scholarly journals MR measures of renal perfusion, oxygen bioavailability and total renal blood flow in a porcine model: noninvasive regional assessment of renal function

2011 ◽  
Vol 27 (1) ◽  
pp. 128-135 ◽  
Author(s):  
A. L. Wentland ◽  
N. S. Artz ◽  
S. B. Fain ◽  
T. M. Grist ◽  
A. Djamali ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Porcine Model ◽  
Renal Perfusion ◽  
Regional Assessment ◽  
Total Renal Blood Flow

Influence of renal perfusion pressure on alpha- and beta-adrenergic stimulation of renin release

1985 ◽  
Vol 248 (3) ◽  
pp. E317-E326 ◽  
Author(s):  
M. L. Blair ◽  
Y. H. Chen ◽  
J. L. Izzo
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Neural Stimulation ◽  
Renin Release ◽  
Beta Blockade ◽  
Renal Perfusion Pressure ◽  
Stimulation Of ◽  
Total Renal Blood Flow

Experiments were performed in pentobarbital-anesthetized dogs to 1) determine if neural stimulation of renin release can be mediated by renal alpha-adrenoceptors at renal nerve stimulation (RNS) frequencies that have little or no effect on total renal blood flow (less than or equal to 1.2 Hz) and 2) ascertain whether alpha-adrenergic control of renin release is affected by renal perfusion pressure (RPP). The renal nerves were electrically stimulated both in the absence of RPP control and with RPP controlled near 85 mmHg. Decreased RPP lowered the threshold for neurogenic stimulation of renin release from less than or equal to 1.2 to 0.3 Hz. beta-Adrenoceptor blockade with propranolol blunted the renin secretion rate (RSR) response to graded RNS (0.3-5.0 Hz), but the extent of inhibition during low-frequency RNS was dependent on RPP. Propranolol prevented increased RSR at 0.6-1.2 Hz RNS when RPP was 111-120 mmHg but not when RPP was 85 mmHg. Combined alpha- and beta-blockade with prazosin and propranolol totally prevented increased RSR during 0.6-1.2 Hz RNS at reduced RPP. In summary, both alpha- and beta-adrenoceptors mediate neural stimulation of renin release at RNS frequencies that do not decrease total renal blood flow when RPP is 85 mmHg.

Effect of General Anaesthesia on Renal Haemodynamics in the Rat

1979 ◽  
Vol 57 (5) ◽  
pp. 469-471 ◽  
Author(s):  
B. M. Koeppen ◽  
A. I. Katz ◽  
M. D. Lindheimer
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
General Anaesthesia ◽  
Renal Haemodynamics ◽  
Sodium Pentobarbital ◽  
Radioactive Microspheres ◽  
Anaesthetic Agents ◽  
Total Renal Blood Flow

1. The effect of sodium pentobarbital and Inactin anaesthesia on renal haemodynamics in the rat was evaluated with radioactive microspheres 15 μm in diameter. 2. Both anaesthetic agents caused substantial decrements in total renal blood flow (sodium pentobarbital, −34%; Inactin, −24%) compared with unanaesthetized animals. 3. Measurements of renal function obtained in rats anaesthetized with either of these anaesthetic agents should be interpreted with caution.

Measurement of Intrarenal Blood-Flow Distribution in the Rabbit Using Radioactive Microspheres

1975 ◽  
Vol 48 (1) ◽  
pp. 51-60 ◽  
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Flow Distribution ◽  
Rabbit Kidney ◽  
Radioactive Microspheres ◽  
Injection Dose ◽  
Intrarenal Blood Flow ◽  
Total Renal Blood Flow

1. Total renal blood flow and its distribution within the renal cortex of the conscious rabbit were studied with radioactive microspheres of 15 and 25 μm diameter. 2. The reliability of the microsphere technique was influenced by microsphere diameter and number (dose). The optimum microsphere diameter for determination of flow distribution in the rabbit kidney was 15 μm and dose 100–150 000 spheres. 3. Spheres of 15 μm nominal diameter were randomly distributed within the renal cortex of adult rabbits. The larger spheres in batches nominally 15 μm in diameter in young rabbits and 25 μm diameter in adult rabbits were preferentially distributed to the superficial cortex. 4. In adult rabbits 15 μm diameter spheres lodged in glomerular capillaries. Larger spheres occasionally lodged in interlobular arteries causing intrarenal haemorrhage. 5. Microspheres of 15 μm caused a decrease in renal clearance of creatinine and of p-aminohippurate when the total injection dose was about 200 000 spheres. These effects were greater when the injection dose was increased to 500 000 spheres. 6. The reduction in total renal blood flow observed with large doses of spheres largely reflected decreased outer cortical flow, as measured by a second injection of spheres, and confirmed by a decrease in p-aminohippurate extraction. 7. The reproducibility of multiple injection studies was limited by these intrarenal effects of microspheres. 8. Total renal blood flow measured in six rabbits in acute experiments by the microsphere technique was 107 ± 12 (mean±sd) ml/min and by p-aminohippurate clearance was 100 ± 10 ml/min. 9. Total renal blood flow in twelve conscious, chronically instrumented rabbits was 125 ± 11 ml/min, of which 92 ± 6 ml/min was distributed to the superficial cortex and 33 ± 4 ml/min to the deep cortex.

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.

Autoregulation of renal blood flow in the puppy

1975 ◽  
Vol 229 (4) ◽  
pp. 983-988 ◽  
Author(s):  
PA Jose ◽  
LM Slotkoff ◽  
S Montgomery ◽  
PL Calcagno ◽  
G Eisner
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Electromagnetic Flowmeter ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin System ◽  
Group Of Seven ◽  
Selective Blockade

The ability of the immature kidney to autoregulate blood flow was investigated. Renal blood flow was measured by electromagnetic flowmeter. In six puppies, selective blockade of the intrarenal effects of angiotensin II (AII) by [1-sarcosine, 8-alanine]angiotensin II (anti-AII) administered into the renal artery did not change renal blood flow. During selective renal AII blockade, intravenous AII raised perfusion pressure from 76 +/- 2 to 100 +/- 6 mmHg. Renal blood flow increased from 1.59 +/- 0.29 to 1.98 +/- 0.59 ml/g kidney per min, but returned to control levels within 40 s in spite of persistent arterial pressure elevation. In another group of seven puppies, renal blood flow remained constant despite reduction of renal perfusion pressure by aortic constriction to 60 mmHg. In two of these seven puppies intrarenal anti-AII did not abolish autoregulation. Autoregulation of renal blood flow occurs in the puppy and is not influenced by inhibition of angiotensin. The renin-angiotensin system does not appear to be involved in the normal regulation of renal blood flow in the puppy.

Mechanism of intrarenal blood flow redistribution after carotid artery occlusion

1977 ◽  
Vol 232 (2) ◽  
pp. F167-F172 ◽  
Author(s):  
E. H. Prosnitz ◽  
E. J. Zambraski ◽  
G. F. DiBona
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Outer Cortex ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Perfusion Pressure

Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.

Role of the renal medulla in volume and arterial pressure regulation

1997 ◽  
Vol 273 (1) ◽  
pp. R1-R15 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Fluid Pressure ◽  
Regulatory System ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vasa Recta ◽  
Pressure Natriuresis ◽  
Total Renal Blood Flow

The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W., N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named "hormones," importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.

The Hepatorenal Syndrome

1997 ◽  
Vol 92 (5) ◽  
pp. 433-443 ◽  
Author(s):  
Kevin Moore
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Liver Disease ◽  
Renal Blood Flow ◽  
Hepatorenal Syndrome ◽  
Venous Pressure ◽  
Renal Perfusion ◽  
Filtration Fraction ◽  
Renal Vasoconstriction ◽  
Vasoactive Mediators

1. The hepatorenal syndrome is the development of renal failure in patients with severe liver disease in the absence of any identifiable renal pathology. 2. Decreased glomerular filtration is caused by a reduction in both renal blood flow and the renal filtration fraction. These changes arise as a consequence of a fall in mean arterial pressure due to systemic vasodilatation, activation of the sympathetic nervous system causing renal vasoconstriction, and increased synthesis of several vasoactive mediators, which together modulate both renal blood flow and the glomerular capillary ultrafiltration coefficient, and thence filtration fraction. 3. Patients with liver disease developing renal failure should have hypovolaemia excluded by volume challenge, and all nephrotoxic drugs including diuretics should be stopped. Broad-spectrum antibiotics should be given for subclinical infection, which may be a treatable precipitant of renal failure in cirrhosis. Renal perfusion should be optimized by ensuring that the blood pressure and systemic haemodynamics are adequate, and that if renal venous pressure is elevated, due to tense ascites, it is alleviated. 4. The prognosis of hepatorenal syndrome is poor with a >90% mortality. However, patients can and do recover from the hepatorenal syndrome, but only if there is a significant improvement of their liver function, or if they undergo liver transplantation.

scholarly journals Renal hemodynamics and oxygenation during experimental cardiopulmonary bypass in sheep under total intravenous anesthesia

2020 ◽  
Vol 318 (2) ◽  
pp. R206-R213 ◽  
Author(s):  
Roger G. Evans ◽  
Naoya Iguchi ◽  
Andrew D. Cochrane ◽  
Bruno Marino ◽  
Sally G. Hood ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Conscious State ◽  
Renal Perfusion ◽  
Total Intravenous Anesthesia ◽  
Intravenous Anesthesia ◽  
Isoflurane Anesthesia ◽  
Conscious Sheep

Renal medullary hypoxia may contribute to the pathophysiology of acute kidney injury, including that associated with cardiac surgery requiring cardiopulmonary bypass (CPB). When performed under volatile (isoflurane) anesthesia in sheep, CPB causes renal medullary hypoxia. There is evidence that total intravenous anesthesia (TIVA) may preserve renal perfusion and renal oxygen delivery better than volatile anesthesia. Therefore, we assessed the effects of CPB on renal perfusion and oxygenation in sheep under propofol/fentanyl-based TIVA. Sheep ( n = 5) were chronically instrumented for measurement of whole renal blood flow and cortical and medullary perfusion and oxygenation. Five days later, these variables were monitored under TIVA using propofol and fentanyl and then on CPB at a pump flow of 80 mL·kg−1·min−1 and target mean arterial pressure of 70 mmHg. Under anesthesia, before CPB, renal blood flow was preserved under TIVA (mean difference ± SD from conscious state: −16 ± 14%). However, during CPB renal blood flow was reduced (−55 ± 13%) and renal medullary tissue became hypoxic (−20 ± 13 mmHg versus conscious sheep). We conclude that renal perfusion and medullary oxygenation are well preserved during TIVA before CPB. However, CPB under TIVA leads to renal medullary hypoxia, of a similar magnitude to that we observed previously under volatile (isoflurane) anesthesia. Thus use of propofol/fentanyl-based TIVA may not be a useful strategy to avoid renal medullary hypoxia during CPB.

scholarly journals Global REACH 2018: renal oxygen delivery is maintained during early acclimatization to 4,330 m

2020 ◽  
Vol 319 (6) ◽  
pp. F1081-F1089
Author(s):  
Andrew R. Steele ◽  
Michael M. Tymko ◽  
Victoria L. Meah ◽  
Lydia L. Simpson ◽  
Christopher Gasho ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
High Altitude ◽  
Renal Blood Flow ◽  
Sea Level ◽  
Oxygen Delivery ◽  
Acid Base ◽  
Altitude Acclimatization ◽  
High Altitude Acclimatization ◽  
Renal Oxygen

Early acclimatization to high altitude is characterized by various respiratory, hematological, and cardiovascular adaptations that serve to restore oxygen delivery to tissue. However, less is understood about renal function and the role of renal oxygen delivery (RDO2) during high altitude acclimatization. We hypothesized that 1) RDO2 would be reduced after 12 h of high altitude exposure (high altitude day 1) but restored to sea level values after 1 wk (high altitude day 7) and 2) RDO2 would be associated with renal reactivity, an index of acid-base compensation at high altitude. Twenty-four healthy lowlander participants were tested at sea level (344 m, Kelowna, BC, Canada) and on day 1 and day 7 at high altitude (4,330 m, Cerro de Pasco, Peru). Cardiac output, renal blood flow, and arterial and venous blood sampling for renin-angiotensin-aldosterone system hormones and NH2-terminal pro-B-type natriuretic peptides were collected at each time point. Renal reactivity was calculated as follows: (Δarterial bicarbonate)/(Δarterial Pco2) between sea level and high altitude day 1 and sea level and high altitude day 7. The main findings were that 1) RDO2 was initially decreased at high altitude compared with sea level (ΔRDO2: −22 ± 17%, P < 0.001) but was restored to sea level values on high altitude day 7 (ΔRDO2: −6 ± 14%, P = 0.36). The observed improvements in RDO2 resulted from both changes in renal blood flow (Δ from high altitude day 1: +12 ± 11%, P = 0.008) and arterial oxygen content (Δ from high altitude day 1: +44.8 ± 17.7%, P = 0.006) and 2) renal reactivity was positively correlated with RDO2 on high altitude day 7 ( r = 0.70, P < 0.001) but not high altitude day 1 ( r = 0.26, P = 0.29). These findings characterize the temporal responses of renal function during early high altitude acclimatization and the influence of RDO2 in the regulation of acid-base balance.

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