Effects of chlorothiazide on forearm vascular responses to norepinephrine

1961 ◽  
Vol 16 (3) ◽  
pp. 549-552 ◽  
Author(s):  
Khalil A. Feisal ◽  
John W. Eckstein ◽  
A. W. Horsley ◽  
Hugh H. Keasling
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Pressor Response ◽  
Human Subjects ◽  
Chronic Administration ◽  
Normal Subjects ◽  
Vascular Responses ◽  
Chronotropic Response ◽  
Vasoconstrictor Effect ◽  
Normal Human

The effects of graded doses of norepinephrine on pulse rate, mean blood pressure, forearm blood flow and vascular resistance were studied in normal human subjects before, during, and after chronic administration of chlorothiazide. This drug prevented the negative chronotropic response normally induced by norepinephrine without altering the pressor response. Before giving and after discontinuing chlorothiazide, increasing doses of norepinephrine were associated with progressive decreases in blood flow. After 1 week of chlorothiazide administration, increasing doses of norepinephrine were associated with increases in flow. The results indicate that chlorothiazide decreases the responsiveness of the forearm vessels of normal subjects to the vasoconstrictor effect of norepinephrine. They suggest that chlorothiazide also may modify the effect of norepinephrine on cardiac output. Submitted on December 9, 1960

Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects

2001 ◽  
Vol 100 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Eleanor M. SCOTT ◽  
John P. GREENWOOD ◽  
Stephen G. GILBEY ◽  
John B. STOKER ◽  
David A. S. G. MARY
Keyword(s):  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Human Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Normal Subjects ◽  
Water Ingestion ◽  
Water Drinking ◽  
Arterial Blood ◽  
Normal Human

A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean±S.E.M.) from 42±4 to 58±5 impulses/100 beats (P < 0.01) and from 36±4 to 51±5 bursts/100 beats (P < 0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.

Age-Related Decrease in Cardiac and Peripheral Vascular Responsiveness to Isoprenaline: Studies in Normal Subjects

1981 ◽  
Vol 60 (5) ◽  
pp. 571-577 ◽  
Author(s):  
P. Van Brummelen ◽  
F. R. Bühler ◽  
W. Kiowski ◽  
F. W. Amann
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Peripheral Vascular ◽  
Chronotropic Response ◽  
Arterial Blood ◽  
Age Related ◽  
Young Subjects

1. Changes in forearm blood flow to intra-arterial infusion of isoprenaline and the chronotropic response to intravenous boluses of isoprenaline were measured in 15 healthy volunteer subjects, eight younger than 25 years and seven older than 50 years. Intra-arterial blood pressure and basal plasma renin activity, adrenaline and noradrenaline were also measured. 2. Young subjects exhibited a greater increase in forearm blood flow than old subjects, to all four doses of isoprenaline used, a greater cardiac isoprenaline responsiveness (measured by the increase in heart rate; P<0.001) and a higher renin (P<0.02). 3. Resting values of blood pressure, forearm blood flow, adrenaline and noradrenaline were not significantly different in young and old subjects. In the latter, noradrenaline correlated with forearm blood flow (r = −0.77, P<0.05), forearm vascular resistance (r = 0.86, P<0.02) and mean arterial pressure (r = 0.83, P<0.02), whereas in the younger subjects forearm blood flow was related to adrenaline (r = 0.78, P<0.05). 4. These data provide evidence for an age-related parallel reduction in cardiac, peripheral vascular and renal β-adrenoceptor-mediated responses.

Viscosity of normal human blood under normothermic and hypothermic conditions

1964 ◽  
Vol 19 (1) ◽  
pp. 117-122 ◽  
Author(s):  
Peter W. Rand ◽  
Eleanor Lacombe ◽  
Hamilton E. Hunt ◽  
William H. Austin
Keyword(s):  
Blood Flow ◽  
Shear Rate ◽  
Heart Surgery ◽  
Blood Rheology ◽  
Normal Subjects ◽  
Future Studies ◽  
Flow Impedance ◽  
Normal Human ◽  
Technical Details ◽  
Normal Human Blood

Although blood viscosity varies in relation to shear rate, hematocrit, and temperature, equipment is now available with which it may be measured in respect to each of these variables. A simple, clinically practical technique for such measurement is presented. Blood from 60 normal subjects was adjusted to hematocrits 0, 20, 40, 60, and 80, and the viscosity-shear rate relationships measured at 37.0, 32.0, 27.0, and 22.0 C. The data obtained are presented as a reference for future studies using this method. Technical details are discussed and some deserving areas of application are considered. shear rate; cone-plate viscometer; hematocrit-viscosity relationships; blood, plasma; hematocrit; temperature; blood flow impedance; perfusion; shock; oliguria; dyspnea; coma; heart surgery; blood rheology; metabolism Submitted on May 31, 1963

Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation

2001 ◽  
Vol 280 (6) ◽  
pp. H2470-H2477 ◽  
Author(s):  
Julian P. J. Halcox ◽  
Suresh Narayanan ◽  
Laura Cramer-Joyce ◽  
Rita Mincemoyer ◽  
Arshed A. Quyyumi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Epoxyeicosatrienoic Acid ◽  
Healthy Human ◽  
Human Forearm ◽  
Oxide Synthase ◽  
Cytochrome P 450

The identity of endothelium-dependent hyperpolarizing factor (EDHF) in the human circulation remains controversial. We investigated whether EDHF contributes to endothelium-dependent vasomotion in the forearm microvasculature by studying the effect of K+ and miconazole, an inhibitor of cytochrome P-450, on the response to bradykinin in healthy human subjects. Study drugs were infused intra-arterially, and forearm blood flow was measured using strain-gauge plethysmography. Infusion of KCl (0.33 mmol/min) into the brachial artery caused baseline vasodilation and inhibited the vasodilator response to bradykinin, but not to sodium nitroprusside. Thus the incremental vasodilation induced by bradykinin was reduced from 14.3 ± 2 to 7.1 ± 2 ml · min−1 · 100 g−1( P < 0.001) after KCl infusion. A similar inhibition of the bradykinin ( P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl. Miconazole (0.125 mg/min) did not inhibit endothelium-dependent or -independent responses to ACh and sodium nitroprusside, respectively. However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and N G-monomethyl-l-arginine, the forearm blood flow response to bradykinin ( P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole. Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF. In the human forearm microvasculature, EDHF appears to be a cytochrome P-450 derivative, possibly an epoxyeicosatrienoic acid.

Role of vagal feedback from the lung in hypoxic-induced tachycardia in humans

1995 ◽  
Vol 78 (4) ◽  
pp. 1522-1530 ◽  
Author(s):  
P. M. Simon ◽  
B. H. Taha ◽  
J. A. Dempsey ◽  
J. B. Skatrud ◽  
C. Iber
Keyword(s):  
Lung Transplant ◽  
Human Subjects ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Chronotropic Response ◽  
Transplant Patients ◽  
Marked Variability ◽  
Arterial O2 Saturation ◽  
Mild Hypoxia

We assessed the cardiovascular responses to systemic normocapnic hypoxia in five normal subjects, five double lung transplant patients with lung denervation and intact hearts, and five patients with denervated hearts. Progressive normocapnic hypoxia was induced over 10–15 min and maintained for 2–3 min each at 90, 87, 84, and 80% arterial O2 saturation (SaO2). Normal subjects showed the most pronounced mean increase in heart rate (dHR/dSaO2 = 0.86 +/- 0.13 beat/min per 1% SaO2). Three lung-denervated subjects had normal tachycardiac responses (1.6, 0.9, and 0.69 beats/min per 1%), whereas the other two had distinctly lower responses (0.34 and 0.39 beat/min per 1%). Most of the lung-denervated subjects also showed a significant tachycardia with even mild hypoxia; none showed a bradycardiac response to any level of hypoxia. In the heart-denervated group, hypoxic tachycardia was significantly lower than normal (0.29 +/- 0.13 beat/min per 1%). We conclude that vagal feedback from the lungs is not required for the normal chronotropic response to hypoxia in humans; however, this mechanism may contribute significantly to the marked variability in hypoxic-induced tachycardia found among human subjects. These data in humans contrast with the progressive bradycardiac response to hypoxia reported in vagally denervated (or nonhyperpneic) dogs and cats.

Adenosine contributes to hypoxia-induced forearm vasodilation in humans

1999 ◽  
Vol 87 (6) ◽  
pp. 2218-2224 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Kris Gray ◽  
Michael D. Herr
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Brachial Artery ◽  
Adenosine Receptors ◽  
Forearm Blood Flow ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Normal Subjects ◽  
Local Release ◽  
Forearm Vascular Resistance

In humans, hypoxia leads to increased sympathetic neural outflow to skeletal muscle. However, blood flow increases in the forearm. The mechanism of hypoxia-induced vasodilation is unknown. To test whether hypoxia-induced vasodilation is cholinergically mediated or is due to local release of adenosine, normal subjects were studied before and during acute hypoxia (inspired O210.5%; ∼20 min). In experiment I, aminophylline (50–200 μg ⋅ min−1 ⋅ 100 ml forearm tissue−1) was infused into the brachial artery to block adenosine receptors ( n = 9). In experiment II, cholinergic vasodilation was blocked by atropine (0.4 mg over 4 min) infused into the brachial artery ( n = 8). The responses of forearm blood flow (plethysmography) and forearm vascular resistance to hypoxia in the infused and opposite (control) forearms were compared. During hypoxia (arterial O2 saturation 77 ± 2%), minute ventilation and heart rate increased while arterial pressure remained unchanged; forearm blood flow rose by 35 ± 6% in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm ( P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the aminophylline-treated forearm ( P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.

AN EFFECT OF REDUCED BAROMETRIC PRESSURE ON THE PERIPHERAL CIRCULATION

1957 ◽  
Vol 35 (10) ◽  
pp. 777-783
Author(s):  
F. Girling ◽  
F. A. Sunahara
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Peripheral Circulation ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
The Past

Several groups of investigators have noted in the past that exposure to a reduced barometric pressure results in a decrease in peripheral blood flow.In the present study human subjects were exposed to a pressure of 225 mm. Hg with maintenace of arterial oxygen saturation, and forearm and hand blood flows were measured plethysmographically. Forearm blood flow was not affected by the exposure whereas hand blood flow was reduced in all subjects. Blood pressure and heart rate were also measured and showed no change during the experiment.

Contribution of prostaglandins to exercise-induced vasodilation in humans

1993 ◽  
Vol 265 (1) ◽  
pp. H171-H175 ◽  
Author(s):  
J. R. Wilson ◽  
S. C. Kapoor
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Catheter ◽  
Normal Subjects ◽  
Wrist Flexion ◽  
Arterial Infusion ◽  
Prostaglandin Release ◽  
Exercise Induced ◽  
Arteriolar Vasodilation

It has been postulated that endothelial release of prostaglandins contributes to exercise-induced vasodilation of skeletal muscle arterioles. To test this hypothesis, 12 normal subjects underwent brachial arterial and venous catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow and arterial and venous 6-ketoprostaglandin F1 alpha (PGF1 alpha) and prostaglandin E2 (PGE2) were then measured during two levels of wrist flexion exercise (0.2 and 0.4 W). In nine of the subjects, exercise was repeated after intra-arterial infusion of indomethacin (0.3 mg/100 ml forearm vol). Exercise increased forearm blood flow (2.0 +/- 0.2 to 12.1 +/- 1.1 ml.min-1.100 ml-1) and forearm release of PGF1 alpha (162 +/- 28 to 766 +/- 193 pg.min-1.100 ml-1) and PGE2 (26 +/- 6 to 125 +/- 46 pg.min-1.100 ml-1) (all P < 0.05). Indomethacin virtually abolished forearm prostaglandin release and reduced forearm blood flow at rest (2.2 +/- 0.2 to 1.7 +/- 0.2 ml.min-1.100 ml-1), at 0.2 W (6.3 +/- 0.7 to 5.4 +/- 0.7 ml.min-1.100 ml-1), and at 0.4 W (12.2 +/- 1.5 to 10.3 +/- 1.3 ml.min-1.100 ml-1) (all P < 0.02). These data suggest that release of vasodilatory prostaglandins contributes to exercise-induced arteriolar vasodilation and hyperemia in skeletal muscle.

Platelet catecholamines and platelet function in normal human subjects

1987 ◽  
Vol 73 (1) ◽  
pp. 99-103 ◽  
Author(s):  
A. P. Wilson ◽  
C. C. T. Smith ◽  
B. N. C. Prichard ◽  
D. J. Betteridge
Keyword(s):  
Platelet Function ◽  
High Performance ◽  
Human Subjects ◽  
Normal Subjects ◽  
Noradrenaline Content ◽  
Collagen Concentration ◽  
Normal Human ◽  
Wall Interaction ◽  
Local Release

1. We have used high-performance liquid chromatography with electrochemical detection to measure plasma and platelet catecholamines in 24 normal subjects. 2. In the same subjects platelet function was assessed by measuring platelet aggregation in response to adenosine 5′-pyrophosphate, thrombin, adrenaline and collagen. Platelet sensitivity to prostacyclin was also examined. 3. Platelet noradrenaline showed a positive correlation with extent of aggregation induced by ‘low-dose’ collagen (1 μg/ml). No correlation was seen at the higher collagen concentration. 4. Platelet noradrenaline content also correlated with sensitivity of platelets to prostacyclin. High platelet noradrenaline concentrations appeared to result in decreased sensitivity to prostacyclin. 5. No other correlations were observed. 6. These data suggest that platelet noradrenaline rather than plasma levels may be involved in modifying platelet function in vivo. Local release of platelet catecholamines may affect the platelet/vessel wall interaction, the primary physiological step in platelet activation.

Effects of posture on peripheral vascular responses to lower body positive pressure

2007 ◽  
Vol 293 (1) ◽  
pp. H670-H676 ◽  
Author(s):  
Takeshi Nishiyasu ◽  
Shigeko Hayashida ◽  
Asami Kitano ◽  
Kei Nagashima ◽  
Masashi Ichinose
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Positive Pressure ◽  
Upper Limbs ◽  
Lower Body ◽  
Peripheral Vascular ◽  
Vascular Responses ◽  
Lower Body Positive Pressure ◽  
Body Positive

We tested the hypothesis that peripheral vascular responses (in the lower and upper limbs) to application of lower body positive pressure (LBPP) are dependent on the posture of the subjects. We measured heart rate, stroke volume, mean arterial pressure, leg and forearm blood flow (using the Doppler ultrasound technique), and leg (LVC) and forearm (FVC) vascular conductance in 11 subjects (9 men, 2 women) without and with LBPP (25 and 50 mmHg) in supine and upright postures. Mean arterial pressure increased in proportion to increases in LBPP and was greater in supine than in upright subjects. Heart rate was unchanged when LBPP was applied to supine subjects but was reduced in upright ones. Leg blood flow and LVC were both reduced by LBPP in supine subjects [LVC: 4.8 (SD 4.0), 3.6 (SD 3.5), and 1.4 (SD 1.8) ml·min−1·mmHg−1 before LBPP and during 25 and 50 mmHg LBPP, respectively; P < 0.05] but were increased in upright ones [LVC: 2.0 (SD 1.2), 3.4 (SD 3.4), and 3.0 (SD 2.0) ml·min−1·mmHg−1, respectively; P < 0.05]. Forearm blood flow and FVC both declined when LBPP was applied to supine subjects [FVC: 1.3 (SD 0.6), 1.0 (SD 0.4), and 0.9 (SD 0.6) ml· min−1·mmHg−1, respectively; P < 0.05] but remained unchanged in upright ones [FVC: 0.7 (SD 0.4), 0.7 (SD 0.4), and 0.6 (SD 0.5) ml·min−1·mmHg−1, respectively]. Together, these findings indicate that the leg vascular response to application of LBPP is posture dependent and that the response differs in the lower and upper limbs when subjects assume an upright posture.

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