A novel method for infusing drugs continuously into the renal artery of rats

1995 ◽  
Vol 268 (5) ◽  
pp. F967-F971 ◽  
Author(s):  
N. Parekh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Kidney Volume ◽  
Membrane Pump ◽  
Arterial Blood ◽  
Novel Method ◽  
Kidney Functions ◽  
Higher Doses

A method is described to achieve a homogeneous intravascular distribution of drugs infused into the renal artery of anesthetized rats. The device for intrarenal infusion consisted of a multiple-catheter system with a cannula inserted into the renal artery, which was connected to different lines for drug infusions and to one line for oscillating blood back and forth in the renal cannula with a magnetic membrane pump. The blood oscillation served to mix the drugs with renal arterial blood. To verify the usefulness of this procedure, Lissamine green was infused into the renal artery; without the mixing pump the dye was located on a small portion of the kidney surface, whereas the dye could be visualized evenly distributed and less concentrated over the entire kidney with the pump. With the mixing device, intrarenal infusion of angiotensin II, 5 pmol.kg-1.min-1, or norepinephrine, 150 pmol.kg-1.min-1, reduced renal blood flow by approximately 25% without affecting blood pressure. Tenfold higher doses given intravenously had comparable renal effects, but these increased systemic pressure. Without the mixing pump, vasoactive drugs given into the renal artery had a distinctly smaller effect on renal blood flow than with the pump (angiotensin II, 39%; norepinephrine, 49%; and acetylcholine, at 5 nmol.kg-1.min-1, 33%). The results show that intrarenally infused drugs, without a mixing device, have access to an unpredictably small kidney volume, and estimation of their effects on kidney functions can be equivocal. The present device ensures an adequate mixing of drugs with renal blood.

Characterization of the postocclusive response of renal blood flow in the cat

1978 ◽  
Vol 235 (4) ◽  
pp. F286-F290 ◽  
Author(s):  
W. S. Spielman ◽  
H. Osswald
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Artery Occlusion ◽  
Renal Nerves ◽  
Vasoconstrictor Response ◽  
Renal Artery Occlusion ◽  
Chronic Denervation

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

Abstract 1785: Renal Artery Angioplasty Improves Diastolic Cardiac Function In Patients With heart failure Possessing Renal Artery Stenosis.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eisei Yamamoto ◽  
Hitoshi Takano ◽  
Hiroyuki Tajima ◽  
Jun Tanabe ◽  
Hidekazu Kawanaka ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Function ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Renal Artery Stenosis ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Diastolic Cardiac Function

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.

Aortic blood flow subtraction: an alternative method for measuring total renal blood flow in conscious dogs

2002 ◽  
Vol 282 (5) ◽  
pp. R1528-R1535 ◽  
Author(s):  
N. C. F. Sandgaard ◽  
J. L. Andersen ◽  
N.-H. Holstein-Rathlou ◽  
P. Bie
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Aortic Blood Flow ◽  
Excretory Function ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Bilateral Carotid ◽  
Total Renal Blood Flow

We have measured total renal blood flow (TRBF) as the difference between signals from ultrasound flow probes implanted around the aorta above and below the renal arteries. The repeatability of the method was investigated by repeated, continuous infusions of angiotensin II and endothelin-1 seven times over 8 wk in the same dog. Angiotensin II decreased TRBF (350 ± 16 to 299 ± 15 ml/min), an effect completely blocked by candesartan (TRBF 377 ± 17 ml/min). Subsequent endothelin-1 infusion reduced TRBF to 268 ± 20 ml/min. Bilateral carotid occlusion (8 sessions in 3 dogs) increased arterial blood pressure by 49% and decreased TRBF by 12%, providing an increase in renal vascular resistance of 69%. Dynamic analysis showed autoregulation of renal blood flow in the frequency range <0.06–0.07 Hz, with a peak in the transfer function at 0.03 Hz. It is concluded that continuous measurement of TRBF by aortic blood flow subtraction is a practical and reliable method that allows direct comparison of excretory function and renal blood flow from two kidneys. The method also allows direct comparison between TRBF and flow in the caudal aorta.

Renal vascular and excretory responses to prostaglandin endoperoxides in the dog

1979 ◽  
Vol 236 (3) ◽  
pp. H427-H433
Author(s):  
J. A. Oliver ◽  
R. R. Sciacca ◽  
P. J. Cannon
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Biologically Active ◽  
Direct Effects ◽  
Cortical Areas ◽  
Anesthetized Dogs ◽  
Renal Vascular ◽  
Higher Doses

To determine whether the prostaglandin endoperoxides PGG2 and PGH2 have direct effects in the kidney, PGG2 and PGH2 were administered into the renal artery of anesthetized dogs and their effects were compared to those of PGE2. Like PGE2, PGG2 and PGH2 induced a dose-related renal vasodilation. A 50% increase in the renal blood flow was observed with 0.05 microgram/kg body wt of PGE2 and with four- and sixfold higher doses of PGH2 and PGG2, respectively. Infusion of all three compounds at doses inducing a 50% increase in the renal blood flow resulted in 1) increases in blood flow to all cortical areas, with the greatest increase occurring in the juxtamedullary area, 2) diuresis with no change in the glomerular filtration rate, and 3) natriuresis and kaliuresis. In vitro incubation of PGH2, a maneuver known to result in its conversion to other prostaglandins, had no influence on its renal effects. The data indicate that PGH2 and PGG2 are biologically active when infused into the renal artery of the anesthetized dog and suggest that the endoperoxides exert their effects after bioconversion to other prostaglandins.

Hemodynamic responses to dopamine and to isoproterenol following acute myocardial injury

1969 ◽  
Vol 47 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Keith L. MacCannell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Myocardial Injury ◽  
Left Renal Artery ◽  
Arterial Blood ◽  
Acute Myocardial Injury ◽  
Cardiac Slowing ◽  
Anesthetized Dogs ◽  
Higher Doses

Severe myocardial injury was produced in eight anesthetized dogs by the injection of microspheres into the coronary circulation. Cardiac output and renal blood flow were monitored continuously with electromagnetic flow probes around the ascending thoracic aorta and left renal artery respectively. Intravenous infusions of isoproterenol and of dopamine (0.01–0.64 and 0.4–32.0 μg/kg per minute respectively) produced an increase in the cardiac output. Renal blood flow increased with small doses of isoproterenol but tended to decrease with higher doses; in contrast, all doses of dopamine increased renal blood flow. Dopamine was more effective in raising the systemic arterial blood pressure, but also increased cardiac work. Occasional extrasystoles were induced at higher doses of both amines. In three unanesthetized dogs sensitized by prior ligation of a coronary artery, the largest doses of dopamine tested (24–64 μg/kg per minute) did not produce cardiac arrhythmias. However, when dopamine was given to anesthetized dogs during vagal-induced cardiac slowing (a condition conducive to the emergence of ventricular automaticity), arrhythmias were induced. These data suggest that dopamine can increase both cardiac output and renal blood flow after severe myocardial injury, and may be a rational agent in the treatment of cardiogenic shock. Its arrhythmogenic properties would not appear to restrict its use.

scholarly journals Pre-treatment with the angiotensin receptor 1 blocker losartan protects renal blood flow and oxygen delivery after propofol-induced hypotension in pigs

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephanie Franzén ◽  
Robert Frithiof
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Oxygen Delivery ◽  
Induced Hypotension ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Pre Treatment ◽  
Renal Oxygen

Abstract Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. We hypothesised that anaesthesia-induced hypotension causes renal vasoconstriction and decreased oxygen delivery via angiotensin II-mediated renal vasoconstriction. Pigs were anaesthetised, surgically prepared and randomised to vehicle/losartan treatment (0.15 mg*kg−1). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mg*kg−1) for 10 min. Renal function and haemodynamics were recorded 60 min before and after hypotension. Propofol induced hypotension in all animals (p < 0.001). Renal blood flow (RBF) and renal oxygen delivery (RDO2) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). During recovery RBF and RDO2 improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 ml*min−1, 95%CI 8–50 ml*min−1, p = 0.01 and + 3.1 ml*min−1, 95%CI 0.3–5.8 ml*min−1, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO2 remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO2 had normalised. Pre-treatment with losartan improved recovery of renal blood flow and renal oxygen delivery after propofol-induced hypotension, suggesting pronounced angiotensin II-mediated renal vasoconstriction during blood pressure reductions caused by anaesthesia.

Differential renal effects of cyclooxygenase inhibition in sodium-replete and sodium-deprived dog

1980 ◽  
Vol 239 (4) ◽  
pp. F360-F365 ◽  
Author(s):  
M. Cynthia Blasingham ◽  
Alberto Nasjletti
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Receptor Blocker ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renal Effects ◽  
Renin Angiotensin ◽  
Arterial Blood

We studied the renal effects of the cyclooxygenase inhibitor sodium meclofenamate (M) (5 mg/kg, iv) in the pentobarbital-anesthetized dog that had been maintained on an elevated (100 meq/day) or on a reduced (<5 meq/day) sodium intake, and during the administration of angiotensin II in the sodium-replete dog, or the angiotensin receptor blocker [Sar1–Ala8]angiotensin II in the sodium-deprived dog. In the sodium-replete dog, M did not affect mean arterial blood pressure (MABP), renal blood flow (RBF), glomerular filtration rate (GFR), or urine volume (V), but reduced the urinary excretion of sodium (UNa V) by 47%, and of immunoreactive PGE2 (iPGE2) by 90%. However, in the sodium-replete dog during angiotensin II infusion (3 ng · kg-1 · min-1, iv), M reduced RBF by 35%, GFR by 24%, V by 71%, and iPGE2m by 94%. Similarly, in the sodium-deprived dog M reduced RBF by 34%, GFR by 28%, and iPGE2 excretion by 89%. However, M did not affect RBF or GFR in the sodium-deprived dog during infusion of [Sar1-Ala8]angiotensin II (6 μg · kg-1 · min-1, iv), although iPGE2 excretion was reduced by 84%. This study demonstrates that the effects of M on renal hemodynamics in the dog vary with the state of sodium balance and suggests that a prostaglandin(s) contributes to maintenance of renal blood flow during activation of the renin-angiotensin system. meclofenamate; renal prostaglandins; renin-angiotensin system; receptor blocker; renal hemodynamic and excretory function Submitted on October 17, 1979 Accepted on May 9, 1980

Renal blood flow changes in contralateral kidney of Goldblatt hypertensive dog

1981 ◽  
Vol 241 (2) ◽  
pp. H145-H148
Author(s):  
B. G. Zimmerman ◽  
C. Mommsen
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

Sequential changes in systemic arterial blood pressure (BP), renal blood flow (RBF) in the contralateral kidney, and plasma renin activity (PRA) were examined on conscious dogs with construction of a single renal artery (RAC). An increase of 24 mmHg in bP occurred within 2 days after RAC, and BP later plateaued at a lower level. RBF in the contralateral kidney transiently increased by 24% and then returned to the control level in 11-14 days. PRA also peaked early after RAC and then returned to control. The clamp was tightened and the renal artery was occluded (RAO) 3-20 days after RAC. BP, RBF, and PRA increased to an even greater degree than after RAC. BP peaked at 145 mmHg, and RBF increased 61.5% at 2-3 days after RAO. BP and RBF both decreased but remained above the control for the duration of the study, BP at 127 mmHg and RBF at 256 ml/min. RBF per gram for the hypertrophied contralateral kidney was calculated from the RBF before death and the weight at death. The final RBF per gram of the contralateral kidney (2.7 ml.min-1.g-1) decreased and renal vascular resistance increased compared with the estimated control RBF/g (3.7 ml.min-1.g-1) and renal vascular resistance. These results suggest that the final RBF of the contralateral kidney is not increased in proportion to its increase in weight and that it may be relatively hypoperfused in two-kidney one-clip Goldblatt hypertension.

Vasodilator capacity of contralateral kidney in Goldblatt hypertensive dog

1983 ◽  
Vol 245 (5) ◽  
pp. H790-H795
Author(s):  
B. G. Zimmerman ◽  
R. D. Largent
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Control Level ◽  
Plasma Renin ◽  
Artery Occlusion ◽  
Angiotensin I ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Artery Occlusion

Because of previous suggestions of impaired renal blood flow in the contralateral kidney of Goldblatt hypertensive animals, we examined the maximal vasodilator capacity of the contralateral kidney in 13 instrumented dogs during progression of Goldblatt hypertension. Constriction of a single renal artery (RAC) followed a week or more later by total renal artery occlusion (RAO) increased mean arterial blood pressure (BP) from a control level of 102 +/- 3 to 135 +/- 7 mmHg (P less than 0.001) and increased plasma renin activity (PRA) from 0.69 +/- 0.16 to 10.2 +/- 3.9 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at 2 wk after RAO. The hypertension was accompanied by an increase in basal renal blood flow (RBF) from 224 +/- 21 to 300 +/- 27 ml/min (P less than 0.01) and RBF at maximal vasodilatation from 505 +/- 24 to 673 +/- 52 ml/min (P less than 0.05). Hypertension and the increase in PRA waned, but BP remained higher than control at 4 wk after RAO (117 +/- 6 mmHg, P less than 0.005). Basal and maximal RBF were sustained at the higher levels throughout the 4-wk period after RAO. When RBF was expressed on a per gram basis, basal and maximal flow before (3.72 +/- 0.40 and 8.26 +/- 0.62 ml X min-1 X g-1, respectively) did not differ from that in the final experiment after RAO (3.85 +/- 0.34 and 8.19 +/- 0.78 ml X min-1 X g-1). The basal and minimal vascular resistances based on flow per gram were increased by 24 +/- 8 and 41 +/- 16% (P less than 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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