Evidence for a preglomerular oxygen diffusion shunt in rat renal cortex

1990 ◽  
Vol 259 (6) ◽  
pp. F910-F915 ◽  
Author(s):  
H. J. Schurek ◽  
U. Jost ◽  
H. Baumgartl ◽  
H. Bertram ◽  
U. Heckmann
Keyword(s):  
Renal Cortex ◽  
Pure Oxygen ◽  
Common Denominator ◽  
High Susceptibility ◽  
Arterial Blood ◽  
Erythropoietin Production ◽  
Arterial Po2 ◽  
Arteries And Veins ◽  
Superficial Glomeruli

Although blood flow to the renal cortex is high and oxygen extraction is low, the renal cortex is remarkably susceptible to hypoxia. Because erythropoietin production has been localized mainly to the renal cortex, the aim of this study was to find a common denominator for both the high susceptibility to hypoxia and oxygen sensing within the renal cortex. By direct measurement of oxygen pressure with microcoaxial needle sensors at superficial glomeruli of the in situ kidney of anesthetized Munich-Wistar-Fromter rats, we obtained mean partial pressure of O2 (PO2) values of 46 +/- 13 (SD) mmHg (n = 71). The simultaneously measured systemic PO2 in arterial blood was 90 +/- 8 mmHg (n = 54). Changing the respirator gas from air to pure oxygen enhanced systemic arterial PO2 to 593 +/- 27 mmHg, whereas PO2 at the superficial glomeruli increased only to a mean of 80 +/- 28 mmHg (n = 71). These data suggest significant preglomerular shunting of oxygen within the cortical vasculature, most likely between interlobular vessels, which are arranged in a countercurrent fashion and represent quantitatively the largest contact area between arteries and veins within the renal cortex.

Effect of increased Hb-O2 affinity on VO2max at constant O2 delivery in dog muscle in situ

1991 ◽  
Vol 70 (6) ◽  
pp. 2656-2662 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Saturation Pressure ◽  
Normal Blood ◽  
Arterial Blood ◽  
O2 Diffusion ◽  
The Mean ◽  
O2 Delivery ◽  
Arterial Po2

We investigated the effect of increasing hemoglobin- (Hb) O2 affinity on muscle maximal O2 uptake (VO2max) while muscle blood flow, [Hb], HbO2 saturation, and thus O2 delivery (muscle blood flow X arterial O2 content) to the working muscle were kept unchanged from control. VO2max was measured in isolated in situ canine gastrocnemius working maximally (isometric tetanic contractions). The muscles were pump perfused, in alternating order, with either normal blood [O2 half-saturation pressure of hemoglobin (P50) = 32.1 +/- 0.5 (SE) Torr] or blood from dogs that had been fed sodium cyanate (150 mg.kg-1.day-1) for 3-4 wk (P50 = 23.2 +/- 0.9). In both conditions (n = 8) arterial PO2 was set at approximately 200 Torr to fully saturate arterial blood, which thereby produced the same arterial O2 contents, and muscle blood flow was set at 106 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. VO2max was 11.8 +/- 1.0 ml.min-1.100 g-1 when perfused with the normal blood (control) and was reduced by 17% to 9.8 +/- 0.7 ml.min-1.100 g-1 when perfused with the low-P50 blood (P less than 0.01). Mean muscle effluent venous PO2 was also significantly less (26 +/- 3 vs. 30 +/- 2 Torr; P less than 0.01) in the low-P50 condition, as was an estimate of the capillary driving pressure for O2 diffusion, the mean capillary PO2 (45 +/- 3 vs. 51 +/- 2 Torr). However, the estimated muscle O2 diffusing capacity was not different between conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of Angiotensin II on Erythropoietin Production in the Kidney and Liver

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5399
Author(s):  
Yukiko Yasuoka ◽  
Yuichiro Izumi ◽  
Takashi Fukuyama ◽  
Hideki Inoue ◽  
Tomomi Oshima ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protein Expression ◽  
Renal Cortex ◽  
The Body ◽  
Outer Medulla ◽  
Main Site ◽  
Erythropoietin Production ◽  
Collecting Ducts ◽  
Mrna And Protein Expression

The kidney is a main site of erythropoietin production in the body. We developed a new method for the detection of Epo protein by deglycosylation-coupled Western blotting. Detection of deglycosylated Epo enables the examination of small changes in Epo production. Using this method, we investigated the effects of angiotensin II (ATII) on Epo production in the kidney. ATII stimulated the plasma Epo concentration; Epo, HIF2α, and PHD2 mRNA expression in nephron segments in the renal cortex and outer medulla; and Epo protein expression in the renal cortex. In situ hybridization and immunohistochemistry revealed that ATII stimulates Epo mRNA and protein expression not only in proximal tubules but also in collecting ducts, especially in intercalated cells. These data support the regulation of Epo production in the kidney by the renin–angiotensin–aldosterone system (RAS).

IN SITU AND PILOT ORGAN PERFUSION TECHNIQUES FOR THE STUDY OF METABOLIC DYNAMICS

1972 ◽  
Vol 68 (2_Supplb) ◽  
pp. S9-S25 ◽  
Author(s):  
John Urquhart ◽  
Nancy Keller
Keyword(s):  
Cardiac Output ◽  
Large Fraction ◽  
Experimental Studies ◽  
Test Substance ◽  
Organ Perfusion ◽  
Systemic Blood ◽  
Experimental Control ◽  
Arterial Blood ◽  
Vascular Connections

ABSTRACT Two techniques for organ perfusion with blood are described which provide a basis for exploring metabolic or endocrine dynamics. The technique of in situ perfusion with autogenous arterial blood is suitable for glands or small organs which receive a small fraction of the animal's cardiac output; thus, test stimulatory or inhibitory substances can be added to the perfusing blood and undergo sufficient dilution in systemic blood after passage through the perfused organ so that recirculation does not compromise experimental control over test substance concentration in the perfusate. Experimental studies with the in situ perfused adrenal are described. The second technique, termed the pilot organ method, is suitable for organs which receive a large fraction of the cardiac output, such as the liver. Vascular connections are made between the circulation of an intact, anaesthetized large (> 30 kg) dog and the liver of a small (< 3 kg) dog. The small dog's liver (pilot liver) is excised and floated in a bath of canine ascites, and its venous effluent is continuously returned to the large dog. Test substances are infused into either the hepatic artery or portal vein of the pilot liver, but the small size of the pilot liver and its blood flow in relation to the large dog minimize recirculation effects. A number of functional parameters of the pilot liver are described.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Accounting for oxygen in the renal cortex: a computational study of factors that predispose the cortex to hypoxia

2017 ◽  
Vol 313 (2) ◽  
pp. F218-F236 ◽  
Author(s):  
Chang-Joon Lee ◽  
Bruce S. Gardiner ◽  
Jennifer P. Ngo ◽  
Saptarshi Kar ◽  
Roger G. Evans ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Renal Cortex ◽  
Computational Study ◽  
Ischemia Reperfusion ◽  
Sodium Reabsorption ◽  
Model Parameters ◽  
Arterial Blood ◽  
Increased Risk ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

We develop a pseudo-three-dimensional model of oxygen transport for the renal cortex of the rat, incorporating both the axial and radial geometry of the preglomerular circulation and quantitative information regarding the surface areas and transport from the vasculature and renal corpuscles. The computational model was validated by simulating four sets of published experimental studies of renal oxygenation in rats. Under the control conditions, the predicted cortical tissue oxygen tension ([Formula: see text]) or microvascular oxygen tension (µPo2) were within ±1 SE of the mean value observed experimentally. The predicted [Formula: see text] or µPo2 in response to ischemia-reperfusion injury, acute hemodilution, blockade of nitric oxide synthase, or uncoupling mitochondrial respiration, were within ±2 SE observed experimentally. We performed a sensitivity analysis of the key model parameters to assess their individual or combined impact on the predicted [Formula: see text] and µPo2. The model parameters analyzed were as follows: 1) the major determinants of renal oxygen delivery ([Formula: see text]) (arterial blood Po2, hemoglobin concentration, and renal blood flow); 2) the major determinants of renal oxygen consumption (V̇o2) [glomerular filtration rate (GFR) and the efficiency of oxygen utilization for sodium reabsorption (β)]; and 3) peritubular capillary surface area (PCSA). Reductions in PCSA by 50% were found to profoundly increase the sensitivity of [Formula: see text] and µPo2 to the major the determinants of [Formula: see text] and V̇o2. The increasing likelihood of hypoxia with decreasing PCSA provides a potential explanation for the increased risk of acute kidney injury in some experimental animals and for patients with chronic kidney disease.

IN SITU MONITORING OF MEAN BLOOD OXYGEN SATURATION USING EXTENDED MODIFIED LAMBERT BEER MODEL

2015 ◽  
Vol 27 (01) ◽  
pp. 1550004 ◽  
Author(s):  
Audrey K. C. Huong ◽  
Xavier T. I. Ngu
Keyword(s):  
Oxygen Saturation ◽  
In Situ Monitoring ◽  
Blood Oxygen ◽  
Optical Monitoring ◽  
Hypertension Status ◽  
Blood Oxygen Saturation ◽  
Fitting Procedure ◽  
Arterial Blood ◽  
The Mean

We present the use of Extended Modified Lambert–Beer model for optical monitoring of mean blood oxygen saturation ( S m O 2) via a fitting procedure. This work focuses on the absorption characteristics of hemoglobin derivatives in the wavelength range of 520–600 nm to give the best estimates of S m O 2. The study of the feasibility of applying this analytic method to skin oximetry is via spectroscopy data collected from fingertips of four healthy volunteers both at rest and during arterial blood occlusion condition. The results revealed a decrease in the mean of mean and standard deviation of S m O 2 value of fingertips from 94.5 ± 2.19% when volunteers were at rest to 56.76 ± 5.8% during the arterial blood occlusion measurement. The larger variation in the value estimated for blood occlusion condition could be a result of differences in volunteers' physical fitness and hypertension status. These estimated S m O 2 values agreed reasonably well with the value reported in most of the previous studies. This work concluded that the proposed technique can potentially be used as a complementary technique to clinical assessment of skin grafts and burnt skin.

Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2795-2800 ◽  
Author(s):  
R. Behm ◽  
H. Mewes ◽  
W. H. DeMuinck Keizer ◽  
T. Unger ◽  
R. Rettig
Keyword(s):  
Carotid Body ◽  
Normobaric Hypoxia ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Excretory Function ◽  
Arterial Blood ◽  
Peripheral Arterial ◽  
Renal Responses ◽  
Arterial Po2 ◽  
Sodium And Potassium

The contribution of peripheral arterial chemoreceptors to cardiovascular and renal responses to acute hypocapnic hypoxia is currently not well understood. We compared the effects of normobaric hypoxia on mean arterial blood pressure (MABP), heart rate, glomerular filtration rate (GFR), renal blood flow (RBF), and renal volume and electrolyte excretion in conscious unilaterally nephrectomized carotid body-denervated (n = 10) and sham-operated (n = 10) control rats. Thirty minutes of normobaric hypoxia (12.5% O2) resulted in significant reductions in arterial PO2 and PCO2 as well as decreases in MABP, GFR, RBF, and renal sodium, potassium, and water excretion. These effects occurred more rapidly and/or were significantly more pronounced in carotid body-denervated than in sham-operated rats. These data indicate that moderate acute hypocapnic hypoxia has profound effects on systemic and renal hemodynamics as well as on renal excretory function in conscious rats. We conclude that stimulation of the peripheral arterial chemoreceptors can partially offset the hypoxia-induced decreases in MABP, RBF, GFR, urine flow, and urinary sodium and potassium excretion, thereby helping to maintain cardiovascular as well as fluid and electrolyte homeostasis.

ANG II modifies cardiomyocyte function via extracardiac and intracardiac neurons: in situ and in vitro studies

1997 ◽  
Vol 272 (3) ◽  
pp. R766-R775 ◽  
Author(s):  
M. Horackova ◽  
J. A. Armour
Keyword(s):  
Guinea Pig ◽  
Receptor Antagonist ◽  
Neuronal Activity ◽  
Ang Ii ◽  
Arterial Blood ◽  
Cardiac Ganglia ◽  
In Situ Experiments ◽  
Anesthetized Dogs

To determine whether angiotensin II (ANG II) affects cardiac performance via neurons in intrathoracic cardiac ganglia, studies were performed on anesthetized dogs. To exclude possible vascular regulatory effects of ANG II, experiments were also performed using long-term cultures of adult guinea pig ventricular cardiomyocytes with or without intrathoracic neurons. 1) In in situ experiments in 10 anesthetized dogs, cardiac augmentation occurred when ANG II (10 microl or 0.1 ml; 10-100 microM) was administered into limited loci within acutely decentralized stellate or middle cervical ganglia that were neurally connected to, but not those disconnected from, the heart. In another 18 dogs, ANG II increased intrinsic cardiac neuronal activity when administered adjacent to such neurons or into their local arterial blood supply. Ventricular ionotropic effects elicited by ANG II were eliminated by timolol, whereas increases in intrinsic cardiac neuronal activity were not affected. Effects elicited by ANG II were eliminated by administration of a selective AT1 receptor antagonist (losartan) but not by a selective AT2 receptor antagonist (PD-123319). 2) In in vitro experiments, ANG II (100 nM) induced positive chronotropic effects on cultured adult guinea pig cardiomyocytes innervated with adult extrinsic or intrinsic cardiac neurons, but not those cultured without neurons. The frequency of calcium inward current (Ca(i)) transients (recorded by fura 2 fluorescence) increased in innervated cocultures but not in the noninnervated cardiomyocyte cultures; however, the amplitude of Ca(i) transients was not affected by ANG II in cultures or in freshly isolated adult guinea pig cardiomyocytes. ANG II-induced effects in cocultures were blocked by losartan but not PD-123319 or timolol. Thus 1) ANG II-sensitive neurons exist in intrathoracic extracardiac and intrinsic cardiac ganglia; 2) these neurons possess AT1 receptors; and 3) these neurons appear to act directly and indirectly via adrenergic neurons to enhance cardiomyocyte function.

Novel in situ production of smooth diamond films

1998 ◽  
Vol 13 (7) ◽  
pp. 1735-1737 ◽  
Author(s):  
Donald R. Gilbert ◽  
Dong-Gu Lee ◽  
Rajiv K. Singh
Keyword(s):  
Electron Cyclotron Resonance ◽  
Microwave Plasma ◽  
Ion Beam ◽  
Diamond Films ◽  
Extraction Process ◽  
Pure Oxygen ◽  
Average Roughness ◽  
Process System ◽  
Unique Method

We have developed a unique method to produce smooth diamond films using a modified microwave plasma process system. This method consists of sequential in situ deposition and planarization in an electron cyclotron resonance plasma system. Diamond films were deposited to a thickness of 3.0 μm in this system at a pressure of 1.000 Torr from gas mixtures of methanol and hydrogen. Deposition was followed by planarization using a two-grid ion beam extraction process with a pure oxygen plasma at 10 mTorr. The average roughness of the diamond films so produced was as low as 30 nm, which was a factor of two lower than that of the as-deposited diamond films.

Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ

1996 ◽  
Vol 271 (6) ◽  
pp. H2238-H2245
Author(s):  
M. Szentivanyi ◽  
G. L. Nadasy ◽  
L. Dezsi ◽  
G. Mozes ◽  
T. Tulassay ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Saphenous Vein ◽  
Vessel Diameter ◽  
Outer Diameter ◽  
Synthesis Inhibitor ◽  
Vascular Effects ◽  
Venous Diameter ◽  
Arteries And Veins ◽  
Saphenous Artery

The vascular effects of somatostatin (ST) and its mechanism of action are not well understood. In the present study, we investigated the direct effects of ST on the vascular tone of rat saphenous artery and vein using videomicroangiometry in situ. ST was administered either in superfusion or in infusion. We found opposite effects in arteries and veins: ST (10(-12)-10(-7) M) dilated the artery (outer diameter increased from 533 +/- 28 to 600 +/- 29 microns, administered in superfusion) and contracted the vein (from 709 +/- 26 to 640 +/- 26 microns and from 775 +/- 30 to 708 +/- 60 microns in superfusion and infusion, respectively). These effects of ST were completely abolished after deendothelization (air bolus maintained for 6 min in vessel lumen) and after local infusion of NG-nitro-L-arginine (L-NNA; 10(-4) M), a nitric oxide (NO) synthesis inhibitor. An NO-dependent basal vasodilator tone in the rat saphenous vein responsible for 10.9 +/- 0.3% of the total vessel diameter was found. After ST administration the venous diameter reduction was similar to that measured after deendothelization or L-NNA. We conclude that ST in situ induces NO release from endothelial cells of rat saphenous artery causing vasodilation, whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone of the saphenous vein inducing vasoconstriction.

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