Renal blood flow before and after portosystemic shunt in children with portal hypertension

Lipopolysaccharide (LPS) and endothelin- (ET-) 1 may aggravate portal hypertension by increasing intrahepatic resistance and splanchnic blood flow. In the portal vein, after TIPS shunting, LPS and ET-1 were significantly decreased. Our study suggests that TIPS can benefit cirrhotic patients not only in high hemodynamics related variceal bleeding but also in intestinal bacterial translocation associated complications such as endotoxemia.

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Plasma dopamine in regulation of canine renal blood flow

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.255.3.r379 ◽

1988 ◽

Vol 255 (3) ◽

pp. R379-R387 ◽

Cited By ~ 2

Author(s):

D. R. Kapusta ◽

N. W. Robie

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Sch 23390 ◽

Renal Perfusion ◽

Receptor Activation ◽

Renal Autoregulation ◽

Alpha Adrenoceptor ◽

Before And After ◽

Anesthetized Dogs ◽

Control Infusion

Studies were performed in pentobarbital-anesthetized dogs to determine whether circulating plasma dopamine (DA) is involved in renal blood flow (RBF) regulation. During graded reductions in renal perfusion pressure (RPP), total renal venous (RV) DA content significantly increased at RPPs below the autoregulatory range. The RBF response to decrements in RPP was also examined during control, infusion of DA (1.2 micrograms.kg(-1).min(-1)ia), and after DA receptor blockade by SCH 23390 (30 micrograms/kg iv). During DA infusion, autoregulation was still evident over the same RPPs, although at higher flow rates. At pressures below the autoregulatory range, RBF decreased linearly and the autoregulatory curve merged with control at 50 mmHg. After SCH 23390, autoregulation ceased at a higher RPP than during control, and RBF was significantly less than control rates at pressures of 80 mmHg and below. To elucidate reasons for this latter response, reductions in RPP were repeated before and after administration of both prazosin (0.1 mg/kg iv) and SCH 23390. The results indicated that RBF rates were not different from control at any RPP. Further, prazosin alone did not alter renal autoregulation but significantly increased RBF at RPP below the autoregulatory range. Thus these results indicate that dopamine does not participate in RBF control at pressures above the inflection point for the lowest limit of RBF autoregulation but may be released at lower RPP to act as a vasodilator agent to oppose alpha-adrenoceptor-mediated reductions in RBF. Moreover, tonic DA receptor activation may influence the setting of the lower limit of canine RBF autoregulation.

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The Effect of Artificial Portocaval Anastomosis or Splenectomy on Hepatic and Portal Haemodynamics in Cirrhotics

Nuklearmedizin ◽

10.1055/s-0038-1624676 ◽

1969 ◽

Vol 08 (03) ◽

pp. 232-241

Author(s):

J. Vosmík ◽

V. Bláha

Keyword(s):

Blood Flow ◽

Liver Cirrhosis ◽

Portal Hypertension ◽

Liver Blood Flow ◽

Severe Liver ◽

Portocaval Anastomosis ◽

Average Decrease ◽

Modified Method ◽

Portosystemic Shunts ◽

Before And After

SummaryUsing their own modified method the authors simultaneously examined the blood clearances of 198Au colloid and 131I-Rose Bengal and determined the ratio1. in a group of 11 patients with severe liver cirrhosis, portal hypertension and portosystemic shunts, both before and after artificial portocaval anastomosis, and2. in two patients with thrombosis v. lienalis, excessive splenomegaly and extensive portosystemic shunts before and after splenectomy. Ad 1. In 6 patients 55%) a reduction of the effective liver blood flow occured due to the artificial portosystemic anastomosis; the average decrease was ~ 20%. In 7 patients a significant enlargement of the total splenosystemic flow was observed as a result of the artificial communication.Ad 2. In both patients an increase of the effective liver blood flow occured after splenectomy. The minimal preoperative splenosystemic flow was ~ 0.152 and ~ 0.089 of the circulating blood per minute (expressed by means of kAu).The authors discuss the significance of the kAu and kBR values as well as that of the ratio for the estimation of changes in hepatic and portal haemodynamics.

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P0544INHIBITION OF 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE (15-PGDH) PROTECTS MICE AGAINST CONTRAST-INDUCED ACUTE KIDNEY INJURY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0544 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Byeong Woo KIm ◽

Sun hee Kim ◽

Ki beom Bae

Keyword(s):

Acute Kidney Injury ◽

Blood Flow ◽

Protective Effect ◽

Renal Blood Flow ◽

Smooth Muscle Actin ◽

Kidney Injury ◽

Plasma Creatinine ◽

Histological Evaluation ◽

Vehicle Group ◽

Before And After

Abstract Background and Aims Although the mechanism of contrast-induced acute kidney injury (CI-AKI) is not fully known, the imbalance of vasoconstrictive and vasodilative mediators plays a major role. Prostaglandin E2 (PGE2) is one of the vasodilators involved in this process. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) causes elevation of PGE2 level in tissue by delaying the rapid degradation of PGE2 by the enzyme. We tested the hypothesis that the 15-PGE2 inhibitor would protect against CI-AKI in a mouse model and attempted to elucidate the mechanism involved. Method 10-week aged male C57/BL6 Mice were injected with 10gI/kg of iodixanol by tail vein. Renal blood flow measurement, right nephrectomy, and blood sampling were taken at 48 hours after iodixanol injection. The 15-PGDH inhibitor was injected before and after iodixanol administration. Plasma creatinine, NGAL, KIM-1 were measured as biomarkers for renal function. Histological evaluation was analyzed by the necrosis scoring system and TUNEL assay. Arteriolar area of outer medulla was analyzed by α-smooth muscle actin stain. Renal blood flow was measured by the non-invasive laser doppler. Results Plasma creatinine (1.94±0.75 vs 1.11±0.44 mg/dL, p=0.005), NGAL (299.7±115.87 vs 140.4±76.56 ng/mL, p=0.004), and KIM-1 (2.09±2.34 vs 0.43±0.89 ng/mL, p=0.024) levels were significantly lower when the 15-PGDH inhibitor was injected before and after iodixanol administration than the vehicle group. But no significant renal protective effect was shown when the 15-PGDH inhibitor was injected before or after iodixanol administration. The 15-PGDH inhibitor administration before and after iodixanol injection showed a significantly wider renal arteriolar area (683.63±248.46 vs 1132.97±357.46 μm2, p=0.039) and larger renal blood flow (360.0±49.72 vs 635.1±27.20, p=0.011) than vehicle administration. Conclusion The 15-PGDH inhibitor has a renal protective effect against CI-AKI in mice by increasing renal blood flow when injected intravenously before and after iodine contrast media administration.

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Renal Blood Flow Changes Induced by Captopril before and after Angioplasty in Renal Arterty Stenosis

Clinical Science ◽

10.1042/cs076030pb ◽

1989 ◽

Vol 76 (s20) ◽

pp. 30P-30P

Author(s):

AM Peters ◽

J Brown ◽

D Crossman ◽

DJ Allison ◽

CT Dollery

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Before And After ◽

Flow Changes

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Renal Vascular Response to Haemorrhage in the Rabbit after Pentobarbitone, Chloralose–Urethane and Ether Anaesthesia

Clinical Science ◽

10.1042/cs0540489 ◽

1978 ◽

Vol 54 (5) ◽

pp. 489-494

Author(s):

D. J. Warren ◽

J. G. G. Ledingham

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Renal Cortex ◽

Ether Anaesthesia ◽

Before And After ◽

Conscious Rabbits ◽

Urethane Anaesthesia ◽

Renal Vascular ◽

Cortical Distribution ◽

Total Renal Blood Flow

1. Total renal blood flow and its cortical distribution were measured by the microsphere technique before and after haemorrhage in conscious rabbits, and after haemorrhage in rabbits anaesthetized with pentobarbitone, chloralose—urethane or ether. 2. The average blood loss necessary to achieve a fall in systolic blood pressure to about 65 mmHg was 101 ml in conscious rabbits and 38, 90 and 118 ml in weight-matched groups of rabbits anaesthetized with pentobarbitone, chloralose—urethane and ether respectively. 3. After haemorrhage in conscious rabbits total renal blood flow fell by 25%, this fall being confined to the superficial renal cortex. 4. In rabbits subject to haemorrhage under pentobarbitone anaesthesia renal blood flow fell by a further 23% when compared with the conscious bled rabbits. This reduction in blood flow was confined to the superficial cortex. 5. Haemorrhage in the rabbits subjected to chloralose—urethane anaesthesia caused no significant change in renal blood flow, as compared with conscious bled rabbits. 6. Haemorrhage under ether anaesthesia was associated with a further 33% fall in total renal blood flow, as compared with conscious bled rabbits. This was associated with a fall of 32% and 34% in superficial and deep cortical blood flow respectively. 7. Animals subjected to general anaesthesia may be particularly susceptible to the renal haemodynamic effects of haemorrhage.

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Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

AJP Renal Physiology ◽

10.1152/ajprenal.0186.2001 ◽

2002 ◽

Vol 282 (1) ◽

pp. F51-F58 ◽

Cited By ~ 10

Author(s):

Silene L. S. Pires ◽

Claude Julien ◽

Bruno Chapuis ◽

Jean Sassard ◽

Christian Barrès

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Renal Blood Flow ◽

Coefficient Of Variation ◽

Tubuloglomerular Feedback ◽

Before And After ◽

Renal Blood Flow Autoregulation ◽

Limited Accuracy ◽

Weibull Equation ◽

Intact Rats

These experiments examined whether the conscious sinoaortic baroreceptor-denervated (SAD) rat, owing to its high spontaneous arterial pressure (AP) variability, might represent a model for renal blood flow (RBF) autoregulation studies. In eight SAD and six baroreceptor-intact rats, AP and RBF were recorded (1-h periods) before and after furosemide (10 mg/kg followed by 10 mg · kg−1 · h−1 iv)administration. In control conditions, AP variability was markedly enhanced in SAD rats (coefficient of variation: 16.0 ± 1.2 vs. 5.4 ± 0.5% in intact rats), whereas RBF variability was only slightly increased (8.7 ± 0.6 vs. 6.1 ± 0.5% in intact rats), suggesting buffering by autoregulatory mechanisms. In SAD rats, but not in intact rats, the AP-RBF relationships could be modeled with a four-parameter sigmoid Weibull equation ( r 2 = 0.24 ± 0.07, 3,600 data pairs/rat), allowing for estimation of an autoregulatory plateau (10.1 ± 0.7 ml/min) and a lower limit of RBF autoregulation (PLL = 93 ± 6 mmHg, defined as AP at RBF 5% below the plateau). After furosemide treatment, autoregulation curves ( r 2 = 0.49 ± 0.07) in SAD rats were shifted downward (plateau = 8.6 ± 0.8 ml/min) and rightward (PLL = 102 ± 5 mmHg). In five of six intact rats, PLL became measurable (104 ± 1 mmHg), albeit with limited accuracy ( r 2 = 0.09 ± 0.03). In conclusion, the conscious SAD rat offers the possibility of describing RBF autoregulation curves under dynamic, unforced conditions. The tubuloglomerular feedback and myogenic mechanisms cooperate in setting PLL and thus in stabilizing RBF during spontaneous depressor episodes.

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cGMP-Mediated Inhibition of cAMP Degradation Stimulates Renin Secretion Without Affecting Renal Hemodynamics.

Hypertension ◽

10.1161/hyp.36.suppl_1.711 ◽

2000 ◽

Vol 36 (suppl_1) ◽

pp. 711-711

Author(s):

Cecilia M Sayago ◽

William H Beierwaltes

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Renal Blood Flow ◽

Direct Effect ◽

Venous Blood ◽

Second Messenger ◽

Renal Hemodynamics ◽

Secretion Rate ◽

Renin Secretion ◽

Before And After

P100 The stimulatory second messenger for renin is cAMP, which is degraded by phosphodiesterase (PDE)-3. PDE-3 is inhibited by cGMP, while PDE-5 degrades cGMP. We hypothesized that if endogenous cGMP was increased, it could inhibit PDE-3, increasing cAMP, and stimulating renin. We used the selective PDE-5 inhibitor Zaprinast at a dose we determined would not change either blood pressure or renal blood flow (RBF). In inactin-anesthetized rats, renin secretion rate (RSR) was determined by collecting arterial and renal venous blood while measuring RBF before and 75 min after administering 20 mg/kg bw Zaprinast (n=9) ip, or vehicle (n=7). Blood pressure before and after Zaprinast was unchanged at 102 ±2 and 98 ±2 mmHg, respectively, similar to vehicle controls (107 ±3 to 105 ±4 mmHg). RBF was unchanged by either Zaprinast (5.57 ±0.38 to 5.77 ±0.41 ml/min/gkw) or vehicle (6.21 ±0.47 to 6.25 ±0.42 ml/min/gkw). Zaprinast increased RSR 6-fold (from 2.95 ±1.74 to 17.62 ±5.46 ng Ang1/hr/min, p <0.024), while vehicle had no effect (4.08 ±2.02 to 3.87 ±1.53 ng Ang1/hr/min). Zaprinast also increased renal cGMP excretion from 12.75 ±1.57 to 18.67 ±1.87 p mol/min (p<0.003), while cGMP excretion was unchanged by vehicle (13.07 ±1.76 to 12.42 ±2.16 p mol/min). Thus, inhibition of cGMP degradation by the PDE-5 inhibitor Zaprinast increased endogenous cGMP (as reflected in excretion) and also stimulated renin secretion, despite not significantly changing renal hemodynamics. These data suggest that endogenous cGMP may indirectly regulate renin through its direct effect on cAMP degradation.

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Failure to abolish reactive hyperemia by indomethacin in denervated kidneys of rabbits

AJP Renal Physiology ◽

10.1152/ajprenal.1977.233.2.f89 ◽

1977 ◽

Vol 233 (2) ◽

pp. F89-F93

Author(s):

C. Aizawa ◽

N. Honda

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Reactive Hyperemia ◽

Fractional Flow ◽

Outer Cortex ◽

Cortical Blood Flow ◽

Before And After ◽

Inner Cortex ◽

Postocclusive Reactive Hyperemia

The effect of indomethacin (10 mg/kg) on the distribution of cortical blood flow during postocclusive reactive hyperemia was evaluated in denervated kidneys of anesthetized rabbits by the radioactive microsphere technique. Renal denervation caused a slight but not significant increase in renal blood flow with no remarkable alteration in the distribution of cortical blood flow. After release of 1-min occlusion of the renal artery, hyperemic responses developed with a fractional flow redistribution toward the inner cortex. The absolute perfusion rate increased in the inner cortex but did not significantly change in the outer cortex. Indomethacin produced a decrease in renal blood flow despite elevated blood pressure. Even in the indomethacin-treated animals, postocclusive reactive hyperemia appeared concomitantly with the fractional flow redistribution to the inner cortex. The percentage repayment by reactive hyperemia of ischemia during the artery clamping was not significantly different before and after indomethacin administration. The findings indicate that indomethacin did not significantly affect the postocclusive vascular response in denervated kidneys of rabbits, thereby giving evidence against the role of prostaglandins as mediators of reactive hyperemia.

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Blockade of renal effects of dopamine in the dog by the DA1 antagonist SCH 23390

AJP Renal Physiology ◽

10.1152/ajprenal.1985.249.2.f236 ◽

1985 ◽

Vol 249 (2) ◽

pp. F236-F240 ◽

Cited By ~ 4

Author(s):

E. D. Frederickson ◽

T. Bradley ◽

L. I. Goldberg

Keyword(s):

Blood Flow ◽

Renal Artery ◽

Renal Blood Flow ◽

Intravenous Infusion ◽

Sch 23390 ◽

Receptor Subtypes ◽

Base Line ◽

Electrolyte Excretion ◽

Pentobarbital Sodium ◽

Before And After

Dopamine (DA) acts on two receptor subtypes, DA1 and DA2. The purpose of this study was to determine which subtype is involved in the increments in renal blood flow (RBF) and electrolyte excretion produced by DA. Mongrel dogs were anesthetized with pentobarbital sodium. Phenoxybenzamine (10 mg X kg-1 ia) and propranolol (5 mg X kg-1 iv) were administered to exclude effects mediated by alpha- and beta-adrenoceptors. DA was infused into the renal artery before and after administration of either the selective DA1 antagonist SCH 23390 or the selective DA2 antagonist domperidone. With DA alone, RBF increased by 52 +/- 7%, Na+ excretion increased by 35 +/- 8%, and K+ excretion increased by 35 +/- 5%. Infusion of SCH 23390 (0.5 micrograms X kg-1 X min-1) completely blocked DA-induced increase in RBF and electrolyte excretion. Intravenous infusion of domperidone (1 microgram X kg-1 X min-1) did not attenuate the responses to DA. Neither SCH 23390 nor domperidone affected base-line RBF or electrolyte excretion, suggesting that in these experiments endogenous DA was not active. In conclusion, these data indicate that the effects of DA to increase RBF and electrolyte excretion are the result of action on DA1 receptors.

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