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Superficial thermal gradients during mild body cooling and its relationship to forearm blood flow.

Forearm and fingertip temperature gradients were related to simultaneously measured forearm blood flow in eleven adult subjects at rest and during a mild cold stimulus. The change in temperature gradients were converted into a percentage change of the potential capacity for heat exchange and this was found to correlate well (r = 0.73: P < 0.001) with the absolute reduction in forearm blood flow.

Adolescent↗

The effect of warmth or/and vitamin E supplementation on forearm blood flow and forearm vascular resistance in sickle cell and non sickle cell anaemia subjects.

The effects of warmth stimulation and/or supplementation with vitamin E (300 mg/day for 6 weeks) on forearm blood flow (FBF) and forearm vascular resistance (FVR) were measured in 8 sickle cell anaemia (SCA) (mean age = 22.8 + 0.8 years) and 11 non sickle cell anaemia (NSCA) subjects (mean age = 23.2 + 1.1 years) of both sexes. Warmth stimulation was induced by immersing the left foot in warm water at 400C for 2 minutes. Forearm blood flow was measured with the venous occlusion plethysmography method. Warmth increased FBF (p <0.01 in each group) and reduced FVR (p <0.05) in NSCA subjects. The change in FBF was greater (p < 0.05) in the NSCA subjects than in the SCA subjects. Supplementation with vitamin E reduced systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MAP) (p < 0.001 in each case) in the NSCA subjects but had little or no effect on the SCA subjects. Vitamin E increased FBF in NSCA subjects (p < 0.05) and SCA subjects (p < 0.01) and decreased FVR in both groups (p < 0.05 in NSCA and p < 0.01 in SCA subjects). The change in FVR seen in the NSCA subjects was less (p < 0.01) than the change in SCA subjects. After supplementation with vitamin E, warmth further decreased SBP (p < 0.01 in each group) and FVR (p < 0.01 in each case) and increased FBF in both groups (p < 0.01 respectively). The changes caused by warmth after vitamin E supplementation on the blood pressure parameters, FBF and FVR were similar in the two groups of subjects.

Adult↗

Forearm blood flow response to posture change in the very old: non-invasive measurement by venous occlusion plethysmography.

Little is known about the peripheral vascular response to posture change in very elderly people who are vulnerable to the development of orthostatic hypotension. This is due, in part, to the risks of currently utilized invasive vascular monitoring techniques in the elderly population. We studied the forearm vascular response to active standing in 18 healthy young, 10 healthy old, and 19 impaired elderly subjects, using the non-invasive technique of venous occlusion plethysmography. In six subjects this technique was compared to duplex doppler ultrasonography for the measurement of postural changes in forearm blood flow. Forearm blood flow changes determined by venous occlusion plethysmography were 11% larger than doppler measurements, but the two methods strongly correlated (r = 0.90, P less than .001). Mean forearm vascular resistance increased to a significantly greater extent at 1 minute of standing in young subjects than in both groups of old, although the response was quite variable in all groups. Two healthy elderly (20%) and eight impaired elderly (40%) subjects had unexpected forearm vasodilatation at 1 minute of standing. By 3 minutes, forearm vascular resistance had increased by similar amounts in all three groups of subjects. Five impaired elderly and no healthy young or healthy old subjects had orthostatic hypotension, defined as greater than or equal to 10 mm Hg decline in mean arterial blood pressure at 1 or 3 minutes of standing. Forearm vascular resistance changes did not correlate with blood pressure response to standing. Thus, forearm vascular response to 1 minute of active standing is attenuated in many elderly subjects. This abnormality may impair adaptation to orthostatic stress in advanced age.

Adult↗

Effects of regional intravenous anaesthesia on blood flow.

Forearm blood flow after regional i.v. anaesthesia in volunteers was compared with the predicted blood flow after arterial occlusion alone, using venous occlusion plethysmography. After arterial occlusion alone for 20 min, marked hyperaemia occured after cuff release. Flows returned to normal within 5 min. Both prilocaine and bupivacaine reduced the hyperaemic response to arterial occlusion. Forearm muscle paralysis using gallamine triethiodide was also associated with a statistically significant but smaller reduction in the hyperaemic response.

Adult↗

Effect of pethidine premedication and halothane anaesthesia on upper limb blood flow.

Forearm blood flow (FBF), hand blood flow (HBF) and arterial pressure were measured in 12 patients, before and after premedication with pethidine and during halothane anaesthesia. After pethidine there was a significant (P less than 0.01) increase in HBF (180%) and decreased hand vascular resistance; heart rate also increased significantly (P less than 0.05), whilst mean arterial pressure (MAP) did not change. The large increase in HBF without hypotension suggests a local effect. With halothane, there was a significant (P less than 0.05) decrease in MAP, increase in HBF and decrease in hand vascular resistance compared with either control or effects produced by pethidine; there was a significant decrease in FBF and reversal of the action of pethidine on forearm vascular resistance.

Adult↗

Effect of luteal phase elevation in core temperature on forearm blood flow during exercise.

Forearm blood flow (FBF) as an index of skin blood flow in the forearm was measured in five healthy women by venous occlusion plethysmography during leg exercise at 80% peak aerobic power and ambient temperature of 35 degrees C (relative humidity 22%; dew-point temperature 10 degrees C). Resting esophageal temperature (T(es)) was 0.3 +/- 0.1 degrees C higher in the midluteal than in the early follicular phase of the menstrual cycle (P < 0.05). Resting FBF was not different between menstrual cycle phases. The T(es) threshold for onset of skin vasodilation was higher (37.4 +/- 0.2 degrees C) in midluteal than in early follicular phase (37.0 +/- 0.1 degrees C; P < 0.05). The slope of the FBF to T(es) relationship was not different between menstrual cycle phases (14.0 +/- 4.2 ml x 100 ml(-1) x min(-1) x degrees C(-1) for early follicular and 16.3 +/- 3.2 ml x 100 ml(-1) x min(-1) x degrees C(-1) for midluteal phase). Plateau FBF was higher during exercise in midluteal (14.6 +/- 2.2 ml x 100 ml(-1) x min(-1) x degrees C(-1)) compared with early follicular phase (10.9 +/- 2.4 ml x 100 ml(-1) x min(-1) x degrees C(-1); P < 0.05). The attenuation of the increase in FBF to T(es) occurred when T(es) was 0.6 degrees C higher and at higher FBF in midluteal than in early follicular experiments (P < 0.05). In summary, the FBF response is different during exercise in the two menstrual cycle phases studied. After the attenuation of the increase in FBF and while T(es) was still increasing, the greater FBF in the midluteal phase may have been due to the effects of increased endogenous reproductive endocrines on the cutaneous vasculature.

Adult↗

Interaction of local and reflex thermal effects in control of forearm blood flow.

We measured forearm blood flow (ABF) bilaterally on six subjects during 15-min periods of leg exercise and the first 10 min of recovery. One forearm (control) was kept at about 33 degrees C skin temperature in all experiments. In experiments at ambient temperature (Ta) of 15 degrees C, the other arm (experimental) was kept at about 26, 33, and 40 degrees C, respectively, during three successive cycles of exercise and recovery. ABF in the 26 degrees C forearm was linearly related to and averaged 42% of control. The relation of ABF in the 40 degrees C forearm to control ABF showed a bend at control ABF of 4-5 ml X 100 ml-1 X min-1. Below the bend, experimental ABF average 213% of control. Above the bend, experimental ABF averaged 5.09 ml X 100 ml-1 X min-1 above control. In four subjects, after heating the experimental forearm to 40 degrees C, we measured ABF for 25-30 min at rest in Ta of both 15 and 25 degrees C. At 25 degrees C Ta, ABF in the heated forearms rose gradually, but control ABF showed little change. At 15 degrees C Ta, the effect on ABF of local heating to 40 degrees C was much reduced, apparently due to reflex vasoconstrictor signals.

Adult↗

Enhanced forearm blood flow during mental stress in children of hypertensive parents.

This study compared changes in forearm blood flow, forearm vascular resistance, blood pressure, and heart rate elicited by mental stress (mental arithmetic) in 12 adolescents with a hypertensive parent and 13 age-matched adolescents with normotensive parents. The two groups did not differ in resting forearm blood flow, forearm vascular resistance, heart rate, or blood pressure. During mental stress, children with a family history of hypertension had a significantly greater increase in forearm blood flow than did children of normotensive parents (+37.5 +/- 8.0 vs +12.8 +/- 7.5%; p less than 0.05) and a trend toward reduced forearm vascular resistance (p = 0.08). Mental stress significantly increased systolic blood pressure (p less than 0.0001), diastolic blood pressure (p less than 0.001), and heart rate (p less than 0.03) in both groups. The blood pressure and heart rate responses to stress were not significantly different between groups. There was no evidence of a prolonged response or a different pattern of recovery in children with a family history of hypertension. This study indicates that regional blood flow responses underlying similar blood pressure increases during mental stress may be different in adolescents with and without a family history of hypertension.

Adolescent↗

Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans.

Activation of ATP-sensitive potassium (KATP) channels present on vascular smooth muscle cells causes membrane hyperpolarization and vasodilation. The purpose of this study was to determine whether KATP channels contribute to reactive hyperemia in humans. Accordingly, we studied the effect of tolbutamide, a KATP channel inhibitor, on reactive hyperemic forearm blood flow. Forearm blood flow was measured by venous occlusion plethysmography. Forearm ischemia was produced by inflating a sphygmomanometric cuff on the arm to suprasystolic pressures for 5 min. After cuff release, forearm blood flow was measured during the reactive hyperemic phase for 5 min. Tolbutamide (1 mM blood concentration, n = 6) did not affect basal (2.4 +/- 0.2 to 2.2 +/- 0.1 ml.100 ml-1.min-1) or peak reactive hyperemic forearm blood flow (21.9 +/- 3.8 to 22.6 +/- 2.9 ml.100 ml-1.min-1, each P = NS), but it significantly attenuated total hyperemic volume (12.6 +/- 1.7 vs. 9.2 +/- 1.8 ml/100 ml, P < 0.02). Vehicle (n = 6) did not affect basal flow, peak reactive hyperemic flow, or total hyperemia. To determine whether adenosine or endothelium-derived nitric oxide contribute to reactive hyperemia via KATP channels, adenosine (1.5-500 micro grams/min, n = 6) and acetylcholine (30 micrograms/min, n = 6) were infused before and during tolbutamide coinfusion. Tolbutamide did not significantly alter the forearm blood flow response to either adenosine or acetylcholine. In conclusion, KATP channels contribute to vasodilation during reactive hyperemia in humans.

Acetylcholine↗

IGF-I increases forearm blood flow without increasing forearm glucose uptake.

Decreased insulin-mediated muscle glucose uptake is a characteristic feature of non-insulin-dependent diabetes mellitus and other insulin-resistant states. It has been suggested that an impairment in the ability of insulin to augment limb blood flow, resulting in diminished glucose delivery to muscle, may contribute to this abnormality. In this study, we used human insulin-like growth factor (IGF) I in conjunction with the forearm balance technique to determine whether forearm glucose uptake could be stimulated by increasing blood flow without directly stimulating the intrinsic ability of the muscle to extract glucose. IGF-I was infused intra-arterially in healthy controls at a rate of either 0.4 microg . kg-1 . min-1 (high IGF) or 0.04 microg . kg-1 . min-1 (low IGF) for 140 min. With high IGF, forearm blood flow increased approximately twofold (34 +/- 3 vs. 64 +/- 8 ml . min-1 . l forearm volume-1, P < 0.01), and arteriovenous glucose concentration difference (a-v difference) increased modestly (0.19 +/- 0.05 vs. 0.31 +/- 0.08 mM, P = 0.32), resulting in an increased forearm glucose uptake (6.4 +/- 1.7 vs. 21.7 +/- 7.4 micromol . min-1 . l forearm volume-1, P = 0.09 vs. basal). With low IGF, forearm blood flow increased by 59% (29 +/- 4 vs. 46 +/- 9 ml . min-1 . l forearm volume-1, P < 0.05) and was associated with a proportional decrease in the a-v difference (0. 29 +/- 0.04 vs. 0.18 +/- 0.05 mM, P < 0.05). Forearm glucose uptake therefore was not significantly different from basal values (7.6 +/- 0.6 vs. 6.9 +/- 1.8 micromol . min-1 . kg-1). These data demonstrate that increasing blood flow without increasing the intrinsic ability of the muscle to extract glucose does not increase forearm muscle glucose uptake.

Adult↗

The effect of varying sodium intake on blood volume, forearm blood flow and vascular responsiveness to sympathetic stimulation in pre-ascitic cirrhosis.

OBJECTIVES: To assess, in patients with well-compensated pre-ascitic cirrhosis, (1) the extent of vasodilatation, if any, in the forearm circulation and (2) the effect of sodium status on its response to reflex sympathetic stimulation. DESIGN: Case-control study. SETTING: Clinical investigation unit of the Toronto Hospital, a tertiary referral hospital. PATIENTS: Eight male, alcoholic patients with pre-ascitic cirrhosis and 10 age- and sex-matched controls. INTERVENTIONS: Patients and controls were given a diet containing 20 mmol of sodium per day for 7 days, then a diet containing 200 mmol of sodium per day for the subsequent 7 days. On the seventh day of each diet, systemic hemodynamics, forearm circulation and effective arterial blood volume were assessed. A cold pressor test was performed after both diets to assess the response of the forearm circulation to reflex sympathetic stimulation. OUTCOME MEASURES: Heart rate, mean arterial pressure, forearm blood flow, forearm vascular resistance, central venous pressure, atrial natriuretic factor concentrations and neurohumoral pressor levels (plasma renin activity, aldosterone and plasma norepinephrine levels). RESULTS: No forearm vasodilatation was evident in the patients with pre-ascitic cirrhosis; their forearm blood flow and forearm vascular resistance were similar to those of the controls. Sodium loading did not influence baseline forearm blood flow. Cold pressor stimulus resulted in a significant decrease in forearm blood flow and a significant increase in forearm vascular resistance, mean arterial pressure, heart rate and plasma norepinephrine levels in both groups after the low-sodium diet. High sodium intake resulted in significantly greater reduction in forearm blood flow (-19%, standard error of the mean [SEM] 3% v. -8%, SEM 3%; p < 0.05) and significantly greater increase in forearm vascular resistance (+46%, SEM 7% v. +25%, SEM 8%; p < 0.05) in the patients with cirrhosis than in the controls. CONCLUSIONS: Well-compensated pre-ascitic cirrhotic patients do not have forearm vasodilatation. Sodium loading does not increase baseline forearm blood flow in these patients, but it does lead to a heightened response to reflex sympathetic stimulation. Sodium loading, with the associated sympathetic hyper-responsiveness, may therefore contribute to further sodium retention in these patients.

Adult↗

Effects of tumour necrosis factor-alpha in the human forearm: blood flow and endothelin-1 release.

Increased circulating concentrations of tumour necrosis factor-alpha (TNF-alpha) are seen in several pathological conditions associated with vascular disease. TNF-alpha induces the synthesis of endothelin-1 (ET-1), a potent vasoconstictor, by the endothelium. However, there is profound vasodilatation in sepsis, where circulating levels of both ET-1 and TNF-alpha are elevated. The details of the interaction between ET-1 and TNF-alpha and the predominant resulting haemodynamic effect in healthy humans are unclear. The aim of the present study was to determine the effects of intra-arterial TNF-alpha on ET-1 spillover, vascular tone and endothelial function in the healthy human forearm. Brachial arterial and deep venous blood samples, forearm plasma flow measurements and blood flow responses to acetylcholine and sodium nitroprusside were obtained in six healthy subjects before and during a 6 h infusion of TNF-alpha into the brachial artery. Forearm blood flow was significantly greater than baseline during exposure to TNF-alpha [median (lower quartile, upper quartile): baseline, 2.6 (2.1, 2.8) ml.min(-1).100 ml(-1); TNF-alpha, 4.6 (4.5, 5.1) ml.min(-1).100 ml(-1); P <0.05]. The rate of release of ET-1 was significantly greater than baseline after 30 and 260 min of TNF-alpha infusion [median (lower quartile, upper quartile): baseline, 0.8 (0.6, 1.1) pg.min(-1).100 ml(-1); 30 min, 2.4 (1.9, 3.2) pg.min(-1).100 ml(-1); 260 min, 4.1 (3.1, 4.2) pg.min(-1).100 ml(-1); P <0.05]. The vasodilatory response to acetylcholine was diminished during TNF-alpha infusion, whereas the response to sodium nitroprusside remained unchanged. We thus demonstrate for the first time that local TNF-alpha increases ET-1 spillover from the human forearm and impairs endothelium-dependent vasodilatation. In spite of this action, TNF-alpha has a vasodilatory effect, resulting in an increase in forearm blood flow.

Acetylcholine↗

Contribution of prostaglandins to exercise-induced vasodilation in humans.

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.

Adult↗

Contribution of endothelium-derived relaxing factor to exercise-induced vasodilation in humans.

Release of endothelium-derived relaxing factor (EDRF) from the vascular endothelium may contribute to skeletal muscle arteriolar vasodilation during exercise. The present study was undertaken to test this hypothesis. Ten normal subjects underwent brachial arterial catheter insertion and instrumentation of their forearm to measure plethysmographic forearm blood flow. Forearm blood flow was then measured at rest, during two levels of wrist flexion exercise (0.2 and 0.4 W), and during 0.4-W exercise with concurrent infusion of norepinephrine (100 ng.min-1 x 100 ml forearm volume-1). Measurements were made with and without infusion of N-monomethyl-L-arginine (L-NMMA) (0.1-0.2 mg.min-1 x 100 ml forearm volume-1), a specific inhibitor of EDRF synthesis. Infusion of L-NMMA reduced resting forearm blood flow (control: 2.5 +/- 0.4 vs. L-NMMA: 1.5 +/- 0.1 ml.min-1 x 100 ml-1) and markedly reduced forearm blood flow response to acetylcholine (5 micrograms.min-1 x 100 ml forearm volume-1) (control: 20.2 +/- 2.9 vs L-NMMA: 4.0 +/- 1.0 ml.min-1 x 100 ml-1; both P < 0.01). However, L-NMMA had no significant effect on flow responses to exercise (0.2 W: 8.3 +/- 1.1 vs. 8.3 +/- 1.2; 0.4 W: 13.8 +/- 1.7 vs. 13.5 +/- 1.7; 0.4 W + norepinephrine: 10.3 +/- 2.4 vs. 9.4 +/- 2.6 ml.min-1 x 100 ml-1; all P = NS). These findings suggest that release of EDRF from the vascular endothelium contributes to skeletal muscle arteriolar vasodilation at rest but does not contribute to the arteriolar vasodilation produced by exercise.

Acetylcholine↗

Increased renal and forearm vasoconstriction in response to exercise after heart transplantation.

OBJECTIVE: To test the hypothesis that the loss of the inhibitory effect of the cardiac ventricular afferent fibres on the vasomotor centre would result in increased vasoconstrictor drive to the forearm and renal vascular beds during supine exercise in heart transplant recipients. DESIGN: Comparison of regional haemodynamic response to exercise in heart transplant recipients and two age matched control groups. SETTING: Regional heart transplant unit. PATIENTS AND METHODS: Orthotopic heart transplant recipients (n = 10), patients with NYHA class II heart failure (n = 10), and normal controls (n = 10) underwent short duration maximal supine bicycle exercise. MAIN OUTCOME MEASURES: Simultaneous measurements were made of heart rate, systemic blood pressure, oxygen consumption (VO2), forearm blood flow, and renal blood flow. Forearm blood flow was measured by forearm plethysmography and renal blood flow by continuous renal vein thermodilution. RESULTS: The peak forearm vascular resistance was significantly greater in the transplant group than in the controls (mean (SEM) 75 (18) v 40 (7) resistance units, p < 0.05). The percentage fall in renal blood flow at peak exercise was significantly greater in heart transplant recipients than in the controls (44% (4%) v 32% (4%), p < 0.05) as was the percentage increase in renal vascular resistance (transplants: 116% (19%) v controls: 78% (17%), p < 0.05). Regional haemodynamics during exercise in the heart failure group were not significantly different from those in the controls. CONCLUSIONS: These findings suggest that surgical division of the cardiac ventricular afferent fibres results in increased vasoconstrictor drive to the kidneys and non-exercising muscle during exercise. This mechanism may contribute to persistent exercise limitation and renal impairment after heart transplantation.

Adult↗

Accuracy of portal and forearm blood flow measurements in the assessment of the portal pressure response to propranolol.

BACKGROUND/AIMS: The portal pressure response to propranolol varies significantly in individual patients with cirrhosis. At present, propranolol responders can be identified only by measuring the hepatic venous pressure gradient. The aims of this study were: 1) to investigate whether the noninvasive monitoring of portal blood flow by pulsed Doppler ultrasound and forearm blood flow by strain-gauge plethysmography can predict the hepatic venous pressure gradient response to propranolol in patients with cirrhosis, and 2) to analyze the factors that may influence this response. METHODS: Hemodynamic measurements were undertaken in 80 patients with cirrhosis before and after receiving propranolol (0.15 mg/kg i.v., n = 60) or placebo (n = 20). RESULTS: No changes were observed in the placebo group. Propranolol lowered (p < 0.01) hepatic venous pressure gradient from 17.6 +/- 3.8 to 14.7 +/- 3.8 mmHg, portal blood flow from 1122 +/- 363 to 897 +/- 332 ml/min and forearm blood flow from 7.52 +/- 3.1 to 6.12 +/- 2.3 ml/min%. Changes in hepatic venous pressure gradient were correlated (p < 0.01) with those of portal blood flow (r = 0.82) and forearm blood flow (r = 0.54). The reduction in hepatic venous pressure gradient was > 20% in 23 patients ("responders"). The accuracy of portal Doppler flowmetry in identifying responders was higher than that of forearm plethysmography (88.3 vs. 68.3%, p < 0.05). Multivariate analysis proved that previous variceal bleeding was the only factor independently associated with a lack of response to propranolol (relative risk 3.42, 95% CI 1.5-7.4, p < 0.01). Hepatic venous pressure gradient reduction by propranolol was higher in non-bleeders than in bleeders (-19.9 +/- 9.4 vs. -11.3 +/- 8.6%, p < 0.01). CONCLUSIONS: Portal Doppler ultrasound can be used as a reliable surrogate indicator of the hepatic venous pressure gradient response to acute propranolol administration. In addition, our study indicates that this response is mainly influenced by previous variceal hemorrhage.

Adrenergic beta-Antagonists↗

The variance of forearm blood flow as an indicator of emotional stress.

Forearm blood flow was measured four times per minute by venous occlusion plethysmography during rest and during a brief emotionally stressful mental task. During emotional stress not only was the mean forearm blood flow increased, but the single blood flow values fluctuated more than at rest. The greater fluctuation, expressed statistically as the variance, was an indicator of emotional stress, at least as sensitive as the mean increase in the blood flow. Both a tranquillizer (thioridazine) and a beta-blocker (toliprolol) reduced the greater variance during the emotionally stressful situation in doses insufficient to diminish the mean increase in forearm blood flow.

Adult↗

Relationship between insulin sensitivity and maximal forearm blood flow in young men.

Insulin resistance is a part of the metabolic cardiovascular syndrome. We aimed to test the hemodynamic hypothesis of insulin resistance, which suggests that a decreased skeletal muscle blood supply with subsequent reduced nutritional flow causes insulin resistance in skeletal muscle. We assessed determinants of peripheral blood flow such as maximal forearm blood flow (MFBF), minimal forearm vascular resistance (MFVR), and whole blood viscosity (WBV) in 27 young men with borderline elevation of blood pressure. Insulin sensitivity measured as glucose disposal rate (GDR) correlated with MFBF (r=0.55, P=0.003), MFVR (r=-0.58, P=0. 002), and WBV (r=-0.39, P=0.046 at shear rate 201 s-1). There was no correlation between GDR and myocardial thickness or left ventricular mass. In a stepwise multiple regression analysis, MFVR and WBV explained 54% of the variation in GDR. The relative increase in mean arterial blood pressure during a mental stress test, as a marker of reactivity or an alert reaction, was correlated with MFVR (r=0.56, P=0.002) and inversely with GDR (r=-0.45, P=0.018) and MFBF (r=-0.49, P=0.01) but not with cardiac dimensions. In a stepwise multiple regression analysis, 48% of the increase in blood pressure during a mental stress test was explained by MFVR and WBV. Fasting insulin correlated with MFVR (r=0.41, P=0.036) and GDR (r=-0.62, P=0.001). These data show a positive association between the appearance of peripheral structural vascular changes as quantified through a hemodynamic technique and insulin resistance in young men with borderline elevation of blood pressure. The cause-effect relationship of this finding needs further evaluations.

Adult↗