%) in C57BL/6 mice even at 24 weeks after 5/6 nephrectomy or 18 weeks after 7/8 nephrectomy. In contrast, glomerulosclerosis was marked in both 129/Sv mice and Swiss-Webster mice as early as 9 weeks after 5/6 nephrectomy: 42% of glomeruli showed sclerosis in 129/Sv mice [average sclerosis index (SI), 0 to 4+ scale, 1.08] vs. 24% in Swiss-Webster mice (average SI, 0.57). Tubulointerstitial fibrosis developed in parallel with glomerulosclerosis in both 129/Sv and Swiss-Webster mice. We conclude that genetic background is one of the important factors determining the susceptibility to the development of glomerulosclerosis in mice. We speculate that the superior effects of renal artery ligation plus cautery to produce glomerulosclerosis may result from higher blood pressure responses due to local ischemia activating the renin-angiotensin system.

Functional evaluation of normothermic ischemia and reperfusion injury in dog kidney by combining MR diffusion-weighted imaging and Gd-DTPA enhanced first-pass perfusion.

To evaluate functional alterations of renal ischemia and reperfusion injury using MR diffusion-weighted imaging and dynamic perfusion imaging. Twelve dogs were randomly divided into four groups. Animal renal ischemia was respectively induced for 30 (group 1), 60 (group 2), 90 (group 3), and 120 (group 4) minutes by left renal artery ligation under anesthesia. Using a 1.5 T MR system, true-FISP, TSE, EPI, and DWI sequences were acquired in five different periods; specifically, pre-ischemia, onset-ischemia, late ischemia, onset-reperfusion, and post-reperfusion. Moreover, a turbo-FLASH sequence (TR/TE/TI/FA = 5.8/3.2/400 msec/10 degrees ) with a temporal resolution of 1.16 seconds was acquired. Signal intensity (SI) was measured in the cortex, outer medulla, and inner medulla of kidney. Apparent diffusion coefficient (ADC) values were calculated, and SI was plotted as a function of time. In all animals, significant SI changes of the left kidney on T2/T2*WI were detected following ischemia-reperfusion insult compared to corresponding values of the right kidney. Following ligation, the ADC values decreased in all layers of the left kidney. Immediately after the release of ligation, ADC values in both outer and inner medulla of the left kidney remained lower than those of the right kidney in those animals which were induced with renal ischemia for 60, 90, and 120 minutes. In all groups, a uniphasic enhancement pattern was observed in the outer and inner medulla of the left kidney, accompanied by a decrease of the area under the curve. Our results suggest that MR diffusion-weighted imaging and dynamic perfusion imaging are useful in identifying renal dysfunction following normothermic ischemia and reperfusion injury.

Depolymerized holothurian glycosaminoglycan (DHG), a novel alternative anticoagulant for hemodialysis, is safe and effective in a dog renal failure model

Depolymerized holothurian glycosaminoglycan (DHG) is a new agent with anticoagulant properties quite different from those of unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) in terms of antithrombin III-dependency, and exerts an antithrombotic effect with less bleeding than UFH and LMWH in vivo. In this study, the anticoagulant and hemorrhagic effects of DHG were investigated on hemodialysis in a dog model of renal failure and compared with those of UFH, LMWH, and nafamostat mesilate (FUT). The dog renal failure model was prepared by 7/8 renal artery ligation. Effectiveness was based on completion of 3-hour hemodialysis, no marked clot deposition in the extracorporeal circuit, and permeability of blood urea nitrogen (BUN) and creatinine. Template bleeding was measured by determining the hemoglobin content of the blood from the wound. DHG induced no major bleeding or clot formation during 3-hour hemodialysis, in contrast to UFH and LMWH, each of which induced marked bleeding. These glycosaminoglycans (GAGs) were equally effective in decreasing plasma levels of BUN and creatinine. On the other hand, dogs treated with FUT failed to complete 3-hour hemodialysis. These anticoagulants prolonged activated partial thromboplastin time (APTT) to different extents and GAGs prolonged thrombin clotting time markedly but FUT did not. Our findings suggest that thrombin clotting time prolongation can contribute to prevention of clot formation in extracorporeal circuits, and the non-antithrombin III-dependent activities of DHG may be related to its low risk of hemorrhage for hemodialysis. DHG appears to be promising as an alternative anticoagulant with low risk of hemorrhage for hemodialysis.

Effects of activated factor X inhibitor, JTV-803, in a pig model of hemodialysis

JTV-803 (4-[(2-amidino-1,2,3,4-tetrahydroisoquinolin-7-yloxy)methyl]-1-(4-pyridinyl)piperidine-4-carboxylic acid monomethanesulfonate trihydrate), a specific inhibitor of factor Xa, was evaluated in a pig hemodialysis model with ligation of renal arteries. In this model, JTV-803 administered into the dialysis circuit showed an anticoagulant effect (prolongation of dialysis time) at doses of 0.3 mg/kg+0.3, 1.0 and 3.0 mg/kg/h. The prolongation of dialysis time in the 0.3 mg/kg+1.0 mg/kg/h JTV-803 group was comparable to that in the 15 U/kg+7.5 U/kg/h heparin group. The plasma concentrations of JTV-803 following 0.3 mg/kg+1.0 mg/kg/h infusion of the drug into the dialysis circuit was 500 ng/ml or less, and prothrombin time was 1.5-fold or less than the pretreatment value. JTV-803 was removed by passing the blood through a dialyzer, resulting in a clearance rate of 53.4–81.8%. After the end of dialysis, plasma concentrations of JTV-803 decreased rapidly with time. These results suggest that human factor Xa inhibitor JTV-803 may have good potential as an antithrombotic agent during hemodialysis, with lower likelihood of bleeding after the end of dialysis.

Functional assessment of canine kidneys after acute vascular occlusion on Gd-DTPA-enhanced dynamic echo-planar MR imaging.

To assess the alteration in renal transit of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) in dog kidneys after acute vascular occlusion on dynamic echo-planar imaging (EPI). Dynamic 240-ms EPI series (repetition time/echo time/inversion time [TR/TE/TI] = 3000/42.1/100 ms) of the midcoronal plane of both kidneys of dogs anesthetized by intravenous administration of phenobarbital sodium and ketamine hydrochloride were obtained before and after ligation of the left renal vein (n = 6) or artery (n = 6) for 40 minutes after a 2-second-rate bolus injection of a 0.05 mmol/kg dose of Gd-DTPA. Renal Gd-DTPA transit was analyzed on the time-DeltaR2* curves in each layer of the outer cortex (OC), juxtamedullary cortex and outer zone of the medulla (JMC-OM), and the inner zone of the medulla (IM). The results were compared with those in six normal animals and those of a fast gradient-echo T1-weighted dynamic study performed in other vein- (n = 6) or artery- (n = 6) occluded animals and six normal animals. The histopathological basis of the altered Gd-DTPA transit was also evaluated. The dynamic EPI showed rapid Gd-DTPA transit through each of the five concentric layers, with three separate peaks on the time-DeltaR2* curves. The vein-occluded kidneys showed immediate swelling, with a significant increase in the cross-sectional area proportion of the JMC-OM layer compared with normals (32% +/- 2% vs 24% +/- 2%, P < 0.0001) and intensely congested capillaries, tubular, obliterated material, and gradual and persistent enhancement of the OC and JMC-OM layers but poor Gd-DTPA migration to the IM layer. The artery-occluded kidneys showed a significant reduction in the entire cross-sectional area compared with normals (1352 +/- 69 vs 1432 +/- 47 mm(2), P < 0.05) and poor enhancement, with significant decreases in the area under the time-DeltaR2* curve of the OC and JMC-OM layers compared with the vein-occluded kidneys (79 +/- 50 vs 324 +/- 108 and 82 +/- 42 vs 326 +/- 113, respectively; both P < 0.0001), despite minimal histological damage. In both models, the nonaffected kidneys showed significant increases in the area under the time-DeltaR2* curves compared with baseline. The time course of vascular and tubular Gd-DTPA transit was more detailed by the EPI study than by the T1-weighted imaging study. Echo-planar imaging has an excellent ability to follow the rapid, renal Gd-DTPA transit through the regional anatomy of the canine kidney. After venous occlusion, the JMC-OM layer may be the most affected site, primarily causing renal swelling and interruption of tubular Gd-DTPA transit and concentration. In contrast, an initial block of vascular Gd-DTPA inflow is the primary effect of arterial occlusion. Nonaffected kidneys seem to compensate by increasing excretion of Gd-DTPA.

Role of aquaporin water channels in pleural fluid dynamics.

Continuous movement of fluid into and out of the pleural compartment occurs in normal chest physiology and in pathophysiological conditions associated with pleural effusions. RT-PCR screening and immunostaining revealed expression of water channel aquaporin-1 (AQP1) in microvascular endothelia near the visceral and parietal pleura and in mesothelial cells in visceral pleura. Comparative physiological measurements were done on wild-type vs. AQP1 null mice. Osmotically driven water transport was measured in anesthetized, mechanically ventilated mice from the kinetics of pleural fluid osmolality after instillation of 0.25 ml of hypertonic or hypotonic fluid into the pleural space. Osmotic equilibration of pleural fluid was rapid in wild-type mice (50% equilibration in <2 min) and remarkably slowed by greater than fourfold in AQP1 null mice. Small amounts of AQP3 transcript were also detected in pleura by RT-PCR, but osmotic water transport was not decreased in AQP3 null mice. In spontaneously breathing mice, the clearance of isosmolar saline instilled in the pleural space ( approximately 4 ml. kg(-1). h(-1)) was not affected by AQP1 deletion. In a fluid overload model produced by intraperitoneal saline administration and renal artery ligation, the accumulation of pleural fluid (approximately 0.035 ml/h) and was not affected by AQP1 deletion. Finally, in a thiourea toxicity model of acute endothelial injury causing pleural effusions and lung interstitial edema, pleural fluid accumulation in the first 3 h ( approximately 4 ml. kg(-1). h(-1)) was not affected by AQP1 deletion. These results indicate rapid osmotic equilibration across the pleural surface that is facilitated by AQP1 water channels. However, AQP1 does not appear to play a role in clinically relevant mechanisms of pleural fluid accumulation or clearance.

DRAINAGE VEIN OF LEFT RENAL CELL CARCINOMA COMMUNICATING WITH INFERIOR MESENTERIC VEIN

No AccessJournal of UrologyClinical Urology: Case Reports1 May 1999DRAINAGE VEIN OF LEFT RENAL CELL CARCINOMA COMMUNICATING WITH INFERIOR MESENTERIC VEIN YUTAKA INOUE and HIDEKI SUGAO YUTAKA INOUEYUTAKA INOUE More articles by this author and HIDEKI SUGAOHIDEKI SUGAO More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(05)68956-2AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "DRAINAGE VEIN OF LEFT RENAL CELL CARCINOMA COMMUNICATING WITH INFERIOR MESENTERIC VEIN." The Journal of Urology, 161(5), p. 1562 References 1 : Renal cell cancer invading the inferior vena cava: clinical review and anatomical approach. J. Urol.1980; 123: 157. Link, Google Scholar From the Department of Radiology, Toyonaka Municipal Hospital, Toyonaka and Department of Urology, Minoo City Hospital, Minoo, Osaka, Japan© 1999 by American Urological Association, Inc.FiguresReferencesRelatedDetails Volume 161Issue 5May 1999Page: 1562 Advertisement Copyright & Permissions© 1999 by American Urological Association, Inc.MetricsAuthor Information YUTAKA INOUE More articles by this author HIDEKI SUGAO More articles by this author Expand All Advertisement PDF downloadLoading ...

Increase in Functional Ca 2+ Channels in Cerebral Smooth Muscle With Renal Hypertension

The hypothesis that availability of functional Ca2+ channels in vascular smooth muscle is augmented in hypertension was tested in basilar artery cells from Wistar rats exhibiting stable systolic blood pressure (BPsys) for 2 to 11 weeks after partial renal artery ligation (Goldblatt 2-kidney 1-clip [2K1C] model). Cells were freshly isolated and patch-clamped using a nystatin-perforated patch method. BPsys ranged from 110 to 280 mm Hg and correlated with normalized kidney mass. Macroscopic current-voltage curves were fit to a Boltzmann function to obtain maximum conductance (gmax), steepness and midpoint potential for the voltage dependence of activation (k and E1/2, respectively), and extrapolated reversal potential for the chord conductance (Erev). Linear regression of normalized conductance (ng(max)=g(max)/cell capacitance) versus BPsys for 103 cells indicated a strong relationship, with a slope of 0.0019 nS x pF(-1) x mm Hg(-1) (P<0.0001). Similar analysis of data from 35 other cells exposed to 500 nmol/L Bay K 8644 gave a slope of 0.0041 nS x pF(-1) x mm Hg(-1) (P=0.001). Voltage-dependent parameters, k, E1/2, and Erev, were not significantly related to BPsys. Single-channel measurements in cell-attached patches revealed that the number of channels in 32 patches was significantly related to BPsys (P=0.0024) but that slope conductance, open dwell times at 0 mV, and distribution between 2 open states were not. Finally, in a subgroup of 61 cells from animals made hypertensive (180 mm Hg<BPsys<200 mm Hg) for approximately 1/2 to 6 weeks, we found that elevation of ngmax depended on duration of hypertension (P=0.003), with no elevation at approximately 1/2 week. We conclude that in the 2K1C model, availability of functional Ca2+ channels increases with BPsys with no change in channel properties and that measurable BPsys elevation occurs before the increase in functional channels.

MR Imaging Findings of Renal Infarction Induced by Renal Artery Ligation in Rabbits: The Usefulness of Diffusion-weighted Imaging

MR Imaging Findings of Renal Infarction Induced by Renal Artery Ligation in Rabbits: The Usefulness of Diffusion-weighted Imaging

Interaction of nitric oxide and renin angiotensin system in pulmonary arterial circulation of RHR

We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated pulmonary arterial tension and pulmonary arterial pressure (PAP) in renal hypertensive rats (RHR) made by complete ligation of left renal artery. Losartan induced a depressor response that was smaller in RHR than in normotensive rats (NR) (3.3 and 7.0 mmHg, respectively, at 3.0 mg/kg, p<0.05), and the response was significantly reduced by N(G)-nitro-L-arginine methyl ester (L-NAME). Angiotensin II elevated the PAP (7.6 and 10.8 mmHg at 0.1 mug/kg; 20.3 and 23.6 mmHg at 1.0 mug/kg, respectively) and contracted the isolated pulmonary artery (pD(2): 8.79 and 8.71, respectively) from both NR and RHR with similar magnitude, and these effects were significantly enhanced by L-NAME in NR, but not in HRR. Acetylcholine lowered the PAP slightly less effectively in RHR than in NR (3.8 and 6.0 mmHg at 10 mug/kg, respectively) and relaxed the pulmonary artery precontracted with norepinephrine in both rats with similar magnitude (E(max): 60.8 and 63.6%, respectively), and the effect being completely abolished after pretreatment with L-NAME or removal of endothelial cells. These results suggest that nitric oxide interacts with renin angiotensin system to control the pulmonary vascular tension and pulmonary arterial circulation of RHR.

Influence of Renal Artery Ligation on the Contralateral Kidney and Life Span of Rats.

We examined the life span and blood biochemical data of Sprague-Dawley rats after left renal artery ligation (RAL). The survival rate of rats with a single kidney was 50% at the 66th week, 50% survival of control (sham-operated) rats was at the 92nd week. The RAL group showed an average life span of 68 weeks, as compared with 96 weeks for the control rats. When the RAL group was divided into three subgroups depending on the life span, we found that the body weight in the subgroup with the shortest life span was increased significantly for 25 weeks after the operation, whereas that in the subgroup with the longest life span increased more slowly. Moreover, even 10 weeks before death, the body weight in the subgroup with the shortest life span was found to be heavier than that in either of the other two subgroups. The blood urea nitrogen and creatinine levels already showed high values in the RAL group by the 4th week after the operation, and they were more than two-fold the values in the control rats by the 48th week. These results suggest that unilateral ligation of the renal artery causes abnormal metabolism of proteins and anemia due to malfunction of the remaining kidney and may be a factor in shortening the life span.

A novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system

The present study describes a novel renal hypertensive guinea pig model for comparing different inhibitors of the renin-angiotensin system (RAS). Renal hypertension was induced by a two-step procedure consisting of ligation of the left caudal renal artery and right nephrectomy. Sham-operated animals were used as controls. Arterial blood pressure and heart rate were monitored in conscious animals. Left caudal renal artery ligation and subsequent right nephrectomy led to a significant increase (32% over sham-operated controls, p < .05) in mean arterial blood pressure (MABP), 3 to 4 weeks following surgery. Renal hypertensive animals had increased urine production (from 63 ± 8 mL/kg per day to 143 ± 29 mL/kg per day, p < .05) and an increased incidence of proteinuria ( 11 13 animals had urine protein levels higher than 20 mg/kg per day). Five of the 13 renal hypertensive animals also had hematuria. On autopsy, an 83% increase in the left kidney/body weight ratio and a 37% increase in the heart/body weight ratio were observed in the renal hypertensive animals, compared to the sham-operated controls. Changes in blood pressure and heart rate were assessed before and after an intravenous bolus injection of the drug to be tested. Captopril reduced MABP in both sham-operated and renal hypertensive animals with equal efficacy (up to a maximum of 42%). In contrast, BILA 2157 BS, one of our human renin inhibitors, produced a similar maximum MABP decrease but only in renal hypertensive animals. This selective antihypertensive effect was also observed with enalkiren, another renin inhibitor. These results indicate that the renal hypertensive guinea pig is an useful model for comparing and contrasting different RAS inhibitors.

Magnetic resonance imaging of renal ischemia experimentally induced by renal artery ligation

Magnetic resonance imaging of renal ischemia experimentally induced by renal artery ligation

Analysis of nucleotides and their derivatives in renal tissue of rat during ischemia by HPLC

In rat kidney, the changes in concentrations of nucleotides and their derivatives during ischemia induced by renal artery ligation was measured quantitatively with high performance liquid chromatography(HPLC). After the ligation of renal artery for 60minutes, the concentrations of the nucleotides and derivatives were measured. In ischemic tissue, IDP was significantly decreased from in control to (p to (p to (P, to (P to (P to (p to (P to (P to (P