Scand J Urol Nephrol 10:52-55. 1976
THE EFFECT OF TEMPORARY CLAMPING OF THE RENAL VESSELS ON THE VASCULAR RESISTANCE IN RABBIT KIDNEYS Torben Bilde
Scand J Urol Nephrol Downloaded from informahealthcare.com by University of Auckland on 10/28/14 For personal use only.
From Surgiccrl Depcrrttnent D . Rigshospitulet. University Hospital of Copenhagen, Denmork
(Submitted for publication August 9, 1974)
Ahstrucr. In studies of 45 rabbits, either the renal artery (35 animals), or the renal artery and vein (10 animals) were the warm clamped in situ. The effect of the clamping-f ischemia-n the vascular resistance of the kidney after reestablishment of the circulation was examined in perfusion studies made after removal of the kidneys from groups of 5 animals between I and 5 days after revascularization. Resistance patterns were measured during hypothermic perfusion. The results confirm earlier findings that vascular resistance increases in proportion to the duration of warm ischemia up to 60 min, but not thereafter. The renal vascular resistance falls over the days following revascularization, more slowly after longer periods of ischemia. Thus after 60 min of warm ischemia the vascular resistance became normal within 24 hours, but after 180 min of warm ischemia, the normal resistance range was not reached until 96 hours after reestablishment of the circulation. When both the renal artery and the renal vein were clamped, the pattern was the same but much less emphatic. The vascular resistance never attained such high values as seen after clamping of the renal artery alone, and became normal after 24 hours of revascularization, even when the period of warm ischemia was as long as 180 min.
An earlier study (Bilde, 1976) showed that warm ischemia induced by in situ clamping of the rabbit renal artery gave an increase in renal vascular resistance, measured during subsequent perfusion studies. Maximal resistance values were measured after 60 min of clamping, and thereafter remained unchanged up to and after 180 min of clamping. If both the renal artery and the renal vein were clamped, renal vascular resistance also increased, but only to half that value seen when the renal artery alone was clamped. This study concerns the degree and the rate at Scand J Urol N e p h m l 10
which renal vascular resistance becomes normal when revascularization is effected after varying periods of clamping of the renal vessels. MATERIAL Experiments were conducted in 45 rabbits of white Danish country breed, of average weight 2.7 kg. The animals were fasted for 14 hours before operation. Serum creatinine was determined on the day of operation, and if this value was over 0.18 mmol/l, the animals were excluded from the study. Anesthesia was effected with Nembutal 10 mg per kg i.v. Isotonic saline and Heparine 500 i.u. were given at the beginning of operation. Fluid supplements, either isotonic glucose or saline, 15 ml/kg/hr were given during operation. Continuous transducer blood pressure measurement was made through a cannula inserted in the central artery of the ear.
OPERATIVE T E C H N I Q U E The abdomen was opened through a midline incision. The left renal vessels were isolated close to the aorta and clamped. IJI 35 of the animals, only the artery was clamped-for 60 min in 10 animals, and for 180 min in the remaining 25. In 10 animals both the artery and the vein were clamped for 180 min. After the predetermined period of clamping, clamps were removed, and experiments continued only when the kidney in question became red and pulsation could be detected in the renal artery. The abdominal incision was closed. At intervals of 24,48,96 and 120 hours, the left kidneys were removed from groups of 5 animals, and perfused. All kidneys were perfused at 4°C with 5 % Dextran of low molecular weight in balanced saline solutions, with addition of 5 mg% Papaverin. Flow rates were adjusted to 0.5 ml/g renal tissuelmin. Perfusion pressures were measured at 2, 5, 10, 20, 30,40 and SO min. A detailed description of the perfusion system has been given earlier (Bilde, 1975 u ) .
Eflc~ctof clumping of r e n d vessels on vascular resistunce
53
Table I . Perjirsion prc.s.sr{re.s (niniHg) in kidneys ufter in sitrr nrteriul clamping ,for 60 niin follou~rdby restorution of circrrlntion ,fi)r 24 lioitrs ( I ) und 48 liorrrs ( 2 ) Mean values and standard deviations Duration of perfusion (rnin)
Scand J Urol Nephrol Downloaded from informahealthcare.com by University of Auckland on 10/28/14 For personal use only.
Groups
2
Control, no occlusion" 56.0(19.3) Control, 60 min occlusion'' 147.0 (35.8) ( I ) 60 min occlusion, 24 hours recirc. 44.0 (7.4) ( 2 ) 6 0 minocclusion, 47.0 (5.7) 48 hours recirc. ~
10
5
20
30
50
40
42.0(11.8)
37.0 (7.5)
32.5 (5.4)
32.5 (5.4)
31.5 (4.7)
32.0 (4.8)
129.0 (24.4)
113.0 (27.5)
108.0 (31.2)
106.0 (29.0)
105.5 (29.3)
105.5 (29.3)
37.0 (8.4) 40.0 (7.1)
34.0 (6.5) 37.0 (5.5)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
~
These groups have been published earlier (T. Bilde. 1975).
RESULTS Table I records the results of perfusion studies after the renal artery had been clamped in sitrr for 60 min, and, thereafter, revascularized in situ after removal of the clamp. Two groups are concerned, those in which revascularization in situ was permitted for, respectively, 24 and 48 hours. For comparison, results in two control groups are appended-in one no vessels were clamped and the kidney was simply removed and placed in the perfusion system. In the other the kidney was removed immediately after a 60 min period of arterial clamping, and placed in the perfusion system. These latter two control groups are described previously (Bilde, 19764). Perfusion pressures in all groups were initially high, but fell to a stable level after 20 min perfusion, whereafter perfusion pressures remained unchanged. These 20 min perfusion pressure values are applied in characterization of the different groups. The perfu-
sion pressures in group I , after 60 min clamping and 24 hours recirculation, are significantly lower than in the control group without revascularization @
THE EFFECT OF TEMPORARY CLAMPING OF THE RENAL VESSELS ON THE VASCULAR RESISTANCE IN RABBIT KIDNEYS Torben Bilde
Scand J Urol Nephrol Downloaded from informahealthcare.com by University of Auckland on 10/28/14 For personal use only.
From Surgiccrl Depcrrttnent D . Rigshospitulet. University Hospital of Copenhagen, Denmork
(Submitted for publication August 9, 1974)
Ahstrucr. In studies of 45 rabbits, either the renal artery (35 animals), or the renal artery and vein (10 animals) were the warm clamped in situ. The effect of the clamping-f ischemia-n the vascular resistance of the kidney after reestablishment of the circulation was examined in perfusion studies made after removal of the kidneys from groups of 5 animals between I and 5 days after revascularization. Resistance patterns were measured during hypothermic perfusion. The results confirm earlier findings that vascular resistance increases in proportion to the duration of warm ischemia up to 60 min, but not thereafter. The renal vascular resistance falls over the days following revascularization, more slowly after longer periods of ischemia. Thus after 60 min of warm ischemia the vascular resistance became normal within 24 hours, but after 180 min of warm ischemia, the normal resistance range was not reached until 96 hours after reestablishment of the circulation. When both the renal artery and the renal vein were clamped, the pattern was the same but much less emphatic. The vascular resistance never attained such high values as seen after clamping of the renal artery alone, and became normal after 24 hours of revascularization, even when the period of warm ischemia was as long as 180 min.
An earlier study (Bilde, 1976) showed that warm ischemia induced by in situ clamping of the rabbit renal artery gave an increase in renal vascular resistance, measured during subsequent perfusion studies. Maximal resistance values were measured after 60 min of clamping, and thereafter remained unchanged up to and after 180 min of clamping. If both the renal artery and the renal vein were clamped, renal vascular resistance also increased, but only to half that value seen when the renal artery alone was clamped. This study concerns the degree and the rate at Scand J Urol N e p h m l 10
which renal vascular resistance becomes normal when revascularization is effected after varying periods of clamping of the renal vessels. MATERIAL Experiments were conducted in 45 rabbits of white Danish country breed, of average weight 2.7 kg. The animals were fasted for 14 hours before operation. Serum creatinine was determined on the day of operation, and if this value was over 0.18 mmol/l, the animals were excluded from the study. Anesthesia was effected with Nembutal 10 mg per kg i.v. Isotonic saline and Heparine 500 i.u. were given at the beginning of operation. Fluid supplements, either isotonic glucose or saline, 15 ml/kg/hr were given during operation. Continuous transducer blood pressure measurement was made through a cannula inserted in the central artery of the ear.
OPERATIVE T E C H N I Q U E The abdomen was opened through a midline incision. The left renal vessels were isolated close to the aorta and clamped. IJI 35 of the animals, only the artery was clamped-for 60 min in 10 animals, and for 180 min in the remaining 25. In 10 animals both the artery and the vein were clamped for 180 min. After the predetermined period of clamping, clamps were removed, and experiments continued only when the kidney in question became red and pulsation could be detected in the renal artery. The abdominal incision was closed. At intervals of 24,48,96 and 120 hours, the left kidneys were removed from groups of 5 animals, and perfused. All kidneys were perfused at 4°C with 5 % Dextran of low molecular weight in balanced saline solutions, with addition of 5 mg% Papaverin. Flow rates were adjusted to 0.5 ml/g renal tissuelmin. Perfusion pressures were measured at 2, 5, 10, 20, 30,40 and SO min. A detailed description of the perfusion system has been given earlier (Bilde, 1975 u ) .
Eflc~ctof clumping of r e n d vessels on vascular resistunce
53
Table I . Perjirsion prc.s.sr{re.s (niniHg) in kidneys ufter in sitrr nrteriul clamping ,for 60 niin follou~rdby restorution of circrrlntion ,fi)r 24 lioitrs ( I ) und 48 liorrrs ( 2 ) Mean values and standard deviations Duration of perfusion (rnin)
Scand J Urol Nephrol Downloaded from informahealthcare.com by University of Auckland on 10/28/14 For personal use only.
Groups
2
Control, no occlusion" 56.0(19.3) Control, 60 min occlusion'' 147.0 (35.8) ( I ) 60 min occlusion, 24 hours recirc. 44.0 (7.4) ( 2 ) 6 0 minocclusion, 47.0 (5.7) 48 hours recirc. ~
10
5
20
30
50
40
42.0(11.8)
37.0 (7.5)
32.5 (5.4)
32.5 (5.4)
31.5 (4.7)
32.0 (4.8)
129.0 (24.4)
113.0 (27.5)
108.0 (31.2)
106.0 (29.0)
105.5 (29.3)
105.5 (29.3)
37.0 (8.4) 40.0 (7.1)
34.0 (6.5) 37.0 (5.5)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
33.0 (5.7) 35.0 (5.0)
~
These groups have been published earlier (T. Bilde. 1975).
RESULTS Table I records the results of perfusion studies after the renal artery had been clamped in sitrr for 60 min, and, thereafter, revascularized in situ after removal of the clamp. Two groups are concerned, those in which revascularization in situ was permitted for, respectively, 24 and 48 hours. For comparison, results in two control groups are appended-in one no vessels were clamped and the kidney was simply removed and placed in the perfusion system. In the other the kidney was removed immediately after a 60 min period of arterial clamping, and placed in the perfusion system. These latter two control groups are described previously (Bilde, 19764). Perfusion pressures in all groups were initially high, but fell to a stable level after 20 min perfusion, whereafter perfusion pressures remained unchanged. These 20 min perfusion pressure values are applied in characterization of the different groups. The perfu-
sion pressures in group I , after 60 min clamping and 24 hours recirculation, are significantly lower than in the control group without revascularization @
