Metabolic and functional consequences of blunted myocardial reactive hyperemia

1991 ◽  
Vol 261 (3) ◽  
pp. H892-H900 ◽  
Author(s):  
G. G. Schwartz ◽  
S. Schaefer ◽  
S. D. Trocha ◽  
S. Steinman ◽  
J. Gober ◽  
...  
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Coronary Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Blood Flow Rate ◽  
Intracellular Acidosis ◽  
Ischemic Region ◽  
Phosphorus Metabolites ◽  
Contractile Recovery

This study determined whether the rapidity of myocardial metabolic and contractile recovery after brief coronary occlusion depends upon the intensity of reactive hyperemia. We also tested the hypothesis that coronary flow rate modulates contractility after brief myocardial ischemia, independent of changes in phosphorus metabolites. Eight open-chest pigs were studied with phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy with 14 s time resolution. After a 29-s anterior descending coronary occlusion, peak Doppler coronary flow velocity was alternately unrestricted (normal hyperemia, 443 +/- 40% of control) or limited to 159 +/- 9% of control. During 29 s coronary occlusion, phosphocreatine-to-inorganic phosphate ratio (PCr/Pi) and systolic segment shortening in the ischemic region fell to 28 +/- 4 and 7 +/- 7% of control, respectively. With normal hyperemia, PCr/Pi and segment shortening recovered within 29 s. With blunted hyperemia, recovery of both parameters was delayed an additional 29-43 s, associated with reduced subendocardial blood flow (measured with radioactive microspheres) and persistent intracellular acidosis. However, the relationship between segment shortening and PCr/Pi was unaffected by the intensity of reactive hyperemia. Thus blunted reactive hyperemia significantly delays metabolic and contractile recovery from brief ischemia, probably via transient maldistribution of transmural perfusion. However, coronary blood flow rate does not independently modulate contractility after brief reversible ischemia.

Myocardial reactive hyperemia in the unanesthetized dog

1965 ◽  
Vol 208 (2) ◽  
pp. 224-230 ◽  
Author(s):  
Ray A. Olsson ◽  
Donald E. Gregg
Keyword(s):  
Coronary Artery ◽  
Flow Rate ◽  
Myocardial Contractility ◽  
Coronary Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Control Flow ◽  
Flow Curves ◽  
Diastolic Flow ◽  
Average Figure

Studies of myocardial reactive hyperemia in dogs 5–24 days after the implantation of electromagnetic flowmeters on coronary artery branches reveal that the duration of occlusion and the control flow rate are independent determinants of the volume of reactive hyperemia flow. Flow debt is almost always overpaid, the average figure being 500 ± 200%. Phasic coronary flow curves show an increase in both systolic and diastolic flow during reactive hyperemia, the increase in systolic flow being due in part to decreased myocardial contractility. Myocardial reactive hyperemia is thought to be due to the accumulation of vasodilator metabolites during the period of coronary occlusion.

Effects of neuropeptide Y on regulation of blood flow rate in canine myocardium

1990 ◽  
Vol 259 (6) ◽  
pp. H1709-H1717
Author(s):  
J. H. Svendsen ◽  
S. P. Sheikh ◽  
J. Jorgensen ◽  
J. D. Mikkelsen ◽  
W. P. Paaske ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Neuropeptide Y ◽  
Coronary Arteries ◽  
Flow Rate ◽  
Reactive Hyperemia ◽  
Blood Flow Rate ◽  
Nerve Fibers ◽  
Tension Development ◽  
Mean Values

The effect of neuropeptide Y (NPY) on tension development was examined in isolated canine coronary arteries, and the effects on local myocardial blood flow rate were studied in open-chest anesthetized dogs by the local 133Xe washout technique. By immunohistochemistry, numerous NPY-like immunoreactive nerve fibers were identified in the adventitia of canine coronary arteries. NPY (10(-9)-10(-6) M) supplied to isolated epicardial segments of the left anterior descending coronary artery induced a modest vasoconstriction, with a maximum tension of 0.95 mN, that was only 6.9% of the response to K+. In contrast, intracoronary NPY (0.01-10 micrograms) induced a considerable degree of vasoconstriction; the reduction of blood flow rate was dose related, with a maximum reduction to 52% of control values. The effect of intracoronary NPY (1 microgram) on maximally relaxed arterioles elicited by 30 s of ischemia was studied in separate experiments during reactive hyperemia. NPY induced a decrease in maximum blood flow during reactive hyperemia (166.6 vs. 214.6% of preocclusive blood flow rate, mean values; P = 0.05), an increase in the cumulative excess blood flow (61.0 vs. 35.3 ml/100 g; P = 0.02), and an increase in the duration of reactive hyperemia compared with control values (66 vs. 41 s; P = 0.02). Thus we conclude that in the heart NPY is a potent vasoconstrictor that seems to act preferentially on smaller intramyocardial arterioles. Furthermore, NPY inhibits vascular relaxation of myocardial resistance vessels after ischemia, suggesting that this peptide may participate in the regulation of myocardial blood flow not only during physiological conditions but also after ischemia.

The Effect of Furosemide on the Intrarenal Blood Flow Distribution in the Dog

1972 ◽  
Vol 50 (8) ◽  
pp. 774-783 ◽  
Author(s):  
Serge Carrière ◽  
Michel Desrosiers ◽  
Jacques Friborg ◽  
Michèle Gagnan Brunette
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Urine Volume ◽  
Flow Distribution ◽  
Blood Flow Rate ◽  
Initial Distribution ◽  
Blood Flow Distribution ◽  
Intrarenal Blood Flow ◽  
Femoral Blood ◽  
Furosemide Administration

Furosemide (40 μg/min) was perfused directly into the renal artery of dogs in whom the femoral blood pressure was reduced (80 mm Hg) by aortic clamping above the renal arteries. This maneuver, which does not influence the intrarenal blood flow distribution, produced significant decreases of the urine volume, natriuresis, Ccreat, and CPAH, and prevented the marked diuresis normally produced by furosemide. Therefore the chances that systemic physiological changes occurred, secondary to large fluid movements, were minimized. In those conditions, however, furosemide produced a significant increase of the urine output and sodium excretion in the experimental kidney whereas Ccreat and CPAH were not affected. The outer cortical blood flow rate (ml/100 g-min) was modified neither by aortic constriction (562 ± 68 versus 569 ± 83) nor by the subsequent administration of furosemide (424 ± 70). The blood flow rate of the outer medulla in these three conditions remained unchanged (147 ± 52 versus 171 ± 44 versus 159 ± 54). The initial distribution of the radioactivity in each compartment remained comparable in the three conditions. In parallel with the results from the krypton-85 disappearance curves, the autoradiograms, silicone rubber casts, and EPAH did not suggest any change in the renal blood flow distribution secondary to furosemide administration.

The Effect of Hematocrit on the Clearance of Small Molecules during Hemodialysis

1983 ◽  
Vol 6 (3) ◽  
pp. 127-130 ◽  
Author(s):  
C. Woffindin ◽  
N.A. Hoenich ◽  
D.N.S. Kerr
Keyword(s):  
Blood Flow ◽  
Regression Analysis ◽  
Small Molecules ◽  
Flat Plate ◽  
Flow Rate ◽  
Distribution Curve ◽  
Blood Flow Rate ◽  
Hollow Fibre ◽  
Urea Clearance ◽  
Flow Rates

Data collected during the evaluation of a series of hemodialysers were analysed to see the effect of hematocrit on the clearance of urea and creatinine. All evaluations were performed on patients with a range of hematocrits with a mean close to 20%. The urea clearance of those in the upper half of the distribution curve (mean hematocrit 29.4%) was not significantly different from that of patients in the lower half of the distribution curve (mean hematocrit 16.9%) whether the clearance was studied at high or low blood flow rates and with hollow fibre or flat plate disposable hemodialysers. Likewise, there was no correlation between hematocrit and urea clearance by regression analysis. In contrast, the clearance of creatinine was affected by hematocrit being greater at lower hematocrit values. This difference was independent of blood flow rate and dialyser type and was confirmed by regression analysis.

Anoxia and adenosine induce increased cerebral blood flow rate in crucian carp

1994 ◽  
Vol 267 (2) ◽  
pp. R590-R595 ◽  
Author(s):  
G. E. Nilsson ◽  
P. Hylland ◽  
C. O. Lofman
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Crucian Carp ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Liver Glycogen ◽  
Glycolytic Flux ◽  
Brain Blood Flow ◽  
Atp Production ◽  
The Brain

The crucian carp (Carassius carassius) has the rare ability to survive prolonged anoxia, indicating an extraordinary capacity for glycolytic ATP production, especially in a highly energy-consuming organ like the brain. For the brain to be able to increase its glycolytic flux during anoxia and profit from the large liver glycogen store, an increased glucose delivery from the blood would be expected. Nevertheless, the effect of anoxia on brain blood flow in crucian carp has never been studied previously. We have used epireflection microscopy to directly observe and measure blood flow rate on the brain surface (optic lobes) during normoxia and anoxia in crucian carp. We have also examined the possibility that adenosine participates in the regulation of brain blood flow rate in crucian carp. The results showed a 2.16-fold increase in brain blood flow rate during anoxia. A similar increase was seen after topical application of adenosine during normoxia, while adenosine was without effect during anoxia. Moreover, superfusing the brain with the adenosine receptor blocker aminophylline inhibited the effect of anoxia on brain blood flow rate, clearly suggesting a mediatory role of adenosine in the anoxia-induced increase in brain blood flow rate.

scholarly journals Patient-specific computational haemodynamics associated with surgical creation of an arteriovenous fistula

2021 ◽  
Author(s):  
George Hyde-Linaker ◽  
Pauline Hall Barrientos ◽  
Sokratis Stoumpos ◽  
Asimina Kazakidi
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Disease Patient ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Transitional Flow ◽  
Patient Specific ◽  
Venous Anastomosis ◽  
End Stage

Abstract Despite arteriovenous fistulae (AVF) being the preferred vascular access for haemodialysis, high primary failure rates (30-70%) and low one-year patency rates (40-70%) hamper their use. The haemodynamics within the vessels of the fistula change significantly following surgical creation of the anastomosis and can be a surrogate of AVF success or failure. Computational fluid dynamics (CFD) can crucially predict AVF outcomes through robust analysis of a fistula’s haemodynamic patterns, which is impractical in-vivo. We present a proof-of-concept CFD framework for characterising the AVF blood flow prior and following surgical creation of a successful left radiocephalic AVF in a 20-year-old end-stage kidney disease patient. The reconstructed vasculature was generated utilising multiple contrast-enhanced magnetic resonance imaging (MRI) datasets. Large eddy simulations were conducted for establishing the extent of arterial and venous remodelling. Following anastomosis creation, a significant 2-3-fold increase in blood flow rate was induced downstream of the left subclavian artery. This was validated through comparison with post-AVF patient-specific phase-contrast data. The increased flow rate yielded an increase in time-averaged wall shear stress (TAWSS), a key marker of adaptive vascular remodelling. We have demonstrated TAWSS and oscillatory shear distributions of the transitional-flow in the venous anastomosis are predictive of AVF remodelling.

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