Measuring forearm blood flow and interpreting the responses to drugs and mediators.

Venous occlusion plethysmography has been widely used to study forearm blood flow. The principle of the technique is straightforward: the rate of swelling of the forearm during occlusion of venous return is used to assess the rate of arterial inflow. Provided that perfusion pressure (arterial blood pressure) remains constant, changes in flow reflect changes in smooth muscle tone in small arteries and arterioles. Local infusion into the brachial artery allows assessment of the direct effect of drugs on vascular tone and has been used to probe the roles of endogenous mediators. The technique is at its most powerful when dose-response relationships to different drugs or mediators within a single study are being compared but can also be used for comparison of responses to drugs between healthy control subjects and patient populations. However, when responses between groups are being compared, it is important to take into account the starting conditions of baseline blood flow and pressure. This article describes venous occlusion plethysmography, discusses the presentation and analysis of data (dose of drug or concentration? forearm blood flow or resistance?), and highlights certain potential problems and limitations of the technique as a means of studying disease states.

[1]  O. Heikinheimo,et al.  Dose-response relationships of RU 486. , 1993, Annals of medicine.

[2]  B. Robinson Altered calcium handling as a cause of primary hypertension. , 1984, Journal of hypertension.

[3]  A. Quyyumi,et al.  Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension. , 1990, The New England journal of medicine.

[4]  H. Barcroft,et al.  On sympathetic vasoconstrictor tone in human skeletal muscle , 1943, The Journal of physiology.

[5]  A. Greenfield,et al.  Reactions of the blood vessels of the human forearm to increases in transmural pressure , 1954, The Journal of physiology.

[6]  R. F. Whelan,et al.  A comparison of the effects of intra-arterial and intravenous infusions of angiotensin and noradrenaline on the circulation in man. , 1965, Clinical science.

[7]  W. Wallace,et al.  Methods for the assessment of the effects of drugs on the arterial system in man. , 1979, British journal of clinical pharmacology.

[8]  B. Folkow The fourth Volhard lecture: cardiovascular structural adaptation; its role in the initiation and maintenance of primary hypertension. , 1978, Clinical science and molecular medicine. Supplement.

[9]  R. Whelan Control of the peripheral circulation in man , 1967 .

[10]  S Moncada,et al.  Role of endothelium-derived nitric oxide in the regulation of blood pressure. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[11]  O G EDHOLM,et al.  The blood flow in skin and muscle of the human forearm , 1955, The Journal of physiology.

[12]  R. Wilkins,et al.  Changes in arterial and venous blood pressure and flow distal to a cuff inflated on the human arm. , 1946, The American journal of physiology.

[13]  Julio A. Panza,et al.  Circadian variation in vascular tone and its relation to α-sympathetic vasoconstrictor activity , 1991 .

[14]  F. Bühler,et al.  Vasodilatory effect of nicardipine and verapamil in the forearm of hypertensive as compared with normotensive man. , 1985, British journal of clinical pharmacology.

[15]  S. Moncada,et al.  Effect of local intra-arterial NG-monomethyl-L-arginine in patients with hypertension: the nitric oxide dilator mechanism appears abnormal. , 1992, Journal of hypertension.

[16]  R. Furchgott,et al.  The pharmacology of vascular smooth muscle. , 1955, Pharmacological reviews.

[17]  H. W. Overbeck,et al.  Attenuated vasodilator responses to K+ in essential hypertensive men. , 1974, The Journal of clinical investigation.

[18]  J. Cooke,et al.  L-arginine improves endothelium-dependent vasodilation in hypercholesterolemic humans. , 1992, The Journal of clinical investigation.

[19]  P. Erne,et al.  The Vasodilating Effect of Atrial Natriuretic Peptide in Normotensive and Hypertensive Humans , 1988, Journal of cardiovascular pharmacology.

[20]  D. Webb,et al.  Local inhibition of converting enzyme and vascular responses to angiotensin and bradykinin in the human forearm. , 1989, The Journal of physiology.

[21]  R. J. Whitney,et al.  The measurement of volume changes in human limbs , 1953, The Journal of physiology.

[22]  R. F. Whelan,et al.  The action of 5-hydroxytryptamine on the blood vessels of the human hand and forearm. , 1955, British journal of pharmacology and chemotherapy.

[23]  A. Doyle,et al.  Reactivity of forearm vessels to vasoconstrictor substances in hypertensive and normotensive subjects. , 1959, Clinical science.

[24]  R. Pedrinelli,et al.  Calcium entry blockade and α‐adrenergic vascular reactivity in human beings: Differences between nicardipine and verapamil , 1989, Clinical pharmacology and therapeutics.

[25]  N Schork,et al.  Mechanism of increased alpha adrenergic vasoconstriction in human essential hypertension. , 1987, The Journal of clinical investigation.

[26]  B. Robinson,et al.  Comparison of effects of locally infused angiotensin I and II on hand veins and forearm arteries in man: evidence for converting enzyme activity in limb vessels. , 1974, Clinical science and molecular medicine.

[27]  B. Robinson,et al.  Effect of prostaglandins A 1 , A 2 , B 1 , E 2 and F 2 on forearm arterial bed and superficial hand veins in man. , 1973, Clinical science.

[28]  S. Moncada,et al.  EFFECTS OF ENDOTHELIUM-DERIVED NITRIC OXIDE ON PERIPHERAL ARTERIOLAR TONE IN MAN , 1989, The Lancet.

[29]  D. Webb,et al.  Pharmacology of endothelin-1 in vivo in humans. , 1991, Journal of Cardiovascular Pharmacology.