Diaphragmatic perfusion heterogeneity during exercise with inspiratory resistive breathing

1990 ◽  
Vol 68 (5) ◽  
pp. 2177-2181 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Exercise Capacity ◽  
Vascular Resistance ◽  
Maximal Exercise ◽  
Perfusion Pressure ◽  
Work Of Breathing ◽  
Regional Distribution ◽  
Resistive Breathing ◽  
Exercise Induced

Regional distribution of diaphragmatic blood flow (Q; 15-microns-diam radionuclide-labeled microspheres) was studied in normal (n = 7) and laryngeal hemiplegic (LH; n = 7) ponies to determine whether the added stress of inspiratory resistive breathing during maximal exercise may cause 1) redistribution of diaphragmatic Q and 2) crural diaphragmatic Q to exceed that in maximally exercising normal ponies. LH-induced augmentation of already high exertional work of breathing resulted in diminished locomotor exercise capacity so that maximal exercise in LH ponies occurred at 25 km/h compared with 32 km/h for normal ponies. The costal and crural regions received similar Q in both groups at rest. However, exercise-induced increments in perfusion were significantly greater in the costal region of the diaphragm. At 25 km/h, costal diaphragmatic perfusion was 154 and 143% of the crural diaphragmatic Q in normal and LH ponies. At 32 km/h, Q in costal diaphragm of normal ponies was 136% of that in the crural region. Costal and crural diaphragmatic Q in LH ponies exercised at 25 km/h exceeded that for normal ponies but was similar to the latter during exercise at 32 km/h. Perfusion pressure for the three conditions was also similar. It is concluded that diaphragmatic perfusion heterogeneity in exercising ponies was preserved during the added stress of inspiratory resistive breathing. It was also demonstrated that vascular resistance in the crural and costal regions of the diaphragm in maximally exercised LH ponies remained similar to that in maximally exercising normal ponies.

Effects of emphysema on diaphragm blood flow during exercise

1998 ◽  
Vol 84 (3) ◽  
pp. 971-979 ◽  
Author(s):  
William L. Sexton ◽  
David C. Poole
Keyword(s):  
Blood Flow ◽  
Treadmill Exercise ◽  
Work Of Breathing ◽  
Regional Distribution ◽  
Blood Flows ◽  
Syrian Golden Hamsters ◽  
Unit Body Weight ◽  
Crural Diaphragm ◽  
Exercise Induced ◽  
And Control

Chronic hyperinflation of the lung in emphysema displaces the diaphragm caudally, thereby placing it in a mechanically disadvantageous position and contributing to the increased work of breathing. We tested the hypothesis that total and regional diaphragm blood flows are increased in emphysema, presumably reflecting an increased diaphragm energetic demand. Male Syrian Golden hamsters were randomly divided into emphysema (E; intratracheal elastase 25 units/100 g body wt) and control (C; saline) groups, and experiments were performed 16–20 wk later. The regional distribution of blood flow within the diaphragm was determined by using radiolabeled microspheres in hamsters at rest and during treadmill exercise (walking at 20 feet/min, 20% grade). Consistent with pronounced emphysema, lung volume per unit body weight was greater in E hamsters (C, 59.3 ± 1.8; E, 84.5 ± 5.0 ml/kg; P < 0.001) and arterial[Formula: see text] was lower both at rest (C, 74 ± 3; E, 59 ± 2 Torr; P < 0.001) and during exercise (C, 93 ± 3; E, 69 ± 4 Torr; P < 0.001). At rest, total diaphragm blood flow was not different between C and E hamsters (C, 47 ± 4; E, 38 ± 4 ml ⋅ min−1 ⋅ 100 g−1; P = 0.18). In both C and E hamsters, blood flow at rest was lower in the ventral costal region of the diaphragm than in the dorsal and medial costal regions and the crural diaphragm. During exercise in both C and E hamsters, blood flows increased more in the dorsal and medial costal regions and in the crural diaphragm than in the ventral costal region. Total diaphragm blood flow was greater in E hamsters during exercise (C, 58 ± 7; E, 90 ± 14 ml ⋅ min−1 ⋅ 100 g−1; P = 0.03), as a consequence of significantly higher blood flows in the medial and ventral costal regions and crural diaphragm. In addition, exercise-induced increases in intercostal ( P < 0.005) and abdominal ( P < 0.05) muscle blood flows were greater in E hamsters. The finding that diaphragm blood flow was greater in E hamsters during exercise supports the contention that emphysema increases the energetic requirements of the diaphragm.

scholarly journals Determinants of Cerebrovascular Reserve in Patients with Significant Carotid Stenosis

2020 ◽  
Author(s):  
Joseph P Archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Patient Specific ◽  
Flow Reserve

AbstractIntroductionIn patients with 70% to 99% diameter carotid artery stenosis cerebral blood flow reserve may be protective of future ischemic cerebral events. Reserve cerebral blood flow is created by brain auto-regulation. Both cerebral blood flow reserve and cerebrovascular reactivity can be measured non-invasively. However, the factors and variables that determine the availability and magnitude and of reserve blood flow remain poorly understood. The availability of reserve cerebral blood flow is a predictor of stroke risk. The aim of this study is to employ a hemodynamic model to predict the variables and functional relationships that determine cerebral blood flow reserve in patients with significant carotid stenosis.MethodsA basic one-dimensional, three-unit (carotid, collateral and brain) energy conservation fluid mechanics blood flow model is employed. It has two distinct but adjacent blood flow components with normal cerebral blood flow at the interface. In the brain auto-regulated blood flow component cerebral blood flow is maintained normal by reserve flow. In the brain pressure dependent blood flow component cerebral blood flow is below normal because cerebral perfusion pressure is below the lower threshold value for auto-regulation. Patient specific values of collateral vascular resistance are determined from a model solution using clinically measured systemic and carotid arterial stump pressures. Collateral vascular resistance curves illustrate the model solutions for reserve and actual cerebral blood flow as a function of percent diameter carotid artery stenosis and mean systemic arterial pressure. The threshold cerebral perfusion pressure value for auto-regulation is assumed to be 50 mmHg. Normal auto-regulated regional cerebral blood flow is assumed to be 50 ml/min/100g. Cerebral blood flow and reserve blood flow solutions are given for systemic arterial pressures of 80, 90, 100, 110 and 120 mmHg and for three patient specific collateral vascular resistance values, Rw = 1.0 (mean patient value), Rw = 0.5 (lower 1 SD) and Rd = 3.0 (upper 1 SD).ResultsReserve cerebral blood flow is only available when a patients cerebral perfusion pressure is in the normal auto-regulatory range. Both actual and reserve cerebral blood flows are primarily from the carotid circulation when carotid stenosis is less than 60% diameter. Between 60% and 75% stenosis the remaining carotid blood flow reserve is utilized and at higher degrees of stenosis all reserve flow is from the collateral circulation. The primary independent variables that determine actual and reserve cerebral blood flow are mean systemic arterial pressure, degree of carotid stenosis and patient specific collateral vascular resistance. Approximate 16% of patients have collateral vascular resistance greater than 5.0 and are predicted to be at high risk of cerebral ischemia or infarction with progression to severe carotid stenosis or occlusion. The approximate 50% of patients with a collateral vascular resistance less than 1.0 are predicted to have adequate cerebral blood flow with progression to carotid occlusion, and most maintain some reserve. Clinically measured values of cerebral blood flow reserve or cerebrovascular reactivity are predicted to be unreliable without consideration of systemic arterial pressure and degree of carotid stenosis. Reserve cerebral blood flow values measured in patients with only moderate 60% to 70% carotid stenosis are in general too high and variable to be of clinical value, but are most reliable when measured near 80% diameter stenosis and considered as percent of the maximum reserve blood flow. Patient specific measured reserve blood flow values can be inserted into the model to calculate the collateral vascular resistance.ConclusionsPredicting cerebral blood flow reserve in patients with significant carotid stenosis is complex and multifactorial. A simple cerebrovascular model predicts that patient specific collateral vascular resistance is an excellent predictor of reserve cerebral blood flow in patients with significant carotid stenosis. Cerebral blood flow reserve measurements are of limited value without accounting for systemic pressure and actual percent carotid stenosis. Asymptomatic patients with severe carotid artery stenosis and a collateral vascular resistance greater than 1.0 are at increased risk of cerebral ischemia and may benefit from carotid endarterectomy.

Regional distribution of blood flow of dogs during graded dynamic exercise

1987 ◽  
Vol 63 (6) ◽  
pp. 2269-2277 ◽  
Author(s):  
T. I. Musch ◽  
D. B. Friedman ◽  
K. H. Pitetti ◽  
G. C. Haidet ◽  
J. Stray-Gundersen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Maximal Exercise ◽  
Regional Blood Flow ◽  
Regional Distribution ◽  
Work Load ◽  
Work Intensity ◽  
Semitendinosus Muscle ◽  
Blood Flows ◽  
Flow Response ◽  
Semimembranosus Muscle

The regional blood flow response to progressive treadmill exercise was measured with radioactive microspheres in 25 untrained mongrel dogs. Incremental increases in work intensity resulted in corresponding increases in blood flows to the gracilis, gastrocnemius, semimembranosus, and semitendinosus muscles of the hindlimb and to the heart. During maximal exercise, blood flow was greatest in the semimembranosus muscle and lowest in the semitendinosus muscle (342 and 134 ml–1.100 g tissue-1.min-1, respectively). Exercise produced a decrease in blood flow to the temporalis muscle, which was classified as nonlocomotive in function. Blood flows to the stomach, pancreas, and large intestine decreased at the lowest exercise work load and remained diminished throughout the continuum to maximal exercise. Blood flows to the small intestine and spleen were maintained during submaximal exercise but were reduced by 50% at maximal O2 consumption (VO2max). No changes in blood flows to the kidneys, adrenal glands, liver, and brain were found. These results demonstrate that 1) renal blood flow is maintained at resting levels during exercise in untrained dogs; 2) blood flow changes in the various organs of the splanchnic region of dogs during exercise are heterogeneous; and 3) blood flows to the working skeletal muscles of dogs progressively increase with increasing work loads up to VO2max.

Intrinsic control of colonic blood flow and oxygenation

1980 ◽  
Vol 238 (6) ◽  
pp. G478-G484
Author(s):  
P. R. Kvietys ◽  
T. Miller ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Reactive Hyperemia ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Colonic Blood Flow ◽  
O2 Extraction ◽  
O2 Delivery

In a denervated autoperfused dog colon preparation, arterial perfusion pressure, venous outflow pressure, blood flow, and arteriovenous O2 difference were measured during graded arterial pressure alterations, arterial occlusion, venous pressure elevation, venous occlusion, and local intra-arterial infusion of adenosine. As perfusion pressure was reduced from 100 to 30 mmHg, colonic blood flow decreased and arteriovenous O2 difference increased. Although blood flow was not autoregulated O2 delivery was maintained within 10% of control between 70 to 100 mmHg and then decreased with further reduction in perfusion pressure. Arterial occlusion (15, 30, and 60 s) resulted in a postocclusion reactive hyperemia; the magnitude of the hyperemia was directly related to the duration of occlusion. Venous occlusion resulted in a postocclusion reactive hypoemia. Elevation of venous pressure from 0 to 20 mmHg increased vascular resistance, O2 extraction, and the capillary filtration coefficient, but decreased O2 delivery. Infusion of adenosine decreased vascular resistance and O2 extraction, but increased O2 delivery. These data suggest that both metabolic and myogenic mechanisms are involved in the control of colonic blood flow and oxygenation.

Choroidal Blood Flow during Exercise-Induced Changes in the Ocular Perfusion Pressure

2003 ◽  
Vol 44 (5) ◽  
pp. 2126 ◽  
Author(s):  
John V. Lovasik ◽  
He´le`ne Kergoat ◽  
Charles E. Riva ◽  
Benno L. Petrig ◽  
Martial Geiser
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Ocular Perfusion Pressure ◽  
Choroidal Blood Flow ◽  
Ocular Perfusion ◽  
Exercise Induced ◽  
Induced Changes

Vasoconstriction is amplified by autoregulation during vasoconstrictor-induced hypertension

1988 ◽  
Vol 254 (4) ◽  
pp. H709-H718 ◽  
Author(s):  
G. A. Meininger ◽  
J. P. Trzeciakowski
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Dose Response ◽  
Flow Curve ◽  
Perfusion Pressure ◽  
Low Doses ◽  
Ang Ii ◽  
Local Pressure ◽  
Pressure Flow

This study investigated the degree to which autoregulation of blood flow interacts with vasoconstrictors to determine vascular resistance. Anesthetized rats were instrumented with a Doppler flow probe on the superior mesenteric artery (SMA) to measure blood flow and for calculation of vascular resistance. An adjustable occluder was placed on the SMA to set local perfusion pressure at values independent of mean arterial pressure (MAP) even when MAP was increased by the vasoconstrictors. Infusion of angiotensin II (ANG II, 50-1,247 ng.kg-1.min-1) produced a dose-dependent rightward shift in the intestinal pressure-flow relationship and elevated MAP from 85 to 127 mmHg. Low doses of phenylephrine (PE, 2.5-12.4 micrograms.kg-1.min-1) failed to shift the pressure-flow curve but did increase arterial pressure from 83 to 102 mmHg. At higher doses (25-62 micrograms.kg-1.min-1), PE also shifted the pressure-flow curve to the right. Maintaining local perfusion pressure at different values during the infusion of ANG II or PE produced a family of dose-response curves, with each exhibiting a different maximum change in resistance. When local pressure was permitted to increase with MAP, the composite dose-response curve for resistance that was obtained reflected the influence of the rise in local pressure (i.e., auto-regulation) and vasoconstrictor dose. At low doses of PE the increase in vascular resistance was attributable solely to an autoregulatory response related to the rise in MAP and not due to the constrictor effects of PE. Thus these data indicate that the rise in MAP accompanying systemic infusion of a vasoconstrictor stimulates autoregulation to amplify the local increase in vascular resistance.

Characteristics of coronary blood flow and transmural distribution in miniature pigs

1978 ◽  
Vol 235 (5) ◽  
pp. H601-H609 ◽  
Author(s):  
M. Sanders ◽  
F. C. White ◽  
T. M. Peterson ◽  
C. M. Bloor
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Oxygen Demand ◽  
Coronary Artery Occlusion ◽  
Adenosine Infusion ◽  
Myocardial Oxygen Demand ◽  
Heavy Exercise ◽  
Miniature Pigs

The relationship between phasic systolic and diastolic coronary blood flow and its transmural distribution has been studied in 29 Yucatan miniature pigs at rest and during heavy exercise, with and without adenosine infusion (1.5 mg . kg-1 . min-1) and with and without a subtotal coronary artery occlusion. Altered factors that affected coronary flow included vascular resistance, perfusion pressure, myocardial oxygen demand, and extra-vascular pressure. The data indicate that, at rest, endomural perfusion is significantly dependent on diastolic blood flow. However, the ability of the myocardial vessels to autoregulate during systole as well as during diastole was clearly shown with the use of adenosine infusion. This ability to regulate flow intrinsically appeared to transcend the endocardial dependency on diastolic perfusion under certain stressful conditions, e.g., during heavy exercise, when the diastolic duration was significantly reduced. Systolic transmural perfusion may then become a significant factor in meeting the blood flow demands of the myocardium. However, due to gradients in vascular resistance, perfusion pressure, and oxygen demand, the coronary reserve of the epicardium appears to be greater than that of the endocardium under any condition.

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

1989 ◽  
Vol 257 (4) ◽  
pp. H1043-H1048 ◽  
Author(s):  
H. M. Wei ◽  
Y. H. Kang ◽  
G. F. Merrill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Vasodepressor Response

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Combined effects of autoregulation and vasoconstrictors on hindquarters vascular resistance

1990 ◽  
Vol 258 (4) ◽  
pp. H1032-H1041 ◽  
Author(s):  
G. A. Meininger ◽  
J. P. Trzeciakowski
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Dose Response ◽  
Perfusion Pressure ◽  
Combined Effects ◽  
Ang Ii ◽  
Response Curves ◽  
Local Pressure ◽  
Pressure Flow ◽  
Dose Dependent

Relative contributions of local autoregulatory tone and vasoconstrictor tone to skeletal muscle vascular resistance were studied in anesthetized rats during hypertension produced by vasoconstrictor infusion. Rats were instrumented with a Doppler flow probe on the sacral aorta (SA) to measure blood flow and to allow calculation of vascular resistance. An occluder was placed on the SA and used to produce stepwise reductions in local perfusion pressure. Pressure-flow curves for the hindquarters were obtained in the absence and presence of elevated mean arterial pressure (MAP) produced by infusion of angiotensin II (ANG II; 50-1,247 ng.kg-1.min-1) or phenylephrine (PE; 2.5-12.4 micrograms.kg-1.min-1). Both ANG II and PE infusion increased MAP. For example, MAP was increased by ANG II from 91 to 134 mmHg and by PE from 89 to 156 mmHg. In addition, infusions of ANG II and PE produced dose-dependent rightward shifts in the hindquarters pressure-flow relationship. To examine the effect of pressure on the dose-response relationships of ANG II or PE, local perfusion pressure was adjusted to remain constant at various pressure levels that were independent of MAP during drug infusions. This produced a series of distinct dose-response curves with each curve defined by a different pressure level and with each characterized by a different maximum change in vascular resistance. If local perfusion pressure was not held constant but was permitted to increase with MAP, a compound dose-response curve was obtained in which the combined effects of the change in local pressure (i.e., autoregulation) and vasoconstrictor dose on vascular resistance could be discerned. These data demonstrate that hindquarters blood flow autoregulation continues to occur in the presence of vasoconstrictors. Consequently, autoregulatory mechanisms may be stimulated by any increase in MAP whether associated with systemic vasoconstrictor infusion or activation of neurohumoral pressor systems. The result is an amplified rise in local vascular resistance.

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