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.

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.

scholarly journals Estimation of changes in instantaneous aortic blood flow by the analysis of arterial blood pressure

2012 ◽  
Vol 112 (11) ◽  
pp. 1832-1838 ◽  
Author(s):  
Tatsuya Arai ◽  
Kichang Lee ◽  
Robert P. Marini ◽  
Richard J. Cohen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Arterial Blood Pressure ◽  
Aortic Blood Flow ◽  
Windkessel Model ◽  
Arx Model ◽  
Arterial Blood ◽  
Aortic Blood

The purpose of this study was to introduce and validate a new algorithm to estimate instantaneous aortic blood flow (ABF) by mathematical analysis of arterial blood pressure (ABP) waveforms. The algorithm is based on an autoregressive with exogenous input (ARX) model. We applied this algorithm to diastolic ABP waveforms to estimate the autoregressive model coefficients by requiring the estimated diastolic flow to be zero. The algorithm incorporating the coefficients was then applied to the entire ABP signal to estimate ABF. The algorithm was applied to six Yorkshire swine data sets over a wide range of physiological conditions for validation. Quantitative measures of waveform shape (standard deviation, skewness, and kurtosis), as well as stroke volume and cardiac output from the estimated ABF, were computed. Values of these measures were compared with those obtained from ABF waveforms recorded using a Transonic aortic flow probe placed around the aortic root. The estimation errors were compared with those obtained using a windkessel model. The ARX model algorithm achieved significantly lower errors in the waveform measures, stroke volume, and cardiac output than those obtained using the windkessel model ( P < 0.05).

Failure of acute saralasin to reverse chronic hypertension in fetal lambs

1991 ◽  
Vol 260 (4) ◽  
pp. R811-R816
Author(s):  
D. F. Anderson ◽  
N. D. Binder
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Upper Body ◽  
Chronic Hypertension ◽  
Aortic Blood Flow ◽  
Flow Reduction ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Blood Flow Reduction

Upper body arterial hypertension developed in 12 fetal lambs after chronic suprarenal aortic blood flow reduction. Sixty minutes after blood flow reduction, intravenous saralasin infusion was able to reduce upper body mean arterial blood pressure to control levels. Although saralasin infusion was able to decrease upper body arterial blood pressure after 1 day of hypertension, it was not able to return blood pressure to control levels. Three or more days later, saralasin was unable to cause a significant reduction in upper body arterial blood pressure. We conclude that, although the renin-angiotensin system has a role in maintaining the elevated blood pressure after greater than or equal to 1 day of suprarenal aortic blood flow reduction, some other mechanism also participates. We have ruled out a role for changing blood volume, and our results suggest that an elevation of plasma catecholamines is not responsible. Some other pathway for fluid regulation available to the fetus may be responsible.

scholarly journals Nitric oxide–endothelin-1 interaction in humans

1997 ◽  
Vol 82 (5) ◽  
pp. 1593-1600 ◽  
Author(s):  
Gunvor Ahlborg ◽  
Jan M. Lundberg
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Metabolic Effects ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Glucose Output ◽  
Change In Mean

Ahlborg, Gunvor, and Jan M. Lundberg. Nitric oxide–endothelin-1 interaction in humans. J. Appl. Physiol. 82(5): 1593–1600, 1997.—Healthy men received N G-monomethyl-l-arginine (l-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1.l-NMMA effects were that heart rate (17%), cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean arterial blood pressure (6%), and systemic (28%) and pulmonary (40%) vascular resistances increased ( P < 0.05 to 0.001). Arterial ET-1 levels (21%) increased due to a pulmonary net ET-1 release ( P < 0.05 to 0.01). Splanchnic glucose output (SGO) fell (26%, P < 0.01). Arterial insulin and glucagon were unchanged. Subsequent ET-1 infusion caused no change in mean arterial pressure, heart rate, or cardiac output, as found in the present controls, or in splanchnic and renal blood flow or splanchnic glucose output as previously found with ET-1 infusion (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 79: 141–145, 1995). In conclusion, l-NMMA like ET-1, induces prolonged cardiovascular effects and suppresses SGO.l-NMMA causes pulmonary ET-1 release and blocks responses to ET-1 infusion. The results indicate that nitric oxide inhibits ET-1 production and thereby interacts with ET-1 regarding increase in vascular tone and reduction of SGO in humans.

Aortic Stiffening, Aortic Blood Flow Reversal, and Renal Blood Flow

Hypertension ◽  
2015 ◽  
Vol 66 (1) ◽  
pp. 10-12 ◽  
Author(s):  
Stéphane Laurent ◽  
Pierre Boutouyrie ◽  
Elie Mousseaux
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Flow Reversal ◽  
Aortic Blood Flow ◽  
Aortic Blood ◽  
Aortic Stiffening

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.

Intrarenal vascular effects of angiotensin I and angiotensin II

1981 ◽  
Vol 240 (6) ◽  
pp. H914-H919
Author(s):  
S. L. Britton
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Left Renal Artery ◽  
Angiotensin I ◽  
Vascular Effects ◽  
Cortical Blood Flow ◽  
Blood Flows ◽  
Renal Cortical Blood Flow ◽  
Total Renal Blood Flow

The effects of angiotensin I (250 pmol) and angiotensin II (7.5 pmol) on total renal blood flow and its cortical distribution were examined in 25 dogs anesthetized with pentobarbital. These peptides were administered as bolus injections directly into the left renal artery. Right and left renal blood flows were measured with noncannulating electromagnetic flow probes. The distribution of renal cortical blood flow was measured with 15-micrometers radioactive microspheres. Because angiotensin I is converted to angiotensin II extrarenally as well as intrarenally, the distribution of renal blood flow in response to the bolus injection of angiotensin agonists was measured before these peptides could have recirculated through the kidney. This maneuver precluded the possibility that blood flow changes were due to the extrarenal formation of vasoactive metabolites of angiotensin I or angiotensin II. Control total renal blood flow averaged 3.0 +/- 0.1 ml.min-1.g kidney wt-1 and was decreased 25% by both angiotensin I and angiotensin II. Outer renal cortical flow (zone I) was 5.1 +/- 0.3 ml.min-1.g-1 and was decreased to 3.9 +/- 0.3 ml.min-1.g-1 by both angiotensin I and angiotensin II. On the average, angiotensin I decreased inner cortical renal blood flow from a control of 1.8 +/- 0.2 to 1.2 +/- 0.2 ml.min-1.g-1; angiotensin II decreased inner cortical renal blood flow from a control of 1.9 +/- 0.2 to 1.4 +/- 0.2 ml.min-1.g-1. Analysis on a per-experiment basis revealed that angiotensin I, compared with angiotensin II, produced a proportionally greater decrease in inner cortical renal blood flow relative to its effects on outer cortical blood flow.

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

Effects of Saralasin Infusion on Bilateral Renal Function in Two-Kidney, One-Clip Goldblatt Hypertensive Rats

1982 ◽  
Vol 62 (6) ◽  
pp. 573-579 ◽  
Author(s):  
Wann-Chu Huang ◽  
D. W. Ploth ◽  
L. G. Navar
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Renal Vascular

1. Previous studies have shown that administration of converting enzyme inhibitor (CEI, SQ 20 881) to two-kidney, one-clip Goldblatt hypertensive (GH) rats clipped for 3–4 weeks resulted in marked increases in glomerular filtration rate (GFR), water and sodium excretion by the non-clipped kidneys. The clipped kidneys exhibited reduced function that was due, in part, to the reductions in arterial pressure. To evaluate further the hypothesis that the renal responses to CEI were due primarily to the inhibition of angiotensin II rather than other factors, we infused the angiotensin II competitive blocker, saralasin, into GH rats under sodium pentobarbital anaesthesia and examined renal haemodynamics and excretory function of each kidney before and during saralasin infusion and after cessation of saralasin infusion. 2. Saralasin reduced mean arterial blood pressure from 164 ± 4 to 124 ± 4 mmHg. Despite the profound fall of arterial pressure, significant increases in renal blood flow from 5.82 ± 0.22 to 9.15 ± 0.76 ml/min and glomerular filtration rate from 1.46 ± 0.10 to 2.18 ± 0.14 ml/min were observed in the non-clipped kidneys. Renal vascular resistance decreased from 2.34 (± 0.14) × 105 to 1.17 (± 0.19) × 105 kPa l−1 s [2.34 (± 0.14) × 106 to 1.17 (± 0.19) × 106 dyn s cm−5]. Also, concomitant diuresis and kaliuresis and a delayed natriuresis occurred. Correspondence: Dr L. G. Navar, University of Alabama in Birmingham Medical Center, University Station, 727 CDLD Bldg, Birmingham, Alabama 35294, U.S.A. 3. The clipped kidneys exhibited reductions in renal blood flow, GFR and excretory function during saralasin infusion. 4. Normal rats receiving the identical dose of saralasin responded with a slight but significant decrease in arterial pressure. The increases in renal blood flow and GFR were less than those observed in the non-clipped kidneys of hypertensive rats. 5. These data provide further support to the hypothesis that an angiotensin II-mediated elevation in renal vascular resistance and impairment of renal function exist in the non-clipped kidneys of GH rats.

Differing effects of anesthetics on splanchnic arterial blood flow during hemorrhagic shock

1994 ◽  
Vol 76 (6) ◽  
pp. 2304-2309 ◽  
Author(s):  
S. I. Myers ◽  
R. Hernandez ◽  
T. A. Miller
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Arterial Blood Flow ◽  
Splanchnic Blood Flow ◽  
Aortic Blood Flow ◽  
Sprague Dawley ◽  
Acute Hemorrhage ◽  
Shed Blood ◽  
Arterial Blood ◽  
Aortic Blood

The effect of anesthesia on splanchnic blood flow was examined during hemorrhagic shock and resuscitation. Sprague-Dawley rats were anesthetized with the inhalation anesthetic, methoxyflurane, or pentobarbital (65 mg/kg). Transonic Doppler flow probes were placed around the superior mesenteric artery (SMA) and the abdominal aorta, and the animals were subjected to acute hemorrhage (or sham) to 30 mmHg for 90 min followed by 30 min of resuscitation with shed blood (n = 6/group). At 90, 105, and 120 min, sham animals in both anesthetic groups showed comparable blood pressures with a 50% decrease in SMA and aortic blood flow. Acute hemorrhage decreased SMA blood flow by 94.5 +/- 0.01 and 86.0 +/- 2.8%, respectively, in the pentobarbital and methoxyflurane groups, with similar changes occurring in aortic blood flow. During resuscitation, arterial pressure remained significantly depressed and SMA blood flow decreased by 65% in the pentobarbital group, whereas blood pressure returned to control levels and SMA blood flow increased to 56% of control values (P < 0.001) in the methoxyflurane group. The findings indicate that the choice of anesthetic agent may significantly impact splanchnic blood flow and needs to be taken into account when designing experiments examining effects of hemorrhagic shock.

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