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.

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.

Differential responses of uterine and umbilical vasculatures to angiotensin II and norepinephrine

1990 ◽  
Vol 259 (1) ◽  
pp. H197-H203 ◽  
Author(s):  
K. E. Clark ◽  
G. L. Irion ◽  
C. E. Mack
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Base Line ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Umbilical Blood ◽  
Arterial Blood ◽  
Pregnant Sheep

Although the uterine vascular responses to endogenous vasoactive substances have been extensively investigated in pregnant sheep, the fetal umbilical responses to angiotensin II (ANG II) and norepinephrine (NE) have not been well characterized. Twenty-five pregnant ewes between 105 and 115 days of gestation were anesthetized and instrumented for hemodynamic measurements, systemic fetal and maternal intravenous infusions, and local maternal uterine arterial infusions of ANG II and NE. Fetal and maternal arterial pressure and heart rate, maternal uterine blood flow (total of left and right middle uterine arteries), and fetoplacental blood flow (common umbilical artery) were measured during continuous infusions of ANG II or NE. Fetal infusions of ANG II (0.03–1.0 micrograms.min-1.kg estimated fetal body wt-1) increased fetal arterial blood pressure by as much as 44% over base-line values, decreased umbilical blood flow by as much as 63%, and increased umbilical vascular resistance by up to 345%. Fetal infusions of NE (0.1–3 micrograms.min-1.kg-1) increased fetal arterial pressure 42% and increased umbilical vascular resistance by up to 38% but did not significantly alter fetoplacental blood flow. No significant maternal changes were observed during fetal infusions. Maternal infusion of ANG II increased maternal arterial pressure by as much as 59% and significantly increased uterine vascular resistance at the two highest doses but significantly decreased uterine blood flow only at the highest dose (17%; P less than 0.05). Maternal infusions of NE increased arterial pressure by as much as 113%, decreased uterine blood flow by as much as 76%, and increased uterine vascular resistance 3- to 10-fold over the base-line value.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoregulation of gastric blood flow and oxygen uptake

1981 ◽  
Vol 241 (2) ◽  
pp. G143-G149
Author(s):  
L. Holm-Rutili ◽  
M. A. Perry ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Oxygen Demand ◽  
Gastric Blood Flow ◽  
Oxygen Extraction ◽  
Sympathetic Denervation

The purpose of this study was to determine whether the ability of the stomach to autoregulate blood flow and oxygen uptake is altered by sympathetic denervation. Blood flow, oxygen extraction, local arterial pressure, and venous pressure were continuously monitored in sympathetically innervated and denervated autoperfused dog stomach preparations. As perfusion pressure was reduced in increments from 120 to 20 mmHg in innervated preparations, blood flow and oxygen uptake decreased while oxygen extraction and vascular resistance increased. Reductions in perfusion pressure in denervated preparations resulted in a decrease in blood flow, oxygen uptake, and vascular resistance, whereas oxygen extraction increased. The ability of the stomach to regulate blood flow and oxygen uptake was significantly improved after denervation, i.e., vascular resistance decreased and oxygen uptake remained relatively constant when arterial pressure was reduced. Oxygen uptake in denervated stomachs was generally higher than that in innervated stomachs. Autoregulation of gastric blood flow therefore appears to be improved by denervation. The better autoregulation observed after denervation may result either from a reduction in sympathetic tone and/or the increase in gastric oxygen demand.

Role of angiotensin II and prostaglandins in the regulation of uteroplacental blood flow

1993 ◽  
Vol 264 (3) ◽  
pp. R584-R590 ◽  
Author(s):  
L. L. Woods
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Perfusion Pressure ◽  
Moderate Degree ◽  
Ang Ii ◽  
Response Curves ◽  
Uteroplacental Blood Flow ◽  
Uterine Perfusion

This study was designed to determine the importance of the renin-angiotensin (RAS) and prostaglandin (PG) systems in regulating uteroplacental blood flow (UBF). Our objectives were to determine: 1) whether angiotensin II (ANG II) acts as a vasodilator or purely as a vasoconstrictor in the uteroplacental circulation, and 2) whether this circulation is capable of autoregulation. In chronically instrumented pregnant dogs (41-54 days gestation), ANG II was infused intravenously at increasing doses (8, 16, and 24 ng.kg-1 x min-1). Arterial pressure rose from 108 +/- 6 to 146 +/- 4 mmHg and UBF did not change but uterine vascular resistance (UVR) progressively increased. When the experiment was repeated while servo-controlling uterine arterial pressure, UBF fell at all doses, reaching 62 +/- 7% of control at the highest dose, and UVR increased as before. Meclofenamate (6 mg/kg i.v.) did not alter the dose-response curves. In separate experiments, uterine perfusion pressure was reduced in steps to 55 mmHg. UBF was well autoregulated down to approximately 85 mmHg, and neither captopril (14 micrograms.kg-1 x min-1) nor meclofenamate altered UBF autoregulation. Thus ANG II appears to act as a vasoconstrictor in the uteroplacental circulation and any preservation of UBF during ANG II appears to be due to the increased arterial pressure. Also, in the dog the uteroplacental circulation possesses a mild to moderate degree of autoregulatory capability, which does not appear to be dependent on the RAS or PGs.

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.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

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.

Pulmonary vascular alpha 1-adrenoreceptor activity in conscious dogs after left lung autotransplantation

1993 ◽  
Vol 74 (2) ◽  
pp. 733-741 ◽  
Author(s):  
K. Nishiwaki ◽  
D. P. Nyhan ◽  
R. S. Stuart ◽  
P. M. Desai ◽  
W. P. Peterson ◽  
...  
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Dose Response ◽  
Vascular Reactivity ◽  
Left Lung ◽  
Conscious Dogs ◽  
Response Relationship ◽  
Dose Response Relationship ◽  
Pressure Flow ◽  
Vascular Regulation

We investigated the extent to which sympathetic alpha 1-adrenoreceptor activation is involved in chronic pulmonary vascular regulation in conscious dogs after left lung autotransplantation (LLA). Continuous left pulmonary vascular pressure-flow plots were generated in conscious dogs 3–4 wk post-LLA and in identically instrumented conscious dogs not subjected to LLA (sham-operated controls). LLA resulted in a marked upward shift in the baseline left pulmonary vascular pressure-flow relationship compared with the control group (P < 0.01), i.e., LLA caused a chronic increase in pulmonary vascular resistance. The sympathetic alpha 1-adrenoreceptor antagonist prazosin partially reversed (P < 0.01) the LLA-induced increase in pulmonary vascular resistance. Circulating concentrations of norepinephrine and epinephrine at 2 and 4 wk post-LLA were not significantly different from values measured in control dogs. However, the dose-response relationship to the exogenous administration of the sympathetic alpha 1-adrenoreceptor agonist phenylephrine was shifted (P < 0.05) to the left post-LLA compared with control, which indicates an increase in pulmonary vascular reactivity to alpha 1-adrenoreceptor activation. This effect was not due to a generalized increase in pulmonary vascular reactivity to vasoconstrictor stimuli because the dose-response relationship to the thromboxane analogue U-46619 was not significantly altered post-LLA compared with control. Thus LLA results in a chronic increase in pulmonary vascular resistance in conscious dogs. A component of the increase in pulmonary vascular resistance resulting from LLA is mediated by an enhanced reactivity to sympathetic alpha 1-adrenoreceptor activation.

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