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Effect of vitamin C on forearm blood flow and glucose metabolism in essential hypertension.

In 9 patients with essential hypertension, we tested whether a high-dose (12 mg. min(-1)) vitamin C infusion into the brachial artery, by improving endothelium-dependent vasodilatation, would also attenuate the insulin resistance of deep forearm tissues. We measured the effect of vitamin C on acetylcholine (Ach)-induced vasodilatation and on forearm glucose uptake during systemic hyperinsulinemia; in all studies, the contralateral forearm served as the control. Intrabrachial Ach infusion produced a stable increase in forearm blood flow, from 2.6+/-0.3 to 10.6+/-2.1 mL. min(-1). dL(-1); when vitamin C was added, a further rise in forearm blood flow (to 13.4 mL. min(-1). dL(-1); P<0.03 vs Ach alone) was observed. In response to insulin, blood flow in both the infused and control forearms did not significantly change from baseline values (+10+/-16% and +2+/-11%, respectively). In contrast, when vitamin C was added, blood flow in the infused forearm increased significantly (to 3.7+/-0.7 mL. min(-1). dL(-1); P<0.02 vs 2.8+/-0.6 mL. min(-1). dL(-1) in the control forearm). Insulin stimulated whole-body glucose disposal to 20+/-2 micromol. min(-1). kg(-1), compatible with the presence of marked insulin resistance. Forearm glucose uptake was similarly stimulated after 80 minutes of insulin infusion (to 2.11+/-0.42 and 2.06+/-0.43 micromol. min(-1). dL(-1), infused and control, respectively). When intrabrachial vitamin C was added, no difference in glucose uptake was observed between the 2 forearms (infused, 2.37+/-0.44 micromol. min(-1). dL(-1)and control, 2.36+/-0. 53 micromol. min(-1). dL(-1)). Forearm O(2) uptake at baseline was also similar in the 2 forearms (infused, 9.7+/-0.7 micromol. min(-1). dL(-1) and control, 9.6+/-1.1 micromol. min(-1). dL(-1)) and was not changed by either insulin or vitamin C. We conclude that in the deep forearm tissues of patients with essential hypertension and insulin resistance, an acute improvement in endothelial function, obtained with pharmacological doses of vitamin C, restores insulin-mediated vasodilatation but does not improve insulin-mediated glucose uptake. Thus, the endothelial dysfunction of essential hypertension is unlikely to be responsible for their metabolic insulin resistance.

Ascorbic Acid↗

C-type natriuretic peptide-induced vasodilation is dependent on hyperpolarization in human forearm resistance vessels.

Animal studies have demonstrated that CNP causes endothelium-independent vasodilation, which is limited by neutral endopeptidase (NEP) activity. However, the vasodilating mechanism of CNP in humans is still unknown. Therefore, we investigated the vasodilator actions of CNP in human forearm resistance vessels before and after inhibition of nitric oxide (NO) and then prostacyclin production and after inhibition of Ca(2+)-dependent potassium channel activation and NEP activity. Three separate studies were performed. In each study, forearm blood flow was recorded by venous occlusion plethysmography in 8 healthy nonsmoking subjects. Brachial artery infusion of CNP (70, 140, 280, and 560 ng per 100 mL forearm volume per minute) caused significant forearm vasodilation in all studies (forearm blood flow from 3.94 to 8.50 mL per 100 mL forearm volume per minute). Inhibition of the endogenous generation of NO by L-N(G)-monomethyl arginine (by use of the NO-clamp technique) did not block the maximal vasodilating effects of CNP (forearm blood flow from 3.69 to 6.93). In addition, when the cyclooxygenase system was inhibited by 600 mg of acetylsalicylic acid (aspirin) administered orally 30 minutes before start of measurements, the rise in forearm blood flow remained intact (forearm blood flow from 3.31 to 8.27 mL per 100 mL forearm volume per minute). However, inhibition of Ca(2+)-dependent potassium channels with tetraethylammonium chloride (0.1 mg per 100 mL forearm volume per minute) significantly attenuated vasodilation caused by CNP (forearm blood flow from 2.28 to 3.06 mL per 100 mL forearm volume per minute), which suggests that CNP opens vascular potassium channels. Vasodilation to all doses of CNP was significantly increased when activity of NEP was blocked with thiorphan (30 nmol/min), which suggests that NEP activity limits vasodilation of CNP. CNP is a dilator of human resistance vessels that mediates its effects through hyperpolarization of the vessel wall independent of the NO and prostaglandin system. Inhibition of local NEP activity increases CNP bioavailability. This may be of relevance to cardiovascular disease, given that vascular tone is well balanced between NO and an endothelium-derived hyperpolarizing factor, which suggests that in pathological situations, impaired NO activity can be compensated for by enhanced endothelium-derived hyperpolarizing factor release to maintain vascular homeostasis.

Adolescent↗

Effects of insulin on hemodynamics and metabolism in human forearm.

We investigated the vascular response (blood flow and resting vascular resistance) and the metabolic response (exchange of metabolites and respiratory gases) to local insulin administration in the forearms of healthy young volunteers with the use of the perfused-forearm technique. In the postabsorptive state, the deep tissues of the forearm (mostly skeletal muscle) took up glucose (mean +/- SE 1.09 +/- 0.17 mumol.min-1.dl-1 forearm vol), beta-hydroxybutyrate (0.267 +/- 0.130 mumol.min-1.dl-1), and O2 (9.96 +/- 1.02 mumol.min-1.dl-1) and released lactate (0.284 +/- 0.098 mumol.min-1.dl-1), glycerol (0.029 +/- 0.012 mumol.min-1.dl-1), citrate (0.091 +/- 0.030 mumol.min-1.dl-1), alanine (0.184 +/- 0.044 mumol.min-1.dl-1), CO2 (7.36 +/- 0.97 mumol.min-1.dl-1), and protons (12.1 +/- 1.4 pmol.min-1.dl-1). Forearm blood flow (by venous occlusion plethysmography) was 2.95 +/- 0.18 ml.min-1.dl-1, and intra-arterial systolic/diastolic blood pressure was 116 +/- 3/76 +/- 2 mmHg. Local indirect calorimetry indicated dominance of fat as the oxidative substrate (RQ 0.76 +/- 0.09) and an energy expenditure rate of 1.03 +/- 0.11 cal.min-1.dl-1 forearm vol. One hundred minutes of intra-arterial insulin infusion (deep venous plasma insulin concn of 125 +/- 11 microU/ml) had no detectable effect on forearm blood flow, resting forearm vascular resistance, heart rate, or blood pressure. Local hyperinsulinemia significantly stimulated glucose uptake (to 4.79 +/- 0.61 mumol.min-1.dl-1 forearm vol, P less than 0.001), lactate and pyruvate release (to 0.710 +/- 0.093 and 0.032 +/- 0.016 mumol.min-1.dl-1 forearm vol, respectively; P less than 0.01 for both), potassium uptake (0.76 +/- 0.22 mueq.min-1.dl-1, P less than 0.001), and free fatty acid uptake (0.123 +/- 0.041 mumol.min-1.dl-1 forearm vol, P less than 0.05); glycerol balance switched to a net uptake (P less than 0.001), alanine release was restrained by 33% (P less than 0.05), and beta-hydroxybutyrate and citrate release were unchanged. Despite these metabolic changes, local rates of substrate oxidation and energy expenditure were not altered by insulin. In contrast, forearm proton release was significantly stimulated by insulin (to 14.8 +/- 1.4 pmol.min-1.dl-1, P less than 0.02). Proton release was also found to be directly related to resting forearm vascular resistance independent of the effect of insulin (multiple r = 0.64, P less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

3-Hydroxybutyric Acid↗

Outcomes of intramedullary nail fixation through the olecranon apophysis in skeletally immature forearm fractures.

The objective of this study was to quantitatively investigate the long-term radiologic and functional outcomes of antegrade intramedullary (IM) nailing through the olecranon apophysis for ulnar fractures in skeletally immature patients. A retrospective review was conducted of skeletally immature patients with ulnar fractures that had antegrade IM nail fixation through the olecranon apophysis. Patients were excluded if they had a previous forearm fracture or a fracture of the contralateral forearm. Functional measures included the Activities Scale for Kids (ASK) questionnaire for patients younger than 15 years of age and the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire for patients older than 15 years of age. Forearm range-of-motion measurements were collected from the fractured forearm and the contralateral control forearm. Radiologic outcomes were evaluated for ulnar, olecranon, coronoid, and trochlear notch proportions. Nineteen patients were evaluated. The average age at operation was 10.8 years (range 1.6-15.9) and the mean follow-up time was 3.4 years (range 1.2-7.2). Nine patients completed the ASK questionnaire, with a mean score of 93.9 (range 68.9-100), and 10 patients completed the DASH questionnaire, with a mean score of 6.0 (range 0-35). The mean fractured forearm supination was 103.2 degrees compared with 109.2 degrees on the control forearm (P < 0.05). Furthermore, the mean fractured forearm trochlear notch width was 17.7 mm compared with 17.1 mm on the control forearm (P < 0.05). Similarly, the mean fractured forearm trochlear notch height was 16.5 mm compared with 17.0 mm on the control forearm (P < 0.05). This retrospective review suggests that antegrade IM nail fixation through the olecranon apophysis for ulnar fractures in skeletally immature patients is a safe procedure. There is no significant ulnar length disruption or functional limitations, despite the differences in trochlear notch measurements and supination between the fractured and control forearms. Overall, IM nail fixation through the olecranon apophysis for surgically indicated ulnar fractures has minimal outcome limitations, with no evidence of prospective growth disruption. A larger randomized prospective trial should be conducted to strengthen the evidence of this study.

Adolescent↗

Does computer use pose an occupational hazard for forearm pain; from the NUDATA study.

AIMS: To determine the occurrence of pain conditions and disorders in the forearm and to evaluate risk factors for forearm pain in a cohort of computer workers. METHODS: A total of 6943 participants with a wide range of computer use and work tasks were studied. At baseline and at one year follow up participants completed a questionnaire. Participants with relevant forearm symptoms were offered a clinical examination. Symptom cases and clinical cases were defined on the basis of self reported pain score and palpation tenderness in the muscles of the forearm. RESULTS: The seven days prevalence of moderate to severe forearm pain was 4.3%. Sixteen of 296 symptom cases met criteria for being a clinical forearm case, and 12 had signs of potential nerve entrapment. One year incidence of reported symptom cases was 1.3%; no subjects developed new signs of nerve entrapment. Increased risk of new forearm pain was associated with use of a mouse device for more than 30 hours per week, and with keyboard use more than 15 hours per week. High job demands and time pressure at baseline were risk factors for onset of forearm pain; women had a twofold increased risk of developing forearm pain. Self reported ergonomic workplace factors at baseline did not predict future forearm pain. CONCLUSION: Intensive use of a mouse device, and to a lesser extent keyboard usage, were the main risk factors for forearm pain. The occurrence of clinical disorders was low, suggesting that computer use is not commonly associated with any severe occupational hazard to the forearm.

Adult↗

Adenosine contributes to hypoxia-induced forearm vasodilation in humans.

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 O(2) 10.5%; approximately 20 min). In experiment I, aminophylline (50-200 microg. 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 O(2) 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.

Adenosine↗

Biphasic forearm vascular responses to intraarterial arginine vasopressin.

Forearm vascular responses to arginine vasopressin (AVP) infused into a brachial artery in a wide range of infusion rates (0.05-2.0 ng/kg per min) were examined in 20 young healthy volunteers. Intraarterial AVP at lower doses (0.05 and 0.1 ng/kg per min) caused forearm vasoconstriction, whereas AVP at a dose of 0.2 ng/kg per min or higher caused forearm vasodilatation. The maximal forearm vasoconstriction was induced at the venous plasma AVP level of 76.3 +/- 8.8 pg/ml. Forearm vasodilatation was associated with the venous plasma AVP level of 369 +/- 43 pg/ml or higher. Forearm vasodilatation was the result of the direct effect of AVP since forearm blood flow and vascular resistance in the contralateral arm did not change. We attempted to explore the mechanisms involved in AVP-induced direct vasodilatation. The treatment with indomethacin, 75 mg/d for 3 d, did not alter AVP-induced forearm vasodilatation. In contrast, intraarterial infusion of isoosmolar CaCl2 totally prevented AVP-induced forearm vasodilatation. Intra-arterial CaCl2 also markedly attenuated forearm vasodilatation induced by intraarterial sodium nitroprusside, but did not alter forearm vasodilatation induced by intraarterial isoproterenol. These results indicate that the direct vascular effects of intra-arterial AVP on the forearm vessels are biphasic, causing vasoconstriction at lower doses and vasodilatation at higher doses. The direct vasodilatation induced by intraarterial AVP at higher doses is not mediated by prostaglandins but may involve cGMP-related mechanisms.

Adult↗

The effect of thyroid hormones on gluconeogenesis and forearm metabolism in man.

The present study was designed to examine the effects of excess T3 on total body glucose production and forearm exchange of glucose, amino acids, and other metabolites. Five healthy male volunteers were studied after an overnight fast, before and 7 days after the administration of 150 micrograms/day T3. Glucose production (milligrams per kg/min) was measured using a primed continuous infusion of [3-3H]glucose and gluconeogenic index (micromoles per kg/min) was measured by following the conversion of infused [14C]alanine to [14C]glucose. Blood flow across the forearm was measured using capacitance plethysmography and forearm release of substrates was determined by the Fick principle. After T3 administration, there was a 3.7-fold rise in T3 from 150 +/- 15 to 530 +/- 12 ng/dl (P less than 0.001), with no change in insulin (12 +/- 1 microU/ml pre-T3 vs. 13 +/- 2 microU/ml post-T3) and glucagon (79 +/- 5 pre-T3 vs. 84 +/- 7 pg/ml post-T3). T3 administration resulted in an increase in plasma glucose (from 83 +/- 5 to 98 +/- 5 mg/dl; P less than 0.05), net glucose uptake by the forearm (from 250 +/- 90 to 712 +/- 60 nmol/100 ml forearm tissue X min; P less than 0.005) and glucose production (1.7 +/- 0.09 to 2.2 +/- 0.08 mg/kg X min; P less than 0.005), without a change in glucose clearance (2.1 +/- 0.02 vs. 2.0 +/- 0.02 ml/kg X min); the rate of conversion of [14C]alanine to [14C]glucose increased by 30% (0.56 +/- 0.03 to 0.74 +/- 0.03 mumol/ kg X min P less than 0.005). These values were associated with a 25% increase in blood lactate to 712 +/- 69 mumol/liter (P less than 0.05) and a 131% increase in lactate release across the forearm to 434 +/- 90 (P less than 0.005). Forearm release of alanine (96 +/- 29 nmol/100 ml forearm tissue X min) and glutamine (151 +/- 41 nmol/100 ml forearm tissue X min) increased by 90% (P less than 0.005 and P = 0.04, respectively), with no change in their concentrations. Forearm release of branched chain amino acids did not change, while those of their ketoacids, alpha-ketoisocaproate (KIC) and alpha-ketoisovalerate (KIV), doubled (to 64 +/- 9 mumol/liter for KIC and 39 +/- 6 mumol/liter for KIV; P less than 0.05). These were associated with a 45% increase in the branched chain amino acid levels and a 46% rise in both KIC and KIV levels to 41 +/- 9 and 28 +/- 7 mumol/liter, respectively (P less than 0.05). There was a concurrent significant (P less than 0.05) change in the arterial levels of phenylalanine (-32%), tyrosine (-29%), threonine (-20%), glycine (-20%), and serine (-15%), without any change in their efflux across the forearm. The data indicate that a pharmacologically induced rise in T3, to levels comparable to those seen in hyperthyroidism, results in enhanced glucose production, with an increase in glucose uptake by the forearm. The former can be partially accounted for by an increase in hepatic gluconeogenesis, glycogenolysis, or possibly increased renal glucose production...

Adult↗

Effect of 12 weeks of wrist and forearm training on high school baseball players.

This study examined the effect of 12 weeks of wrist and forearm training on male high school baseball players (mean age = 15.3 +/- 1.1 years). Participants (N = 43) were tested for 10 repetition maximum (RM) wrist barbell flexion, wrist barbell extension, dominant (D) and nondominant (ND) hand-forearm supination, D and ND forearm pronation, D and ND wrist radial deviation, D and ND wrist ulnar deviation, D and ND grip strength, and a 3RM parallel squat (PS) and bench press (BP). Group 1 (n = 23) and group 2 (n = 20), randomly assigned by a stratified sampling technique, performed the same resistance exercises while training 3 days a week for 12 weeks according to a stepwise periodized model. Group 2 also performed wrist and forearm exercises 3 days a week for 12 weeks to determine if additional wrist and forearm training provided further wrist and forearm strength improvements. All wrist and forearm strength variables were measured before and after 12 weeks of training. The 3RM PS and BP were measured at 0 and after 4, 8, and 12 weeks of training. Both groups significantly increased wrist and forearm strength (kg +/- SD) except 10RM D and ND forearm supination for group 1 (p < 0.05). Group 2 showed statistically greater improvements (p < 0.05) in all wrist and forearm strength variables than did group 1 except for D and ND grip strength. Predicted 1RM (kg +/- SD) PS and BP increased significantly (p < 0.05) after weeks 4, 8, and 12 for both groups. These data indicate that a 12-week stepwise periodized training program can significantly increase wrist, forearm, PS, and BP strength for both groups. Additionally, group 2 had further wrist and forearm strength gains.

Adaptation, Physiological↗

Differences in foot and forearm skin microcirculation in diabetic patients with and without neuropathy.

OBJECTIVE: We have compared the hyperemic response to heat and the endothelium-dependent and endothelium-independent vasodilatation between the dorsum of the foot and the forearm in diabetic neuropathic and non-neuropathic patients and healthy control subjects. RESEARCH DESIGN AND METHODS: We studied the cutaneous microcirculation in the forearm and foot in 15 diabetic patients with neuropathy, in 14 diabetic patients without neuropathy, and in 15 control subjects matched for age, sex, BMI, and in the case of diabetic patients, for the duration of diabetes. Patients with peripheral vascular disease and/or renal impairment were excluded. The cutaneous microcirculation of the dorsum of the foot and the flexor aspect of the forearm was tested in all subjects. Single-point laser Doppler was employed to measure the maximal hyperemic response to heating of the skin to 44 degrees C and laser Doppler imaging scanner was used to evaluate the response to iontophoresis of 1% acetylcholine chloride (Ach) (endothelium-dependent response) and 1% sodium nitroprusside (NaNP) (endothelium-independent response). RESULTS: The transcutaneous oxygen tension was lower in the neuropathic group at both foot and forearm level, while the maximal hyperemic response to heat was similar at the foot and forearm level in all three groups. The endothelium-dependent vasodilation (percent increase over baseline) was lower in the foot compared to the forearm in the neuropathic group (23 +/- 4 vs. 55 +/- 10 [mean +/- SEM]; P < 0.01)], the non-neuropathic group (33 +/- 6 vs. 88 +/- 14; P < 0.01), and the control subjects (43 +/- 6 vs. 93 +/- 13; P < 0.001). Similar results were observed during the iontophoresis of NaNP (P < 0.05). No differences were found among the three groups when the ratio of the forearm:foot response was calculated for both the endothelium-dependent (neuropathic group, 2.25 +/- 0.24; non-neuropathic group, 2.55 +/- 0.35; and control subjects, 2.11 +/- 0.26; P = NS) and endothelium-independent vasodilation (neuropathic group, 1.54 +/- 0.27; non-neuropathic group, 2.08 +/- 0.33; and control subjects, 2.77 +/- 1.03; P = NS). The vasodilatory response, which is related to the C nociceptive fiber action, was reduced at the foot level during iontophoresis of Ach in the neuropathic group. In contrast, no difference was found during the iontophoresis of NaNP at the foot and forearm level and of Ach at the forearm level among all three groups. CONCLUSIONS: In healthy subjects, the endothelial-dependent and endothelial-independent vasodilatation is lower at the foot level when compared to the forearm, and a generalized impairment of the microcirculation in diabetic patients with neuropathy preserves this forearm-foot gradient. These changes may be a contributing factor for the early involvement of the foot with neuropathy when compared to the forearm.

Adult↗

[The innervation of deep muscles of the human forearm extensors].

The innervation of four deep muscles of the human forearm extensors (the abductor pollicis longus, the extensor pollicis brevis, the extensor pollicis longus, and the extensor indicis muscles) were investigated in 24 bodies (48 sides) from those used in the 1989 and 1990 student courses in gross anatomy dissection at the Iwate Medical University School of Medicine. The forearm extensor muscles and the deep branch of the radial nerve were dissected intensively in the student courses in gross anatomy and were removed afterwards. The four deep muscles of the human forearm extensors and the nerves innervating the muscles were observed while they were immersed in the water and with use of a stereomicroscope--with the assistance of which they were drawn. In six sides the intramuscular nerve supply was also examined carefully and drawn. The results were as follows. 1. The nerves to the four deep muscles of the forearm extensors arose usually from the deep branch of the radial nerve after emerging the supinator muscle and sending branches to superficial forearm extensors. In some cases a nerve or nerves to the superficial forearm extensors were observed arising from the deep branch of the radial nerve after sending one or more branches to the deep forearm extensor muscles, or from the branches to the deep muscles themselves. However they were split easily from the deep branch of the radial nerve and from the branches to the four deep forearm extensors proximally near to the emerging of the deep branch from the supinator muscle. Therefore, it was considered to be constant that the nerves to the four deep forearm extensors arose from the deep branch of the radial nerve after branching to the superficial forearm extensors. 2. The radial group of the deep forearm extensors (the abductor pollicis longus and the extensor pollicis brevis muscles) was innervated usually by one branch that arose from the deep branch of the radial nerve just after emerging from the supinator and giving off branches to the superficial forearm extensors. This branch ran on the dorsal (extensor) surface of the abductor pollicis longus muscle distally, sending many twigs to this muscle, and entered into the muscle at various distances from the origin (Figs. 1-6). The abductor pollicis brevis muscle was innervated by some twigs that ran usually inside but occasionally outside of the abductor pollicis longus muscle (Figs. 7-10).(ABSTRACT TRUNCATED AT 400 WORDS)

Forearm↗

The effects of sublingually administered nitroglycerin on forearm vascular resistance in patients with heart failure and in normal subjects.

This study examined the effects of sublingually administered nitroglycerin on forearm resistance vessels in normal subjects (n = 9) and in patients with congestive heart failure (n = 8). Forearm blood flow was measured with a strain-gauge plethysmograph and forearm vascular resistance was calculated. To assess the magnitude of reflex forearm vasoconstriction triggered by decreased central venous pressure after sublingual nitroglycerin, lower body negative pressure (LBNP) was applied to produce a comparable decrease in central venous pressure to that after nitroglycerin. The change in forearm vascular resistance during LBNP was compared with that after nitroglycerin. In normal subjects, LBNP increased but nitroglycerin did not change forearm vascular resistance. In patients with congestive heart failure neither nitroglycerin nor LBNP changed forearm vascular resistance. The direct vasodilator effect of nitroglycerin on forearm resistance vessels assessed by the difference between the change in forearm vascular resistance produced by nitroglycerin and that during LBNP tended to be less in patients with congestive heart failure than in normal subjects, which might have resulted from decreased vasodilator capacity of resistance vessels in patients with congestive heart failure. Changes in forearm vascular resistance with a cold pressor test were not different between normal subjects and patients with congestive heart failure. These data suggest that in normal subjects, nitroglycerin does not alter forearm vascular resistance because its dilator effect is offset by reflex vasoconstriction. In patients with congestive heart failure, reflex vasoconstriction is impaired but the direct vasodilator effect of nitroglycerin also tends to be reduced, so that as a net effect forearm vascular resistance is not altered.

Adult↗

Intersection syndrome: MR imaging with anatomic comparison of the distal forearm.

OBJECTIVE: To correlate the anatomic and MR imaging characteristics of the area of intersection of the first and the second dorsal extensor tendon compartments (DETC) in the distal forearm in an attempt to improve the design of MR imaging protocols used for the evaluation of intersection syndrome. DESIGN AND PATIENTS: Ten forearms of nine cadavers underwent MR imaging in the axial and sagittal-oblique planes before and after tenography with direct injection of a gadolinium-containing contrast agent into the first DETC in four forearms, the second DETC in four forearms, and both compartments in the remaining two forearms. The area of intersection between the first and second DETC was identified in each case as well as its distance from Lister's tubercle. Subsequently all forearms were sectioned in the axial (8 forearms) or sagittal-oblique planes (2 remaining forearms) to parallel the imaging planes. Detailed examination of each of the anatomic slices was performed in a search for anatomic variations and for possible anatomic connections of the tendons sheaths. One forearm was dissected to identify the area of intersection. RESULTS: The area of intersection between the first and second DETC occurred between 3.5 cm and 4.8 cm (mean 4.18 cm) proximal to Lister's tubercle. After tenography, gadolinium solution was noted in the third DETC in two of four specimens in which the second DETC was injected and in one of two specimens in which both the first and second DETC were injected. Extension of the gadolinium solution between the first and second DETC was noted during isolated injections of either compartment, although this finding may have related to iatrogenic injection effects. The axial plane was the most valuable for assessment of the area of intersection of the first and second DETC. CONCLUSION: MR imaging is a noninvasive method that can be used for the evaluation of distal forearm and wrist pain. Standard wrist protocols do not include the area of intersection between the first and second DETC and, in those cases in which intersection syndrome is suspected, the MR examination must be tailored to include the forearm.

Aged↗

Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting.

To investigate whether systemic endothelial function on forearm resistance vessels is related to angiographic restenosis after coronary stenting, 47 men who underwent elective coronary stenting were divided into 2 groups according to the presence (n = 20) or absence (n = 27) of in-stent restenosis 6 months after the procedure. Another 19 risk factor-matched men with normal coronary angiograms served as the control group. Forearm blood flow was assessed by venous occlusive plethysmography. Basal forearm blood flow was similar between restenosis, nonrestenosis, and control groups (2.63 +/- 0.19, 2.58 +/- 0.14, and 3.23 +/- 0.13 ml/100 ml forearm tissue per minute, respectively). In all 3 groups, forearm blood flow increased significantly during reactive hyperemia (5.75 +/- 0.7, 11. 32 +/- 1.23, and 14.52 +/- 1.36 ml/100 ml forearm tissue per minute, p <0.05, respectively) and remained unchanged after sublingual administration of nitroglycerin. The percentage change of forearm blood flow during reactive hyperemia was significantly lower in the restenosis group (117.3 +/- 18.3%) than in the nonrestenosis group (354.2 +/- 46.5%, p <0.01). This difference was still present after sublingual nitroglycerin (37.6 +/- 21.2% vs 226.4 +/- 40.5%, p <0. 01). In contrast, percentage change of hyperemic forearm blood flow was significantly lower in patients with angina (117.5 +/- 49.5%) than in those without angina (290.1 +/- 37.4%, p <0.05) at follow-up. In all patients, the angiographic loss index was correlated negatively to the percentage change of hyperemic forearm blood flow (r = -0.33, p <0.01) and positively to the percentage change of forearm vascular resistance during reactive hyperemia (r = 0.33, p <0.01). In patients with angiographic restenosis after coronary stenting, forearm reactive hyperemia was more impaired compared with those without angiographic restenosis. Systemic endothelial dysfunction might be either a marker or one of the confounding factors in the development of late restenosis after coronary stenting.

Aged↗

Age-independent forearm vasodilatation by acetylcholine and adenosine 5'-triphosphate in humans.

1. Forearm vasodilator responses to acetylcholine, ATP and sodium nitroprusside were examined in healthy young (20 +/- 1 years, n = 9), middle-aged (46 +/- 2 years, n = 6) and old (57 +/- 1 years, n = 6) subjects. 2. A brachial artery was cannulated with a 20-gauge cannula through which drugs at graded doses were locally infused for 2 min at each dose. During drug infusions, forearm blood flow was continuously measured at 15 s intervals using a plethysmograph. Forearm vascular resistance was calculated from forearm blood flow and mean blood pressure obtained in the opposite arm. Basal forearm blood flow and forearm vascular resistance did not differ between the three groups. 3. Acetylcholine and ATP were used to examine endothelium-dependent vasodilatation, and sodium nitroprusside was used to examine endothelium-independent vasodilatation. All three drugs caused dose-dependent increases in forearm blood flow (P less than 0.01) and decreases in forearm vascular resistance (P less than 0.01). The increases in forearm blood flow or decreases in forearm vascular resistance in response to infusions of the three drugs did not differ between the three groups. 4. These results suggest that endothelium-dependent and endothelium-independent vasodilatation in forearm resistance arteries do not alter with ageing in humans.

Acetylcholine↗

[Revascularization and defect coverage of the hand: special applications of the radialis forearm flap].

During the last years, a large number of newly designed flaps have been presented, suitable to cover defects of the hand. Some of them, namely the retrograde interossea-posterior and the lateral arm flaps, found their way into daily clinical routine. They even seem to have replaced the standard flaps for defect coverage to the hand, the pedicled groin flap and the radial forearm flap. Especially the radial forearm flap seems to become an obsolete procedure, as it requires sacrificing a main forearm artery. Three patients are presented who suffered from complex injuries to their hands and were treated with radial forearm flaps in a single-stage primary procedure. In two hands, the arterial palmar arches and the soft-tissues of the palm were reconstructed by use of a distally pedicled radial forearm flap. Collateral arteries of ischemic fingers were implanted into the flap artery to achieve revascularization and a vein graft was interposed between the stumps of the radial artery to reestablish an orthograde blood flow. A free radial forearm flap harvested from the contralateral uninjured forearm was used to replant a torn-out forearm. In all cases, primary healing was achieved without complications. Primary treatment of complex injuries to the hand and forearm often requires revascularization of ischemic parts of the limb and coverage of large soft-tissue defects at the same time. The radial forearm flap, either as a distally pedicled flap or as a free flap, meets all the needs or in particular is appropriate to perform such demanding primary procedures. The destruction of the arterial palmar arches does not present a contraindication against the use of a distally pedicled radial forearm flap, but actually is a strong indication to reconstruct the radial artery by a vein graft.

Adolescent↗

Forearm mixed nerve conduction velocity: questionable role in the evaluation of retrograde axonal atrophy in carpal tunnel syndrome.

The objective of this study was to determine whether forearm mixed nerve conduction velocity (Fmix) reflects the real conduction velocity of forearm motor nerve (Fmot) and forearm sensory nerve (Fsen) fibers passing through the carpal tunnel. Forearm mixed nerve conduction velocity is presumed to be indicative of the conduction velocity of the median nerve over the forearm. Therefore, Fmix is used widely to assess the causes of slowing forearm conduction velocity in carpal tunnel syndrome. However, some authors claim that Fmix comes chiefly from the undamaged fibers in carpal tunnel syndrome, and thus cannot replace Fmot or Fsen in the evaluation of retrograde axonal atrophy. Patients with clinical symptoms and signs of carpal tunnel syndrome confirmed with standard electrodiagnosis were included. Age-matched volunteers served as control subjects. Conduction velocities across the wrist and over the forearm were measured, including those of the wrist sensory (Wsen), wrist motor (Wmot), and wrist mixed nerves (Wmix); and forearm mixed (Fmix), forearm motor (Fmot), and forearm sensory nerves (Fsen). The authors compared and correlated Wsen, Wmot, and Wmix; and Fmix, Fmot, and Fsen respectively. The mean values of Wsen, Wmot, Wmix, Fmix, Fmot, and Fsen of the control subjects less those of corresponding conduction velocity of carpal tunnel syndrome patients were designated Wsen N, Wmot N, Wmix N, Fmix N, Fmot N, and Fsen N respectively and were compared and correlated again. Wrist motor nerve conduction velocity, Wsen, and Wmix were significantly lower in carpal tunnel syndrome patients, and Fmot and Fsen but not Fmix were reduced significantly when compared with control subjects. Mean wrist sensory nerve conduction velocity, Wmot N, and Wmix N; and Fsen N and Fmot N showed good correlation except for Fmix N, suggesting that Fmix reflects the conduction velocity of undamaged fibers in carpal tunnel syndrome. Forearm mixed nerve conduction velocity cannot replace Fmot or Fsen in the assessment of retrograde axonal atrophy in carpal tunnel syndrome. In the disease state, Fmix possibly represents the conduction velocity of the palmar cutaneous branch.

Carpal Tunnel Syndrome↗

Metabolic and endothelial effects of trimetazidine on forearm skeletal muscle in patients with type 2 diabetes and ischemic cardiomyopathy.

The aim of the present study was to evaluate the effect of prolonged inhibition of beta-oxidation on glucose and lipid muscle forearm metabolism and cGMP and endothelin-1 forearm release in patients with type 2 diabetes mellitus and ischemic cardiomyopathy. Fifteen patients were randomly allocated in a double-blind cross-over parallel study with trimetazidine (20 mg tid) or placebo lasting 15 days. At the end of each period, all patients underwent euglycemic hyperinsulinemic clamps with forearm indirect calorimetry and endothelial balance of vasodilator and vasoconstricor factors. Compared with placebo, trimetazidine induced 1) an increase in insulin-induced forearm glucose uptake and glucose oxidation accompanied by a reduction in forearm lipid oxidation and citrate release and 2) a decrease of endothelin-1 release paralleled by a significant increase in forearm cGMP release. Forearm glucose oxidation significantly correlated with cGMP release (r=0.37, P<0.04), whereas forearm lipid oxidation positively correlated with endothelin-1 release (r=0.40, P<0.03). In conclusion, for the first time, we demonstrated that insulin-induced forearm glucose oxidation and forearm cGMP release were increased whereas forearm endothelin-1 release was decreased during trimetazidine treatment. Muscle's metabolic and vascular effects of trimetazidine add new interest in the use of trimetazidine in type 2 diabetic patients with cardiovascular disease.

3-Hydroxybutyric Acid↗