Hypercapnia-induced cerebral and ocular vasodilation is not altered by glibenclamide in humans

2000 ◽  
Vol 278 (6) ◽  
pp. R1667-R1673 ◽  
Author(s):  
Michaela Bayerle-Eder ◽  
Michael Wolzt ◽  
Elzbieta Polska ◽  
Herbert Langenberger ◽  
Johannes Pleiner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Crossover Study ◽  
Flow Velocity ◽  
Forearm Blood Flow ◽  
Resistive Index ◽  
Venous Occlusion ◽  
Mean Flow ◽  
Choroidal Blood Flow ◽  
Double Blind ◽  
Induced Changes

Carbon dioxide is an important regulator of vascular tone. Glibenclamide, an inhibitor of ATP-sensitive potassium channel (KATP) activation, significantly blunts vasodilation in response to hypercapnic acidosis in animals. We investigated whether glibenclamide also alters the cerebral and ocular vasodilator response to hypercapnia in humans. Ten healthy male subjects were studied in a controlled, randomized, double-blind two-way crossover study under normoxic and hypercapnic conditions. Glibenclamide (5 mg po) or insulin (0.3 mU ⋅ kg− 1 ⋅ min− 1iv) were administered with glucose to achieve comparable plasma insulin levels. In control experiments, five healthy volunteers received glibenclamide (5 mg) or nicorandil (40 mg) or glibenclamide and nicorandil in a randomized, three-way crossover study. Mean blood flow velocity and resistive index in the middle cerebral artery (MCA) and in the ophthalmic artery (OA) were measured with Doppler sonography. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation. Forearm blood flow was measured with venous occlusion plethysmography. Hypercapnia increased ocular fundus pulsation amplitude by +18.2–22.3% ( P < 0.001) and mean flow velocity in the MCA by +27.4–33.3% ( P < 0.001), but not in the OA (2.1–6.5%, P = 0.2). Forearm blood flow increased by 78.2% vs. baseline ( P = 0.041) after nicorandil administration. Glibenclamide did not alter hypercapnia-induced changes in cerebral or ocular hemodynamics and did not affect systemic hemodynamics or forearm blood flow but significantly increased glucose utilization and blunted the nicorandil-induced vasodilation in the forearm. This suggests that hypercapnia-induced changes in the vascular beds under study are not mediated by activation of KATPchannels in humans.

Vascular KATP channel blockade by glibenclamide, but not by acarbose, in patients with Type II diabetes

2002 ◽  
Vol 102 (3) ◽  
pp. 307-314
Author(s):  
E.J. ABBINK ◽  
P. PICKKERS ◽  
A. Jansen VAN ROSENDAAL ◽  
J.A. LUTTERMAN ◽  
C.J. TACK ◽  
...  
Keyword(s):  
Blood Flow ◽  
Type Ii Diabetes ◽  
Katp Channel ◽  
Forearm Blood Flow ◽  
Cardiovascular Effects ◽  
Venous Occlusion ◽  
Type Ii Diabetes Mellitus ◽  
Protective Mechanism ◽  
Type Ii ◽  
Double Blind

Glibenclamide inhibits the opening of vascular ATP-sensitive potassium (KATP) channels, which represents a protective mechanism during ischaemia. This effect may imply harmful cardiovascular effects of glibenclamide when used under conditions of ischaemia in patients with Type II diabetes. Acarbose is not associated with effects on the cardiovascular system, because the drug is not absorbed from the bowel. Therefore we hypothesized that treatment of Type II diabetes patients with glibenclamide will impair the vasodilator function of KATP opening, unlike treatment with acarbose. A double-blind randomized cross-over study in 12 patients with Type II diabetes was performed to compare the effects of glibenclamide with those of acarbose on the vasodilator responses to KATP channel opening in the forearm vascular bed. The study consisted of two periods: 8 weeks of treatment with orally administered glibenclamide (10mgċday-1) followed by 8 weeks of treatment with acarbose (300mgċday-1), or vice versa. At the end of each treatment period, forearm blood flow (venous occlusion plethysmography) in response to intra-arterially administered diazoxide, acetylcholine and dipyridamole and to forearm ischaemia was measured. The diazoxide-mediated increase in the forearm blood flow ratio (infused/control arm) was significantly less pronounced after glibenclamide than after acarbose (290±58% and 561±101% respectively; P < 0.0005). Forearm blood flow responses to acetylcholine, dipyridamole and forearm ischaemia were similar during glibenclamide and acarbose treatment. Thus, in patients with Type II diabetes mellitus, treatment with glibenclamide is associated with an attenuated response to KATP opening as compared with treatment with acarbose. This implies that glibenclamide may affect defensive mechanisms under conditions of KATP channel activation.

scholarly journals Effects of 1 MHz Therapeutic Ultrasound on Limb Blood Flow and Microvascular Reactivity: A Randomized Pilot Trial

2021 ◽  
Vol 18 (21) ◽  
pp. 11444
Author(s):  
Megan Waters ◽  
Branko Miljkovic ◽  
Jozelyn Rascon ◽  
Manuel Gomez ◽  
Alvaro N. Gurovich
Keyword(s):  
Blood Flow ◽  
Repeated Measures ◽  
Forearm Blood Flow ◽  
Pilot Trial ◽  
Therapeutic Ultrasound ◽  
Venous Occlusion ◽  
Double Blind ◽  
Effective Treatment Modality ◽  
Group Time ◽  
Before And After

A randomized, double-blind, placebo-controlled, cross-over study where continuous therapeutic ultrasound (CUS; at 0.4 W/cm2), pulsed therapeutic ultrasound (PUS; at 20% duty cycle, 0.08 W/cm2), both at 1 MHz, and placebo (equipment on, no energy provided) were randomized and applied over the forearm of the non-dominant arm for 5 min in 10 young, healthy individuals. Absolute and peak forearm blood flow (FBF) were measured via Venous Occlusion Plethysmography. FBF was measured before, halfway, and after (immediately and 5 min after) the therapeutic ultrasound (TUS) intervention. Post-ischemic peak FBF was measured 10 min before and 10 min after the TUS intervention. A two-way repeated measures ANOVA (group × time) was selected to assess differences in FBF before, during, and after TUS treatment, and for peak FBF before and after TUS treatment. FBF increased 5 min after TUS in CUS compared to placebo (2.96 ± 1.04 vs. 2.09 ± 0.63 mL/min/100 mL of tissue, p < 0.05). PUS resulted in the greatest increase in Peak FBF at 10 min after US (Δ = 3.96 ± 2.02 mL/min/100 mL of tissue, p = 0.06). CUS at 1 MHz was an effective treatment modality for increasing FBF up to 5 min after intervention, but PUS resulted in the greatest increase in peak FBF at 10 min after intervention.

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans

1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Time Course ◽  
Forearm Blood Flow ◽  
Voluntary Contraction ◽  
Double Blind ◽  
Rate Of Increase ◽  
Forearm Exercise ◽  
Blind Manner ◽  
Exercise In Humans

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.

Noninvasive measurement of forearm blood flow and oxygen consumption by near-infrared spectroscopy

1994 ◽  
Vol 76 (3) ◽  
pp. 1388-1393 ◽  
Author(s):  
R. A. De Blasi ◽  
M. Ferrari ◽  
A. Natali ◽  
G. Conti ◽  
A. Mega ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Healthy Subjects ◽  
Near Infrared ◽  
Forearm Blood Flow ◽  
Vascular Occlusion ◽  
Venous Occlusion ◽  
The Subject

We applied near-infrared spectroscopy (NIRS) for the simultaneous measurement of forearm blood flow (FBF) and oxygen consumption (VO2) in the human by inducing a 50-mmHg venous occlusion. Eleven healthy subjects were studied both at rest and after hand exercise during vascular occlusion. FBF was also measured by strain-gauge plethysmography. FBF measured by NIRS was 1.9 +/- 0.8 ml.100 ml-1.min-1 at rest and 8.2 +/- 2.9 ml.100 ml-1.min-1 after hand exercise. These values showed a correlation (r = 0.94) with those obtained by the plethysmography. VO2 values were 4.6 +/- 1.3 microM O2 x 100 ml-1.min-1 at rest and 24.9 +/- 11.2 microM O2 x 100 ml-1.min-1 after hand exercise. The scatter of the FBF and VO2 values showed a good correlation between the two variables (r = 0.93). The results demonstrate that NIRS provides the particular advantage of obtaining the contemporary evaluation of blood flow and VO2, allowing correlation of these two variables by a single maneuver without discomfort for the subject.

Abstract P531: Cerebral Blood Flow Analysis Using Flow Wire Measurements and CFD Analysis

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Aichi Chien ◽  
Huy Dinh ◽  
Viktor Szeder ◽  
Fernando Vinuela
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Cfd Simulation ◽  
Cfd Analysis ◽  
Flow Data ◽  
Velocity Data ◽  
Mean Flow ◽  
Good Agreement ◽  
Cerebral Vascular

Introduction: Clinical reports show that cerebral blood flow conditions are indicative of cerebral vascular disease. While methods for characterizing cerebral vascular flow have been extensively reported in the past, comparative analyses between direct flow measurements (DM) and computational flow dynamic (CFD) analysis remain limited. We hypothesize that flow data can be reliably measured both directly and through CFD in normal vessels. Methods: A left heart replicator was used as a realistic cardiac pump which maintained systolic pressure at 120 mmHg and diastolic pressure at 80 mmHg. A stenotic model with 50% stenosis for the ICA was connected to the replicator. A ComboWire was used for DM and recorded flow pressure and velocity. CFD was used to study flow. Results: In areas at the proximal end of the stenosis, the pressure and flow velocity derived from DM and CFD were in good agreement. At the end of systole and diastole, DM pressure were 145.42 mmHg and 73.53 mmHg, respectively. CFD simulation for the same system obtained the pressure at the end of systole and diastole of 147.16 mmHg and 74.64 mmHg, respectively. The velocity data collected from DM was at 15.40 cm/s and 7.74 cm/s for systolic flow and mean flow velocity. CFD measured flow was 17.85 cm/s and 11.37 cm/s, respectively. In areas at the distal end of the stenosis, pressure data showed good agreement between DM and CFD analysis. The DM were 138 and 70.81 mmHg at the end of systole and diastole, respectively; CFD simulation yielded 145.95 and 74.51 mmHg, respectively. Variations in the velocity data were observed at this location (Fig, pink arrows). Conclusion: DM of pressure showed good agreement with CFD simulation in all areas of the vessel. DM of velocity using the flow wire were highly affected by location of the measurement. CFD analysis can provide more consistent flow data for flow information collection along the vasculature.

Abstract WP432: Non-invasive Respiratory Impedance Enhances Cerebral Perfusion

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Christopher G Favilla ◽  
Ashwin B Parthasarathy ◽  
John A Detre ◽  
Michael T Mullen ◽  
Scott E Kasner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Flow Velocity ◽  
Cerebral Perfusion ◽  
Respiratory Impedance ◽  
Mean Flow ◽  
Non Invasive ◽  
End Tidal ◽  
High Level ◽  
Mean Flow Velocity

Background: Optimization of cerebral blood flow is the cornerstone of clinical management in a number of neurologic diseases, most notably ischemic stroke. Intra-thoracic pressure influences cardiac output and has the potential to impact cerebral blood flow (CBF). Here we aim to quantify cerebral hemodynamic changes in response to increased respiratory impedance using a non-invasive respiratory device. Methods: Cerebral perfusion was measured under varying levels of respiratory impedance (6cm H 2 0, 9cm H 2 0, and 12 cm H 2 0) in 20 healthy volunteers. Simultaneous measurements of microvascular CBF and middle cerebral artery mean flow velocity (MFV), respectively, were performed with optical diffuse correlation spectroscopy (DCS) and transcranial Doppler ultrasound (TCD). Results: At the high level of respiratory impedance, mean flow velocity increased by 6.4% compared to baseline (p=0.004), but changes in cortical CBF were smaller and non-significant (Figure). Heart rate, cardiac output, respiratory rate, and end tidal CO 2 remained stable during all levels of respiratory impedance. There was small increase in mean arterial blood pressure, 1.7% (p=0.006), at the high level of respiratory impedance. In a multivariable linear regression model accounting for end tidal CO 2 and individual variability, respiratory impedance was associated with increases in both mean flow velocity (coefficient: 0.49, p<0.001) and cortical CBF (coefficient: 0.13, p<0.001). Conclusions: Manipulating intrathoracic pressure via non-invasive respiratory impedance was well tolerated and produced a small but measurable increase in cerebral perfusion in healthy individuals. Future studies in acute ischemic stroke patients with impaired cerebral autoregulation is warranted in order to assess whether respiratory impedance is feasible as a novel non-invasive therapy for stroke.

scholarly journals Parathyroid Hormone's Acute Effect on Vasodilatory Function

2010 ◽  
Vol 3 ◽  
pp. CMED.S4650 ◽  
Author(s):  
P. Farahnak ◽  
L. Lind ◽  
K. Mattala ◽  
I-L. Nilsson
Keyword(s):  
Cardiovascular Disease ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Acute Effect ◽  
Venous Occlusion ◽  
Arterial Infusion ◽  
Resistance Vessels ◽  
Vasodilatory Function ◽  
Pth Level

Parathyroid hormone (PTH) seems to affect the risk of cardiovascular disease. The aim of the present study was to investigate PTH's acute effect on endothelial vasodilatory function in forearm resistance vessels. Ten healthy subjects underwent forearm venous occlusion plethysmography. We measured forearm blood flow at baseline and at a stable, locally increased PTH level after intra-arterial infusion of metacholine and nitroprusside. The contralateral arm served as a control. Ionized calcium (Ca++) and PTH values were normal in all subjects at baseline (1.26 ± 0.02 mM/L, 3.6 ± 1.2 pM/L). After 30 minutes of PTH infusion, the PTH level increased in the active arm (13.8 ± 4.0 pM/L P < 0.01), while the Ca++ level was unchanged (1.25 ± 0.04; mM/L). Both the PTH and the Ca++ level in the contralateral arm remained unchanged, which indicates no systemic influence. The endothelial-dependent vasodilation was inversely correlated to the Ca++ level at baseline (r = −0.75, P < 0.05) and after PTH infusion (r = −0.68, P < 0.05). The vasodilatory function was not affected during PTH-infusion.

Action of the endothelin receptor (ETA) antagonist BQ-123 on forearm blood flow in young normotensive subjects

2002 ◽  
Vol 102 (6) ◽  
pp. 661-666 ◽  
Author(s):  
R.C. WIMALASUNDERA ◽  
S.A.McG. THOM ◽  
L. REGAN ◽  
A.D. HUGHES
Keyword(s):  
Blood Flow ◽  
Vascular Tone ◽  
Forearm Blood Flow ◽  
Randomized Study ◽  
Double Blind ◽  
Eta Receptor ◽  
Normotensive Subjects ◽  
Eta Receptor Antagonist ◽  
Forearm Occlusion

Endothelin-1 (ET-1) has been proposed to contribute to the regulation of vascular tone in humans. BQ-123, an ETA receptor antagonist, has also been reported to increase forearm blood flow (FBF) in vivo; however, the efficacy of BQ-123 as an antagonist of ET-1 has not been evaluated in the forearm. The present study investigated the effects of BQ-123 on changes in FBF in response to ET-1 and noradrenaline (NA; norepinephrine), taking into account the possible influence of vasodilator effects of BQ-123 on responses to vasoconstrictors. Six subjects (age 25-34 years) participated in a double-blind randomized study. FBF was measured by forearm occlusion plethysmography. Drugs were infused intra-arterially into the non-dominant arm (study arm) on four separate occasions; the non-infused arm was used as a control. The effects of BQ-123 (50nmol/min for 60min, or 300nmol/min for 5min followed by saline for 55min) were compared with the effects of infusion of sodium nitroprusside (SNP; 12nmol/min for 60min) or saline on vasoconstriction induced by ET-1 (10pmol/min for 7min) and NA (120pmol/min for 7min). Infusion of BQ-123 at either dose did not significantly increase FBF, whereas SNP increased FBF by 134% (P = 0.03). ET-1 significantly reduced FBF, and this effect was almost completely inhibited by both doses of BQ-123, but was unaffected by SNP. NA also reduced FBF, and this action was unaffected by BQ-123 or SNP. The data show that BQ-123 is a selective ET-1 antagonist, but do not confirm a major role for ET-1 in influencing resting forearm vascular tone in young normotensive subjects.

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