Renal 131I-hippurate clearance overestimates true renal blood flow in the instrumented conscious dog

1996 ◽  
Vol 271 (2) ◽  
pp. F269-F274 ◽  
Author(s):  
C. A. Visscher ◽  
D. De Zeeuw ◽  
G. Navis ◽  
A. K. Van Zanten ◽  
P. E. De Jong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Artery Blood Flow ◽  
Venous Outflow ◽  
Flow Probe ◽  
The Difference ◽  
Probe Calibration ◽  
Clearance Technique ◽  
Venous Plasma

We evaluated renal 131I-hippurate clearance (ERPFhip) as a measure of renal blood flow (RBF) in chronically instrumented conscious dogs. When adjusted for renal hippurate extraction (Ehip, 0.77 +/- 0.01) and hematocrit (Hct, 39.7 +/- 1%), calculated RBFhip (656 +/- 37 ml/min) markedly exceeded renal blood flow measured with renal artery blood flow probes (RBFprobe, 433 +/- 27 ml/min). The discrepancy could not be explained by flow probe calibration, because in vivo comparison of flow probe values with renal venous outflow showed only a slight underestimation of renal blood flow (slope 0.93, 95% confidence interval 0.89-0.97). Redistribution of hippurate from erythrocytes into renal venous plasma during or shortly after blood sampling led to an underestimation of Ehip by 4 +/- 1% and thus could only explain a small part of the difference. Extrarenal hippurate clearance was excluded, because the amount of 131I-hippurate cleared from plasma equaled that appearing in the urine (303 +/- 17 and 307 +/- 17 ml/min). Applying these corrections, we found that RBFhip still exceeded RBFprobe by 37 +/- 3%. These data indicate that renal blood flow measured by the hippurate clearance technique markedly overestimates true renal blood flow. Because other errors were excluded, a combination of sampling of nonrenal blood and intrarenal hippurate extraction from erythrocytes might play a role.

Abstract 062: Regulation of Nephron Afferent Arteriole Resistance in Obesity: Role of Connecting Tubule Glomerular Feedback

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sumit R Monu ◽  
Mani Maheshwari ◽  
Hong Wang ◽  
Ed Peterson ◽  
Oscar Carretero
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Tubuloglomerular Feedback ◽  
Afferent Arteriole ◽  
Connecting Tubule ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
The Difference

In obesity, renal damage is caused by increase in renal blood flow (RBF), glomerular capillary pressure (P GC ), and single nephron glomerular filtration rate but the mechanism behind this alteration in renal hemodynamics is unclear. P GC is controlled mainly by the afferent arteriole (Af-Art) resistance. Af-Art resistance is regulated by mechanism similar to that in other arterioles and in addition, it is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to an increase in sodium chloride (NaCl) in the macula densa, via sodium–potassium-2-chloride cotransporter-2 (NKCC2) and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation and is mediated by connecting tubule via epithelial sodium channel (ENaC). CTGF is blocked by the ENaC inhibitor benzamil. Attenuation of TGF reduces Af-Art resistance and allows systemic pressure to get transmitted to the glomerulus that causes glomerular barotrauma/damage. In the current study, we tested the hypothesis that TGF is attenuated in obesity and that CTGF contributes to this effect. We used Zucker obese rats (ZOR) while Zucker lean rats (ZLR) served as controls. We performed in-vivo renal micropuncture of individual rat nephrons while measuring stop-flow pressure (P SF ), an index of P GC. TGF response was measured as a decrease in P SF induced by changing the rate of late proximal perfusion from 0 to 40nl/min in stepwise manner.CTGF was calculated as the difference of P SF value between vehicle and benzamil treatment, at each perfusion rate. Maximal TGF response was significantly less in ZOR (6.16 ± 0.52 mmHg) when compared to the ZLR (8.35 ± 1.00mmHg), p<0.05 , indicating TGF resetting in the ZOR. CTGF was significantly higher in ZOR (6.33±1.95 mmHg) when compared to ZLR (1.38±0.89 mmHg), p<0.05 . When CTGF was inhibited with the ENaC blocker Benzamil (1μM), maximum P SF decrease was 12.30±1.72 mmHg in ZOR and 10.60 ± 1.73 mmHg in ZLR, indicating that blockade of CTGF restored TGF response in ZOR. These observations led us to conclude that TGF is reset in ZOR and that enhanced CTGF contributes to this effect. Increase in CTGF may explain higher renal blood flow, increased P GC and higher glomerular damage in obesity.

scholarly journals Simplified measurement of intra-access pressure.

1998 ◽  
Vol 9 (2) ◽  
pp. 284-289
Author(s):  
A Besarab ◽  
S Frinak ◽  
R A Sherman ◽  
J Goldman ◽  
F Dumler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Delivery Systems ◽  
Chamber Pressure ◽  
Hemodialysis Access ◽  
Fluid Density ◽  
Special Equipment ◽  
Venous Outflow ◽  
Bernoulli’S Equation ◽  
The Difference ◽  
Zero Flow

The measurement of intra-access pressure (P[IA]) normalized by mean arterial BP (MAP) helps detect venous outlet stenosis and correlates with access blood flow. However, general use of P(IA)/MAP is limited by time and special equipment costs. Bernoulli's equation relates differences between P(IA) (recorded by an external transducer as PT) and the venous drip chamber pressure, PDC; at zero flow, the difference in height (deltaH) between the measuring sites and fluid density determines the pressure deltaPH = P(IA) - P(DC) Therefore, P(DC) and PT measurements were correlated at six different dialysis units, each using one of three different dialysis delivery systems machines. Both dynamic (i.e., with blood flow) and static pressures were measured. Changes in mean BP, zero calibration errors, and hydrostatic height between the transducer and drip chamber accounted for 90% of the variance in P(DC), with deltaPH = -1.6 + 0.74 deltaH (r = 0.88, P < 0.001). The major determinants of static P(IA)/MAP were access type and venous outflow abnormalities. In grafts, flow averaged 555 +/- 45 ml/min for P(IA)/MAP > 0.5 and 1229 +/- 112 ml/min for P(IA)/MAP < 0.5. DeltaPH varied from 9.4 to 17.4 mmHg among the six centers and was related to deltaH between the drip chamber and the armrest of the dialysis chair. Concordance between values of P(IA)/MAP calculated from PT and from P(DC) + deltaPH was excellent. It is concluded that static P(DC) measurements corrected by an appropriate deltaPH can be used to prospectively monitor hemodialysis access grafts for stenosis.

scholarly journals Quantification of coronary microvascular resistance using angiographic images for volumetric blood flow measurement: in vivo validation

2011 ◽  
Vol 300 (6) ◽  
pp. H2096-H2104 ◽  
Author(s):  
Zhang Zhang ◽  
Shigeho Takarada ◽  
Sabee Molloi
Keyword(s):  
Blood Flow ◽  
Swine Model ◽  
Distribution Analysis ◽  
Flow Probe ◽  
Flow Measurements ◽  
First Pass ◽  
Microvascular Resistance ◽  
Time Density ◽  
In Vivo Validation

Structural coronary microcirculation abnormalities are important prognostic determinants in clinical settings. However, an assessment of microvascular resistance (MR) requires a velocity wire. A first-pass distribution analysis technique to measure volumetric blood flow has been previously validated. The aim of this study was the in vivo validation of the MR measurement technique using first-pass distribution analysis. Twelve anesthetized swine were instrumented with a transit-time ultrasound flow probe on the proximal segment of the left anterior descending coronary artery (LAD). Microspheres were injected into the LAD to create a model of microvascular dysfunction. Adenosine (400 μg·kg−1·min−1) was used to produce maximum hyperemia. A region of interest in the LAD arterial bed was drawn to generate time-density curves using angiographic images. Volumetric blood flow measurements (Qa) were made using a time-density curve and the assumption that blood was momentarily replaced with contrast agent during the injection. Blood flow from the flow probe (Qp), coronary pressure (Pa), and right atrium pressure (Pv) were continuously recorded. Flow probe-based normalized MR (NMRp) and angiography-based normalized MR (NMRa) were calculated using Qp and Qa, respectively. In 258 measurements, Qa showed a strong correlation with the gold standard Qp (Qa = 0.90 Qp + 6.6 ml/min, r2 = 0.91, P < 0.0001). NMRa correlated linearly with NMRp (NMRa = 0.90 NMRp + 0.02 mmHg·ml−1·min−1, r2 = 0.91, P < 0.0001). Additionally, the Bland-Altman analysis showed a close agreement between NMRa and NMRp. In conclusion, a technique based on angiographic image data for quantifying NMR was validated using a swine model. This study provides a method to measure NMR without using a velocity wire, which can potentially be used to evaluate microvascular conditions during coronary arteriography.

Abstract 529: Statin Therapy Decreases Vascular Inflammation and Prolongs Patency in Murine Arteriovenous Fistula

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Jie Cui ◽  
Harkamal S Jhajj ◽  
Chase W Kessinger ◽  
Jason McCarthy ◽  
Farouc A Jaffer
Keyword(s):  
Blood Flow ◽  
Statin Therapy ◽  
Inflammatory Cell ◽  
Vascular Inflammation ◽  
Neointimal Hyperplasia ◽  
Venous Outflow ◽  
Statin Group ◽  
Cellular Inflammation ◽  
Anti Inflammatory

Background: AVFs are the lifeline of dialysis patients, but can often occlude. The most common cause of AVF failure is inflammation-driven neointimal hyperplasia and thrombosis. Here, we investigated whether statin therapy with well-recognized anti-inflammatory properties can improve murine AVF patency, and further assessed the anti-inflammatory effects. Methods: One week prior to AVF creation, mice were randomized to oral atorvastatin 1.14mg/kg/day or control 100ul PBS (both n=10), administered by daily gavage. AVF were created using an end-to-side internal jugular vein and carotid artery anastomosis. AVF blood flow was measured (Transonic blood flow probe) at day 0 and weekly thereafter until occlusion (blood flow < 0.1ml/min). On day 6, CLIO-VT680, an inflammatory cell-targeted fluorescent nanoparticle, was injected intravenously (10mg/kg). 24 hours later, in vivo survival epifluorescence molecular imaging was performed to visualize inflammatory cell in the AVF venous outflow limb. Histopathological assessment of AVF was performed in on day 7 and 14 mice (6 statin each, 6 control each) to assess venous outflow area, AVF scarring via collagen, and adventitial macrophage content. Results: At day 7, the in vivo venous outflow cellular inflammation signal (CLIO-VT680 TBR) was significantly lower in statin-treated mice (3.5±0.16 vs 4.5±0.5 PBS, p=0.02). Adventitial macrophage content was significantly lower in statin group at day 14 (p=0.01). Positive AVF remodeling, a desirable feature for clinical AVF patency, was higher in the statin group as compared to the PBS group (p=0.02 at week 1, p=0.002 at week 2). In vivo, statin-treated animals exhibited greater AVF blood flow (BF) preservation from day 7 to day 14 (ΔAVF BF +0.14±0.2 ml/min vs. -0.79±0.32 ml/min PBS, p=0.02). The ΔAVF BF from day 7 to day 14 correlated inversely and significantly with the day 7 CLIO-VT680 cellular inflammation (r=-0.56, p=0.02), indicating that baseline inflammation may predict AVF failure. Kaplan Meier survival analysis showed median AVF patency in mice treated with statin was 28 days compared to 14 days in PBS treated group (p<0.05). Conclusion: Statin therapy prolongs AVF patency and preserves AVF blood flow in association with diminished AVF cellular inflammation.

Adrenocortical metabolism of angiotensin in sheep with adrenal transplants.

1978 ◽  
Vol 235 (5) ◽  
pp. E525
Author(s):  
S Lun ◽  
E A Espiner ◽  
D S Hart
Keyword(s):  
Blood Flow ◽  
Adrenal Gland ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Adrenal Tissue ◽  
Rate Analysis ◽  
Venous Plasma

Conscious trained sheep with adrenal gland autotransplants in cervical skin loops were used to study adrenocortical metabolism and clearance of angiotensin (AII) administered by constant systemic infusion. For comparative purposes similar experiments were undertaken in five control sheep with skin loops but no cervical adrenal tissue. During AII infusions (0.33 microgram/min for 30 min), loop venous-arterial AII ratios (0.42--0.62 were similar in both groups of sheep. Measured AII clearances across the skin loop in sheep with and without adrenal transplants were 400--600 and 100--150 pg/min, respectively, which correlated with blood flow (r = 0.79), but showed no relation to aldosterone secretion rate. Analysis of AII immunoreactive fragments showed similar proportions of octa-, hepta-, and hexapeptide fractions (64, 26, and 5%, respectively) in adrenal arterial, adrenal venous, and systemic venous plasma. These studies do not support selective heptapeptide uptake or metabolism by adrenal tissue in vivo and indicate that specific adrenal binding of AII is likely to be less than 400 pg/min at arterial AII concentrations approximating 120 pg/ml.

scholarly journals Measuring peripheral resistance and conduit arterial structure in humans using Doppler ultrasound

2005 ◽  
Vol 98 (6) ◽  
pp. 2311-2315 ◽  
Author(s):  
Louise H. Naylor ◽  
Cara J. Weisbrod ◽  
Gerry O'Driscoll ◽  
Daniel J. Green
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Peripheral Resistance ◽  
Artery Blood Flow ◽  
Brachial Artery Diameter ◽  
Resistance Vessel ◽  
Conduit Artery ◽  
Significant Difference ◽  
Vessel Structure

The purpose of this study was to establish valid indexes of conduit and resistance vessel structure in humans by using edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit artery blood flow and diameter continuously across the cardiac cycle. Nine subjects aged 36.7 (9.2) yr underwent, on separate days, assessment of brachial artery blood flow and diameter response to 5-, 10-, and 15-min periods of forearm ischemia in the presence and absence of combined sublingual glyceryl trinitrate (GTN) administration. Two further sessions examined responses to ischemic exercise, one in combination with GTN. The peak brachial artery diameter was observed in response to the combination of ischemic exercise and GTN; a significant difference existed between resting brachial artery diameter and peak brachial artery diameter, indicating that resting diameter may be a poor measure of conduit vessel structure in vivo. Peak brachial artery flow was also observed in response to a combination of forearm ischemia exercise and GTN administration, the response being greater than that induced by periods of ischemia, GTN, or ischemic exercise alone. These data indicate that noninvasive indexes of conduit and resistance vessel structure can be simultaneously determined in vivo in response to a single, brief, stimulus and that caution should be applied in using resting arterial diameter as a surrogate measure of conduit artery structure in vivo.

scholarly journals Anaesthesia and the Kidney

1983 ◽  
Vol 11 (4) ◽  
pp. 292-320 ◽  
Author(s):  
Michael J. Cousins ◽  
George Skowronski ◽  
John L. Plummer
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Flow Distribution ◽  
Distal Tubule ◽  
Juxtaglomerular Apparatus ◽  
Anaesthetic Management ◽  
Anatomy And Physiology ◽  
Sympathetic Nervous Systems

Applied anatomy and physiology of the kidney are briefly reviewed. This includes an account of renal blood flow, glomerular filtration rate, juxtaglomerular apparatus, renal autoregulation and intra-renal blood flow distribution, tubular transport mechanisms, solute handling in proximal tubule, function of loop of Henle and distal tubule system. This section concludes with a summary of changes in tubule fluid along the length of the nephron. Acute effects of anaesthesia are reviewed in detail. Indirect effects include those on circulatory and sympathetic nervous systems, autoregulation, endocrine systems such as those involving antidiuretic hormone, adrenaline and noradrenaline, renin-angiotensin and aldosterone. Direct effects of anaesthesia on renal function have now been confirmed both in vitro and in vivo. Delayed direct nephrotoxicity of anaesthetics relates predominantly to methoxyflurane (MOF) and its metabolism to inorganic fluoride. Other factors are MOF dose, genetics, age, enzyme induction, obesity, other nephrotoxic drugs. Clinical implications are presented. Enflurane nephrotoxicity is rare but aetiologic factors are similar to the foregoing. Isoflurane and halothane are not nephrotoxic. A consideration of the influence of anaesthetic management on the incidence and severity of postoperative acute renal failure concludes the review.

Hemodynamic responses to glycols and to hemolysis

1969 ◽  
Vol 47 (6) ◽  
pp. 563-569 ◽  
Author(s):  
Keith MacCannell
Keyword(s):  
Blood Flow ◽  
Superior Mesenteric Artery ◽  
Renal Blood Flow ◽  
Mesenteric Artery ◽  
Direct Injection ◽  
Artery Blood Flow ◽  
Passive Response ◽  
Flow Through ◽  
Vascular Beds ◽  
Mesenteric Artery Blood Flow

Ethylene and propylene glycol both decrease renal blood flow in dogs while increasing flow through the superior mesenteric artery. The decrease in renal blood flow is not a passive response to dilatation of major vascular beds since it precedes the increment in superior mesenteric arterial flow and since it can be duplicated by direct injection of glycols into the renal artery. These rheological changes in response to glycols are at least partly due to hemolysis since intravenous injection of plasma from hemolyzed blood or of crystalline hemoglobin produces the same pattern of response, which is not blocked by phenoxybenzamine. However, the production of hemoglobinemia may not be the sole explanation for the vascular responses to the glycols, since a concentration of 2 %, which does not induce detectable hemolysis, still produces the characteristic increase in superior mesenteric artery blood flow.

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