Deep Forearm Vein Research Articles

Valvular function of peripheral veins after hyperemic dilation

We wanted to answer the question of whether physiological dilation of normal extremity veins can induce temporary valvular leakage and reflux. Directional flow was recorded in 22 forearm and popliteal veins by Doppler duplex scanning after distal compression. Reflux was assessed by valve closure time and calculation of a "reflux index," the ratio of backward to forward flow areas. Hyperemia and enhanced flow did not increase but lowered reflux. During control conditions the mean reflux ratio (backward/forward flow area) of 21 veins was 0.058 and decrease to 0.028 (p < 0.05). Reflux was slightly longer in patients in the erect position in the popliteal vein, compared to forearm veins (with the patients in the sitting position). Significantly increased reflux occurred during hyperemia in only one deep forearm vein (valve closure time 0.92 seconds). Most veins of the upper (forearm) and lower extremity (popliteal vein) were competent even after a maneuver that induced venodilation and an increase in blood flow (exercise hyperemia or postocclusion reactive hyperemia). Veins with an inherent valvular weakness can be identified by a hyperemia test with duplex flow analysis.

Metabolism of Big endothelin-1 (1–38) and (22–38) in the human circulation in relation to production of endothelin-1 (1–21)

Healthy male volunteers received intravenous infusions of Big endothelin (ET)-1 (1–38) or Big ET-1 (22–38). Blood samples were drawn from catheters in the brachial and pulmonary arteries and the hepatic, renal, jugular and deep forearm veins. The in vivo half-lives of circulating plasma Big ET-1 (1–38) were 6.6 ± 0.3 min for the initial phase and 23 ± 1.4 min for the late phase. The corresponding half-lives of Big ET-1 (22–38) were considerably shorter, being 0.9 ± 0.03 min ( P < 0.01) and 3.1 ± 0.4 min ( P < 0.01), respectively. This was concordant with the efficient regional clearance of Big ET-1 (22–38), which was most prominent in the forearm muscle (51 ± 3%), liver (44 ± 5%) and kidney (43 ± 3%) and less pronounced in the lungs (14 ± 2%) and brain (22 ± 5%). Significant fractional extraction of Big ET-1 (1–38) was only found for the liver (30 ± 2%) and kidney (44 ± 3%). During the infusion of Big ET-1 (1–38) a positive veno-arterial gradient of ET-1-LI was noted only for the kidney, indicating production of ET-1. In conclusion, whereas Big ET-1 (22–38) is eliminated in skeletal muscle, splanchnic, renal, pulmonary and cerebral vascular beds, Big ET-1 (1–38) is extracted mainly in the renal and splanchnic vasculature. Furthermore, plasma half-life of Big ET-1 (1–38) is much longer than that of both ET-1 and Big ET-1 (22–38) in man. Thus, for investigation of the secretory activity of the ET-1-system measurements of Big ET-1 (1–38) levels may be a better approach.

915-77 Big ET-1-lnfusion in Man Causes Only Renal ET-1-Release but Potent and Long-lasting Systemic, Pulmonary, Renal and Splanchnic Vasoconstriction

Plasma endothelin-1, ET-1, and the precursor, big ET-1, are demonstrable in healthy man and increase during e.g. myocardial infarction (Miyauchi et al 1989). To study the vascular effects of big ET-1 infusion, and its possible conversion of ET-1, healthy subjects received big ET-1 in doses of 4–8 pmol.kg -1 .min -1 intravenously for 20 minutes. Blood samples were taken from systemic arterial and pulmonary arterial as well as jugular, deep forearm, hepatic and renal vein catheters for determination of cardiac output, CO, splanchnic (ESBF) and renal (ERBF) blood flows (indicators: cardiogreen and PAH) forearm blood flow (FBF, pletysmographyl. and big ET-1 and ET-1 like immuno-reactivity, (ET-1-Li). Big ET-1 infusion caused a decrease in heart rate, HR, from 57 ± 4 to 45 ± 3 beats.min-1 (p &lt; 0.001) and increase of mean arterial pressure, MAP, from 86 ± 1.3 to 106 ± 3.2 mmHg (p &lt; 0.001). CO fell by 22 ± 5% (p &lt; 0.01). Pulmonary, splanchnic and renal oxygen uptakes were unchanged indicating that big ET-1 does not influence oxygen consumption. The arterial-jugular venous oxygen difference was unchanged indicating unchanged cerebral blood flow. FBF was unchanged. ERBF and ESBF fell by approximately 40% (both p &lt; 0.001). Only splanchnic and renal tissues extract big ET-1 with fractional extractions of 23 ± 4 and 45 ± 4%. Intravenous infusion of big ET-1 increased arterial ET-1-Li from 4 to 8 pmol.I-1 (p &lt; 0.001) and renal release of ET-1-Li from 1.50 ± 0.18 to 8.68 ± 0.64 pmol.min-1 (p &lt; 0.001). Big ET-1 infusion causes falls in HR and CO, increase in MAP and decreases in splanchnic and renal blood flows. Uptakes of big ET-1 were only noted in the renal and splanchnic regions with two-fold higher values in the kidneys, p &lt; 0.005. Only the kidney showed increased release of ET-1-Li suggesting a unique renal capacity to synthesize and release big ET-1. Compared to ET-l infusion (Weitzberg et al 1991) big ET-l infusion causes, despite lower arterial plasma ET-1-Li levels, more marked haemodynamic effects as reflected in drops in HR and CO and more marked increase in MAP with more pronounced and long-lasting renal vasoconstriction. In addition big-ET-1 had no effect on cerebral or skeletal muscle blood flows while ET-1 caused dilatations in these regions.

Transmembrane glucose transport in skeletal muscle of patients with non-insulin-dependent diabetes.

Insulin resistance for glucose metabolism in skeletal muscle is a key feature in non-insulin-dependent diabetes mellitus (NIDDM). Which cellular effectors of glucose metabolism are involved is still unknown. We investigated whether transmembrane glucose transport in vivo is impaired in skeletal muscle in nonobese NIDDM patients. We performed euglycemic insulin clamp studies in combination with the forearm balance technique (brachial artery and deep forearm vein catheterization) in six nonobese NIDDM patients and five age- and weight-matched controls. Unlabeled D-mannitol (a nontransportable molecule) and radioactive 3-O-methyl-D-glucose (the reference molecular probe to assess glucose transport activity) were simultaneously injected into the brachial artery, and the washout curves were measured in the deep venous effluent blood. In vivo transmembrane transport of 3-O-methyl-D-glucose in forearm muscle was determined by computerized analysis of the washout curves. At similar steady-state plasma concentrations of insulin (approximately 500 pmol/liter) and glucose (approximately 5.15 mmol/liter), transmembrane inward transport of 3-O-methyl-D-glucose in skeletal muscle was markedly reduced in the NIDDM patients (6.5 x 10(-2) +/- 0.56 x 10(-2).min-1) compared with controls (12.5 x 10(-2) +/- 1.5 x 10(-2).min-1, P < 0.005). Mean glucose uptake was also reduced in the diabetics both at the whole body level (9.25 +/- 1.84 vs. 28.3 +/- 2.44 mumol/min per kg, P < 0.02) and in the forearm tissues (5.84 +/- 1.51 vs. 37.5 +/- 7.95 mumol/min per kg, P < 0.02). When the latter rates were extrapolated to the whole body level, skeletal muscle accounted for approximately 80% of the defect in insulin action seen in NIDDM patients. We conclude that transmembrane glucose transport, when assessed in vivo in skeletal muscle, is insensitive to insulin in nonobese NIDDM patients, and plays a major role in determining whole body insulin resistance.

Abnormal sympathetic overactivity evoked by insulin in the skeletal muscle of patients with essential hypertension.

The reason why hyperinsulinemia is associated with essential hypertension is not known. To test the hypothesis of a pathophysiologic link mediated by the sympathetic nervous system, we measured the changes in forearm norepinephrine release, by using the forearm perfusion technique in conjunction with the infusion of tritiated NE, in patients with essential hypertension and in normal subjects receiving insulin intravenously (1 mU/kg per min) while maintaining euglycemia. Hyperinsulinemia (50-60 microU/ml in the deep forearm vein) evoked a significant increase in forearm NE release in both groups of subjects. However, the response of hypertensives was threefold greater compared to that of normotensives (2.28 +/- 45 ng.liter-1.min-1 in hypertensives and 0.80 +/- 0.27 ng.liter-1 in normals; P less than 0.01). Forearm glucose uptake rose to 5.1 +/- .7 mg.liter-1.min-1 in response to insulin in hypertensives and to 7.9 +/- 1.3 mg.liter-1.min-1 in normotensives (P less than 0.05). To clarify whether insulin action was due to a direct effect on muscle NE metabolism, in another set of experiments insulin was infused locally into the brachial artery to expose only the forearm tissues to the same insulin levels as in the systemic studies. During local hyperinsulinemia, forearm NE release remained virtually unchanged both in hypertensive and in normal subjects. Furthermore, forearm glucose disposal was activated to a similar extent in both groups (5.0 +/- 0.6 and 5.2 +/- 1.1 mg.liter-1.min-1 in hypertensives and in normals, respectively). These data demonstrate that: (a) insulin evokes an abnormal muscle sympathetic overactivity in essential hypertension which is mediated by mechanisms involving the central nervous system; and (b) insulin resistance associated with hypertension is demonstrable in the skeletal muscle tissue only with systemic insulin administration which produces muscle sympathetic overactivity. The data fit the hypothesis that the sympathetic system mediates the pathophysiologic link between hyperinsulinemia and essential hypertension.

Adenosine activates a vascular renin-angiotensin system in hypertensive subjects.

In vitro data indicate that the activation of A2 adenosine receptors increases renin release by the accumulation of cyclic AMP. Because in human forearm vessels beta-adrenergic receptor stimulation causes the local release of renin and angiotensin II through the increase of cyclic AMP, we evaluated in six essential hypertensive subjects whether adenosine can release vascular angiotensin II. Adenosine was infused into the brachial artery at cumulatively increasing doses (0.5, 1.5, and 5 micrograms/100 ml forearm tissue per minute for 5 minutes each) during saline infusion and in the presence of the adenosine antagonist theophylline (100 micrograms/100 ml forearm tissue per minute for 15 minutes), while venous (ipsilateral deep forearm vein) and arterial (brachial artery) angiotensin II (picograms per milliliter) were measured at the end of each infusion period, and forearm angiotensin II net balance (picograms per minute) was calculated by venous-arterial differences corrected for forearm blood flow (strain-gauge venous plethysmography) and hematocrit. In control conditions, adenosine, at higher doses, caused a dose-dependent vasodilation and increased venous angiotensin II without affecting arterial values; therefore, the calculated angiotensin II net balance showed an adenosine-mediated dose-dependent release. Theophylline pretreatment blunted adenosine-mediated forearm blood flow increments and angiotensin II release. The local origin of angiotensin II was further confirmed in another group of six hypertensive subjects in whom the angiotensin converting enzyme inhibitor captopril, locally infused at the rate of 2.5 micrograms/100 ml forearm tissue per minute for 15 minutes, abolished the adenosine-mediated venous angiotensin II increments. Our data indicate that exogenous adenosine can stimulate the production of angiotensin II in the forearm vessels of hypertensive patients.

Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition, potassium and lactate.

Six healthy men performed sustained static handgrip exercise for 2 min at 40% maximal voluntary contraction followed by a 6-min recovery period. Heart rate (fc), arterial blood pressures, and forearm blood flow were measured during rest, exercise, and recovery. Potassium ([K+]) and lactate concentrations in blood from a deep forearm vein were analysed at rest and during recovery. Mean arterial pressure (MAP) and fc declined immediately after exercise and had returned to control levels about 2 min into recovery. The time course of the changes in MAP observed during recovery closely paralleled the changes in [K+] (r = 0.800, P < 0.01), whereas the lactate concentration remained elevated throughout the recovery period. The close relationship between MAP and [K+] was also confirmed by experiments in which a 3-min arterial occlusion period was applied during recovery to the exercised arm by an upper arm cuff. The arterial occlusion affected MAP while fc recovered at almost the same rate as in the control experiment. Muscle biopsies were taken from the brachioradialis muscle and analysed for fibre composition and capillary supply. The MAP at the end of static contraction and the [K+] appearing in the effluent blood immediately after contraction were positively correlated to the relative content of fast twitch (% FT) fibres (r = 0.886 for MAP vs % FT fibres, P < 0.05 and r = 0.878 for [K+] vs % FT fibres, P < 0.05). Capillary to fibre ratio showed an inverse correlation to % FT fibres (r = -0.979, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

A compartmental model to quantitate in vivo glucose transport in the human forearm.

Glucose transport is a critical step in the control of glucose disposal that, until presently, has not been quantitated in vivo in humans. We have employed the perfused forearm and euglycemic insulin-clamp techniques in combination with a dual-tracer injection to measure basal and insulin-mediated glucose transport in six normal subjects. L-[3H]glucose, which is not transported, was used to trace extracellular glucose kinetics; 3-O-[14C]-methyl-D-glucose, transportable but not metabolizable, was used to monitor glucose movement across the cell membrane. After bolus intra-arterial injection of the two tracers, plasma samples were obtained every 15-30 s for 10 min from a deep forearm vein to determine the washout curves. A linear compartmental model was developed that accounts for blood flow heterogeneity. It consists of three parallel, two-compartment chains merging into the sampling compartment to which cellular compartments are appended. A priori identifiability analysis was performed. The uniquely identifiable parameterization includes the transport rate constants of glucose into and out of the cell. The model was identified using nonlinear least-squares parameter estimation. Transport parameters are estimated with very good precision, and their reproducibility is satisfactory. The model also allows the estimation of the mean arteriovenous transit times of both the extracellular and the transported tracer. The compartmental model provides a novel approach to investigate glucose transport in vivo in humans.

Prejunctional α2-Adrenoceptors and Norepinephrine Release in the Forearm of Normal Humans

To investigate the prejunctional alpha 2-adrenoceptor-mediated autoinhibitory feedback for norepinephrine (NE) release, we measured the response of forearm blood flow (FAF, mercury in silastic strain gauge plethysmography) and changes of the forearm venous-arterial NE difference (delta VA-NE, deep forearm vein, brachial artery norepinephrine concentration) induced by six intrabrachial artery 5-min infusions of clonidine in 13 normal volunteers. NE spillover into the forearm circulation was estimated as the product of delta VA-NE and FAF after three clonidine infusions. Clonidine caused dose-dependent decreases in FAF with a maximum reduction of FAF after the highest dose of clonidine of 32 +/- 8%, (N = 7, p less than 0.01) indicating postjunctional alpha-adrenergic stimulation. delta VA-NE increased slightly yet calculated norepinephrine spillover remained statistically unchanged after clonidine. The results suggest that auto-inhibitory feedback control of neuronal transmitter release via prejunctional alpha 2-adrenoceptors may not to an important degree modulate norepinephrine release in the forearm vasculature of healthy subjects.

Measurement of water filtration in skeletal muscle in man by an osmotic transient method.

Water filtration in the human forearm was determined with a new method using a hyperoncotic transient of albumin solution infused into the brachial artery. Baseline dilution of labelled albumin in deep forearm vein plasma in excess of the contribution from arterial blood and from infusate was assumed to originate from extravascular water filtered into the blood by the transient. The filtration coefficient (Fc) was determined as the ratio between filtered water and increase in colloid osmotic pressure in the blood samples, and gives the filtrative water permeability in the exchange areas of the microcirculation. In 10 normal volunteers, Fc was 0.00082 ml (ml mmHg)-1 (SD=0.00007). Multiplication of Fc by plasma flow in the forearm gave a filtration capacity (Kf) of 0.0036 ml (100 ml tissue min mmHg)-1 (SD=0.00137). This filtration capacity (Kf) represents that of fast flowing regions in the forearm muscles, but it is of the same order of magnitude as the capillary filtration coefficient (CFC) determined plethysmographically for the entire forearm by the venous stasis technique.

The effect of leucine infusion on substrate flux across the human forearm

In this study we examine the role of leucine infusion on amino acid and carbohydrate flux across the human forearm. Thirteen male volunteers of ideal body weight (103 ± 3%) were studied after an overnight fast. Five received an infusion of l-leucine (2.1 ± 0.07 μmol/kg/min) for 5 hr and 8 received physiologic saline as controls. Blood samples were obtained from arterialized hand vein and a deep forearm vein at 15-min intervals for 1 hr basal period and at 1-hr intervals for a 5-hr experimental period. Blood flow to the forearm was measured by capacitance plethysmography and balance ( Q ̇ ) across the forearm was calculated according to the Fick principle. Leucine infusion resulted in a reversal of Q ̇ leu ) from a net production of 17 ± 5 to a net uptake of 249 ± 23 nmol/100 g muscle/min ( P < 0.001) or 15% of the infused load. α-Keto-isocaproate release increased from 23 ± 4 to 48 ± 7 nmol/100 g muscle/min ( P < 0.05). Alanine output dropped by 57% (125 ± 22 to 53 ± 12 nmol/100 g muscle/min, P < 0.005), while glutamine output increased by 150% (131 ± 20 to 326 ± 31 nmol/100 g muscle/min, P < 0.005). Total alpha amino nitrogen (AAN output) by the forearm dropped by 60 and 48% within 1 and 2 hr of leucine infusion and returned thereafter to basal levels. The output of amino acids, other than the BCAA, progressively increased such that they were 75% of basal values by the end of leucine infusion (370 ± 75 vs 645 ± 115 nmol/100 g muscle/min, P < 0.005). Glucose uptake dropped and lactate release increased by 80% each. Insulin levels increased by 82%. These changes resulted in a 10% drop in glucose and a 25% increase in lactate levels. Ketone bodies and plasma FFA increased by 85 and 21%, respectively. We conclude that leucine infusion in overnight fasted man results in (a) a transient positive effect on nitrogen balance, followed by (b) an increase in glutamine output across the forearm to account for all the leucine retained, and (c) a minimal change in KIC output, thus suggesting that most of the leucine retained was completely oxidized across the forearm tissue. Furthermore leucine infusion exerted a glucose sparing effect by directly inhibiting glucose uptake across the forearm.

Use of a heated superficial hand vein as an alternative site for the measurement of amino acid concentrations and for the study of glucose and alanine kinetics in man

Comparisons were made between the artery and a heated superficial hand vein (HSHV) for the measurements of amino acids, lactate, glycerol, free fatty acids, insulin and glucagon and the measurements of glucose and alanine kinetics in man. Normal subjects ( n = 8) were studied after an overnight fast (12–14 hr). U-14C-alanine and 3, 3H glucose were administered by a constant infusion and blood was sampled from catheters placed in a radial artery and a superficial dorsal vein of a heated hand (68°C environment), during a control period and a period of a steady state hyperaminoacidemia achieved by a constant infusion of an L-amino acid solution. The blood concentrations of all substrates and hormones measured and the concentrations of cold and radioactive glucose and alanine were comparable in the two vessels during both study periods. In contrast, measurements obtained in a deep forearm vein (DV) showed the concentrations of plasma glucose to be lower (3% in the control period and 5% during the experimental period) and those of plasma alanine to be higher (13% and 5% during control and experimental periods respectively) than the artery or the HSHV. The difference in glucose specific activity between the artery or the HSHV and the DV were however slight but non-significant, while plasma alanine specific activity was significantly lower in the DV as compared to the artery or the HSHV (32% in the control period versus 14% in the experimental period) suggesting a process of exchange of alanine and glucose occuring during the transit of blood across the forearm. As a result blood samples obtained from a DV will overestimate the derived total body glucose and alanine turnover rates. Thus the heated superficial hand vein can adequately replace the artery for the measurements of whole blood amino acids, lactate and glycerol and for plasma FFA, insulin and glucagon; its use can obviate the risks associated with arterial catheterization and can be a suitable site for the measurements of total body glucose and alanine kinetics in man.

Arterial concentration and forearm extraction of glucose and insulin during the early phase of a glucose infusion.

The concentrations of glucose and insulin were determined with high precision at half minute intervals in arterial and deep forearm vein blood after a bolus injection of glucose (4 g), followed by a constant i. v. infusion (200 mg/min), in four healthy subjects. The values for the deep vein were corrected for the transit time, which was determined by injection of Cardio-green. Arterial glucose peaked at the end of the bolus injection, venous glucose 1 1/2 min later. Arterial insulin reached its maximum later than glucose, after 2 1/2-4 min. The venous insulin reached its maximum later and was much lower than the arterial level, in two cases only around 50% of the arterial concentration. It is concluded that early after glucose administration there is a considerable extraction of both glucose and insulin by the forearm. Since the insulin extraction was quite variable venous insulin concentrations cannot be used for the assessment of early insulin response to glucose.

Gyrate Atrophy of the Choroid and Retina with Hyperornithinemia

A case of gyrate atrophy of the choroid and retina and hyperornithinemia in a 28-year-old man was subjected to extensive clinical and biochemical investigation. The familial occurrence of the ocular disease and of abnormality of amino acids was unique to this patient, being absent in parents and siblings. He presented with progressive visual loss, and had cataracts and large areas of peripheral lacumar atrophy. Clinically there was no other abnormality. However, he was hyperuricemic and had an abnormal electroencephalogram. Despite otherwise normal biochemical indices of hepatic, renal, and muscle function, selective catheterization of an artery, the hepatic vein, the renal vein, and a deep forearm vein showed all of these circulatory beds to be producing ornithine according to arteriovenous difference measurements. Cerebrospinal fluid and urine contained increased amounts of ornithine. Though electromyography was normal a muscle biopsy specimen was abnormal. Clinical tests including arginine loading, glucose tolerance testing, and other measurements of blood variables provided inferences as to the metabolic locus of the abnormality. The syndrome is a systemic multiorgan disorder in which the choriod and retina would appear to be target organs and the hyperornithinemia to be of as yet undetermined cause and pathogenic significance.

The effects of adrenergic β-blockade with oxprenolol on peripheral metabolism

Summary Peripheral metabolism was studied with the forearm technique in six fasting normal subjects before and after oxprenolol administration. With the forearm technique the product of blood flow and arteriovenous differences is a measure of substrate uptake or release, and, therefore, an index of metabolism. Blood flow was measured with venous occlusion plethysmography, and arterial and venous samples obtained through indwelling catheters in the radial artery and deep forearm vein. Oxprenolol administration influenced both peripheral flow and the basal pattern of substrate exchange. Before oxprenolol blockade a net uptake of glucose, triglycerides, and FFA, and a net release of glycerol were recorded across the forearm. After oxprenolol blockade there was a marked reduction in triglyceride uptake, with augmentation of glucose uptake and inhibition of lipolysis.

The Origin of Blood withdrawn from Deep Forearm Veins during Rhythmic Exercise1

The Origin of Blood withdrawn from Deep Forearm Veins during Rhythmic Exercise¹

Circulatory reactions in the forearm and hand during and after exercise in patients with vasoregulatory asthenia.

1. Investigations were made on 15 patients with vasoregulatory asthenia (VA) and 14 clinically healthy control subjects (CS) concerning the magnitude and variations of the circulation in the resting forearm and hand during supine leg exercise, and in the forearm after exhaustive forearm exercise. Measurements were performed of blood flows in forearm and hand (venous occlusion plethysmography), arterial blood pressure, heart rate, a-v O2 difference between the brachial artery and a deep forearm vein, and blood lactate concentration, and calculations were made of O2 uptake in deep forearm (musculature) and vascular resistances in forearm and hand. 2. The blood flowat rest and duringleg exercise was in VA on the average two to three times higher in the forearm, and significantly lower in the hand, than in CS. The difference was especially pronounced in those patients who showed a marked reduction of physical work capacity (W170).

Circulatory and psychophysiological reactions to adrenaline and noradrenaline in patients with vasoregulatory asthenia.

1. The effects of intravenous and intra-arterial infusion of adrenaline and noradrenaline on the blood flow in the forearm and hand, heart rate, arterial blood pressure, lactate concentration in blood effluent from a deep (muscle) forearm vein, and on the incidence of subjective symptoms were studied in 14 patients with vasoregulatory asthenia (VA) and 9 clinically healthy control subjects (CS). 2. In the VA group the highest intravenously administered catecholamine dose which was tolerated by the average individual person with regard to subjective symptoms, was about 40 per cent lower for adrenaline (10 Μg/min), and between 15 and 65 per cent higher for noradrenaline (29 Μg/min) than that tolerated by the CS subjects. The number of various subjective symptoms which arose on intravenous infusion of catecholamines was twice as high for adrenaline, but less for noradrenaline, in the VA group than in the control subjects. Ten of the VA patients noted their usual typical and personally patterned symptoms on intravenous infusion of adrenaline. 3. The circulatory effects of intravenously or intra-arterially administered adrenaline were at comparable dose rates in some respects different in VA and CS but the differences were not pronounced. With comparable doses of noradrenaline, however, a pronounced difference was found, the increase in arterial blood pressure and the decrease in forearm and hand blood flow (especially on intra-arterial infusion) being less marked in the VA group. Ectopic heart beats occurred less frequently in VA than in CS during these infusions. 4. Infusions of adrenaline at 0.01 and 0.1 Μg/min into the brachial artery caused a gradual slight increase in the lactate concentration of blood effluent from the local forearm musculature, which on the average was of a similar magnitude (about 4 mg/100 ml) in the VA and CS groups. 5. It is concluded that the circulatory sensitivity of the VA patients to noradrenaline was decreased. The sensitivity to intravenous adrenaline was increased in VA with respect to subjective symptomatology. The cause and nature of the altered catecholamine sensitivity are not known.

The source of blood samples withdrawn from deep forearm veins via catheters passed upstream from the median cubital vein.

The source of blood samples withdrawn from deep forearm veins via catheters passed upstream from the median cubital vein.

The effect of venous pressure on the oxygen content of venous blood in the deep forearm veins.

The effect of venous pressure on the oxygen content of venous blood in the deep forearm veins.