Artificial organs · 2005
Renal-portal shunt ameliorates renovascular hypertension in pigs.
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Katsenis Konstantinos, Vlahakos Demetrios V, Antoniadis Pavlos, Kostopanagiotou Georgia, Antoniou Aris, Chatziioannou Achilles, Arapoglou Vassilis, Agroyannis Basil, Dimakakos Panagiotis
Аннотация
BACKGROUND: Renovascular hypertension is the most common curable form of secondary hypertension. Renin angiotensin system activation depends on the balance between renin production by the kidney and renin degradation by the liver. Thus, we aimed to examine whether deviation of renin-rich blood from the affected kidney into the portal circulation (portalization) can ameliorate renovascular hypertension.
METHODS: We selected a porcine model of unilateral renal artery stenosis because the pig's anatomy and physiology are comparable to those of humans and because pigs have already been found capable of developing chronic renovascular hypertension. Angiography and ultrasonography were deliberately used to evaluate renal artery stenosis and the renal-portal shunt. Histology was used to examine the effects of portalization on the kidney and liver after a period of two months.
RESULTS: As expected, following the creation of a left renal artery stenosis both renin activity and mean blood pressure measurements increased from 1.23 +/- 0.06 ng/mL/h and 85.6 +/- 0.5 mm Hg at baseline to 4.59 +/- 0.02 ng/mL/h and 126 +/- 1.76 mm Hg, respectively. After portalization renin activity returned to the normal range (1.59 +/- 0.07 ng/mL/h) followed by a concomitant reduction of mean blood pressure to 91 +/- 2 mm Hg. Moreover, a significant correlation was observed between changes in renin activity and blood pressure measurements during the two stages of the experiment. Both the kidney and liver remained macroscopically and microscopically intact at the end of the experiment.
CONCLUSION: Portalization of the affected kidney can ameliorate renovascular hypertension and therefore, it might be of benefit in those individuals with fibromascular or atheromatous lesions in the renal artery or its branches not amenable to balloon angioplasty or surgical revascularization.
METHODS: We selected a porcine model of unilateral renal artery stenosis because the pig's anatomy and physiology are comparable to those of humans and because pigs have already been found capable of developing chronic renovascular hypertension. Angiography and ultrasonography were deliberately used to evaluate renal artery stenosis and the renal-portal shunt. Histology was used to examine the effects of portalization on the kidney and liver after a period of two months.
RESULTS: As expected, following the creation of a left renal artery stenosis both renin activity and mean blood pressure measurements increased from 1.23 +/- 0.06 ng/mL/h and 85.6 +/- 0.5 mm Hg at baseline to 4.59 +/- 0.02 ng/mL/h and 126 +/- 1.76 mm Hg, respectively. After portalization renin activity returned to the normal range (1.59 +/- 0.07 ng/mL/h) followed by a concomitant reduction of mean blood pressure to 91 +/- 2 mm Hg. Moreover, a significant correlation was observed between changes in renin activity and blood pressure measurements during the two stages of the experiment. Both the kidney and liver remained macroscopically and microscopically intact at the end of the experiment.
CONCLUSION: Portalization of the affected kidney can ameliorate renovascular hypertension and therefore, it might be of benefit in those individuals with fibromascular or atheromatous lesions in the renal artery or its branches not amenable to balloon angioplasty or surgical revascularization.