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PubMed1991

Reduction of complication rate at radial forearm flap donor sites.

The radial forearm flap has become a versatile tissue transfer in head and neck surgery, especially in the reconstruction of the pharynx and oral cavity. Still, many surgeons avoid its application because of the possible donor site complications. In 29 of 51 patients who were operated between July 1987 and April 1990 at the Department of Otorhinolaryngology in Tübingen, we evaluated the function and aesthetic appearance of the radial forearm donor site after surgery. We found a much lower complication rate compared to some reports in the literature. With a questionnaire, the patients were asked how they judged the function and appearance of the forearm donor site. Further tests were made to detect a possible reduced mobility of the hand, and to measure the strength of the hand. Postoperative complications and their management as well as our concept of dealing with the radial forearm flap donor site to minimize complications are discussed.

Consumer Behavior↗
PubMed1985

Digitalis-induced augmentation of cardiopulmonary baroreflex control of forearm vascular resistance.

We sought to determine whether digitalis augments cardiopulmonary baroreflex control of forearm vascular resistance in normal young men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP) at 10 and 20 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate. Decreases in forearm blood flow and increases in forearm vascular resistance with LBNP were greater after administration of lanatoside C (Cedilanid) than before, and the slope of the regression line relating changes in central venous pressure and those in forearm vascular resistance was steeper after lanatoside C. Vasoconstrictor responses to the cold pressor test did not differ before and after lanatoside C, which suggested that augmented responses to LBNP after the drug were not caused by a generalized change in reflex control. These results suggest that lanatoside C augments the tonic inhibitory influence of cardiopulmonary baroreceptors in normal men.

Adult↗
PubMed1988

Atrial natriuretic factor potentiates forearm reflex vasoconstriction induced by cardiopulmonary receptor deactivation in man.

Previous evidence suggests that atrial natriuretic factor (ANF) interferes with the autonomic control of circulation. In the present study we investigated whether ANF modulates forearm vasoconstriction reflexly induced by cardiopulmonary receptor unloading in man. For this purpose, the hemodynamic response to -20 mm Hg lower body negative pressure (LBNP) was assessed under control conditions and during the constant infusion of alpha-human ANF (0.5 micrograms/kg bolus followed by 0.05 micrograms/kg/min) in seven normal subjects. ANF infusion resulted in a slight reduction in blood pressure and right atrial pressure, did not modify heart rate or forearm vascular resistance, but significantly potentiated the reflex increase in forearm vascular resistance during LBNP (+25 +/- 9% under control conditions vs +40 +/- 12% during ANF, p less than .05). In an attempt to clarify the mechanisms underlying the enhanced reflex vasoconstriction during infusion of ANF, in five additional subjects we demonstrated that there was a comparable vascular reflex response to LBNP under control conditions and during nitroglycerin infusion at a dose that induced a reduction in atrial pressure comparable to that observed during ANF. Finally, in seven additional subjects we found that ANF infusion did not alter the reflex hemodynamic responses elicited by carotid baroreceptor unloading induced by a +60 mm Hg increase in external neck pressure. We conclude that during the infusion of a pharmacologic dose of ANF the reflex forearm vasoconstriction in response to selective cardiopulmonary receptor unloading is potentiated. This effect does not seem to be related to the hemodynamic actions of the peptide or to interference with the sympathetic control of peripheral circulation.

Adult↗
PubMed1990

Indirect evidence for release of endothelium-derived relaxing factor in human forearm circulation in vivo. Blunted response in essential hypertension.

In isolated blood vessels, acetylcholine releases endothelium-derived relaxing factor (EDRF). In vivo, the vasodilator action of acetylcholine may be mediated by EDRF, but prostacyclin or prejunctional inhibition of adrenergic neurotransmission may also be involved. Therefore, we investigated whether acetylcholine releases EDRF in humans in vivo and, if so, whether the response altered in essential hypertension. Acetylcholine was infused into the brachial artery, and forearm blood flow measured by venous occlusion plethysmography. In control subjects, acetylcholine (0.02-16 micrograms/min/100 ml tissue) increased flow from 2.4 +/- 5.0 to 20.6 +/- 5.2 ml/min/100 ml tissue (n = 14; p less than 0.05) and decreased forearm vascular resistance from 42.0 +/- 4.1 to 6.0 +/- 1.4 units (p less than 0.03), a response comparable to that of sodium nitroprusside (0.6 micrograms/min ml tissue). Acetylsalicylic acid (500 mg i.v.) given to block vascular prostacyclin production did not alter the response (n = 14). alpha-Adrenoceptor blockade by phentolamine (12 micrograms/min/100 ml tissue) did not prevent the increase in flow evoked by acetylcholine. In hypertensive patients, the decrease in forearm vascular resistance induced by acetylcholine but not evoked by sodium nitroprusside was reduced as compared with controls (14.5 +/- 3.1 and 6.1 +/- 1.6 units, respectively; n = 8; p less than 0.05). Thus, the vascular effects of acetylcholine in the human forearm circulation are independent of prostaglandins and adrenergic neurotransmission and therefore are most likely to be mediated by EDRF; the acetylcholine-induced release of EDRF is blunted in patients with essential hypertension.

Acetylcholine↗
PubMed1990

Attenuated forearm vasodilative response to intra-arterial atrial natriuretic peptide in patients with heart failure.

It has been shown that renal responses to atrial natriuretic peptide (ANP) are markedly attenuated in patients with heart failure. This study aimed to determine if vasodilative response to ANP is altered in patients with heart failure. In patients with heart failure (n = 7) and age-matched normal subjects (n = 7), forearm blood flow was measured using a strain-gauge plethysmograph during intra-arterial infusion of alpha-human ANP (50, 100, 200, and 400 ng/min) or nitroglycerin (100, 200, 400, and 600 ng/min). Forearm vasodilatation evoked with intra-arterial alpha-human ANP in patients with heart failure was considerably less (p less than 0.01) than that in normal subjects. In contrast, nitroglycerin produced comparable forearm vasodilatation in the two groups. Plasma ANP and cyclic guanosine monophosphate (GMP) levels at rest were higher in patients with heart failure than in normal subjects (p less than 0.05 for both), but the increases in plasma ANP and cyclic GMP in the venous effluents during intra-arterial ANP infusion did not differ between the two groups. These results indicate that the direct vasodilative effect of ANP on forearm vessels was attenuated in patients with heart failure as compared with that in normal subjects. The mechanisms responsible for this alteration are not clear but might involve mechanisms other than down-regulation of the ANP receptors because the increases in venous plasma cyclic GMP caused by intra-arterial ANP were comparable between patients with heart failure and normal subjects.

Adult↗
PubMed1994

Pathophysiological correlates of increased serum tumor necrosis factor in patients with congestive heart failure. Relation to nitric oxide-dependent vasodilation in the forearm circulation.

BACKGROUND: Tumor necrosis factor-alpha (TNF alpha), which we and others have shown to be elevated in patients with severe congestive heart failure (CHF), is involved in the regulation of nitric oxide metabolism. Whether increased concentrations of TNF alpha affect nitric oxide-mediated vasodilation in patients with CHF has not been studied previously. METHODS AND RESULTS: Serum concentrations of TNF alpha, interleukin-1 (IL-1), interleukin-2 (IL-2), and interleukin-6 (IL-6) were determined in venous blood (pg/mL) from 17 patients with stable New York Heart Association classes II and III CHF (mean age, 58 +/- 11 years; mean left ventricular ejection fraction, 19.5 +/- 7.3) and 17 age-matched normal subjects with enzyme-linked immunosorbent assays (detection limit of assays, 20 pg/mL). Forearm blood flows were determined with plethysmography (mL/min per 100 mL) in 17 patients and 7 normal subjects in response to brachial artery administration of graded concentrations of acetylcholine (10(-6) mol/L and 10(-5) mol/L) and nitroglycerin (10(-7) mol/L and 10(-6) mol/L). Serum concentrations of TNF alpha were above the detection limits of the assay in 10 of 17 patients with CHF (mean serum concentration, 39.4 +/- 3.8 pg/mL). Forearm blood flow responses to acetylcholine and nitroglycerin were significantly greater in these 10 patients than in the 7 patients without detectable serum TNF alpha and were closely correlated with TNF alpha serum concentrations (r > or = .81, P < .01 and r > or = .65, P < .05 respectively). In 1 of 17 normal subjects, the serum concentration of TNF alpha was just above the detection limit of the assay. Serum concentrations of IL-2 were above the detection limit of the assay in 14 of 17 patients with CHF (mean serum concentration, 112 +/- 19 pg/mL). IL-2 was not detected in the serum of normal subjects. Serum concentrations of IL-1 and IL-6 were below the detection limit of the assays in all patients and normal subjects assayed. CONCLUSIONS: Increased TNF alpha concentrations are closely correlated with forearm blood flow responses to regional administration of acetylcholine and nitroglycerin. The significant correlation between serum concentrations of TNF alpha and forearm blood flow responses to acetylcholine and nitroglycerin suggests that both the inducible and the constitutive forms of nitric oxide synthase are involved in the regulation of peripheral vasomotor tone in patients with CHF.

Adult↗
PubMed1994

Effects of L-arginine on impaired acetylcholine-induced and ischemic vasodilation of the forearm in patients with heart failure.

BACKGROUND: Endothelium-dependent vasodilation in response to acetylcholine (ACh) and ischemic vasodilation during reactive hyperemia are attenuated in the forearm of patients with heart failure (HF). It has been shown that L-arginine augments endothelium-dependent vasodilation in healthy subjects. Thus, the aim of the present study was to determine if L-arginine improves endothelium-dependent and ischemic vasodilation in the forearm in HF. METHODS AND RESULTS: Forearm blood flow was measured by a strain-gauge plethysmograph in 20 patients with HF and in 24 age-matched control subjects (C). Resting forearm vascular resistance (FVR) was significantly higher in HF than in C (37 +/- 4 versus 22 +/- 2 U, P < .01). Intra-arterial infusions of ACh or sodium nitroprusside (SNP) at graded doses progressively decreased FVR in HF as well as in C. The magnitude of ACh-induced vasodilation was attenuated in HF (P < .01), whereas SNP-induced vasodilation was similar between the two groups. The minimal FVR during reactive hyperemia after 10 minutes of arterial occlusion was significantly higher in HF (n = 12) than in C (n = 12) (3.2 +/- 0.4 versus 2.1 +/- 0.1 U, P < .05). L-Arginine significantly augmented maximal vasodilation evoked with ACh and decreased minimal FVR during reactive hyperemia in HF (P < .01) but not in C. L-Arginine did not affect SNP-induced vasodilation in HF or C. CONCLUSIONS: Our results suggest that defective endothelial function may contribute to impaired ischemic vasodilator capacity in HF.

Acetylcholine↗
PubMed1994

Characterization of ATP-induced vasodilation in the human forearm vascular bed.

BACKGROUND: Animal data indicate that ATP derived from aggregating thrombocytes or endothelium induces an endothelium-dependent vasodilator response that is mediated by P2y-purinergic receptors and is reduced when high dosages are administered. This reduced vasodilator response to high ATP doses has been associated with the concomitant release of endothelium-derived contracting factors. In contrast to the endothelium-dependent vasodilator response, ATP as released from sympathetic nerve endings induces a P2x-purinergic receptor-mediated vasoconstrictor response that may contribute to the attenuated vasodilator response to high dosages of luminally applied ATP. The dual action of ATP might be important in the pathophysiology of disease states characterized by an impaired endothelial function and increased thrombocyte aggregation. This study was performed to characterize the vascular response to ATP in humans. METHODS AND RESULTS: The brachial artery was cannulated in 50 healthy male volunteers (age, 18 to 44 years) for drug infusion and measurement of mean arterial pressure. Forearm blood flow was recorded by venous occlusion strain-gauge plethysmography. ATP induced a dose-dependent vasodilator response that was significantly higher than the effect of equimolar adenosine infusion and that was not reduced by concomitant infusion of the P1-purinergic receptor antagonist theophylline. The infusion of the NO synthase antagonist NG-monomethyl-L-arginine (L-NMMA) reduced the average fall in forearm vascular resistance (FVR) to acetylcholine (-59 +/- 6% [mean +/- SEM] versus -42 +/- 8%; P < .05; N = 10) but did not affect the vasodilator response to ATP (-68 +/- 3% versus -64 +/- 6%; P > .1; N = 10) or sodium nitroprusside (SNP; -53 +/- 3% versus -49 +/- 4%; P > .01; N = 6). The L-NMMA-induced increase in FVR appeared to be related to the type of vasodilator pretreatment, being 94.7 +/- 16.7%, 44.9 +/- 8.7%, and 40.8 +/- 7.3% for acetylcholine, ATP, and SNP pretreatment, respectively (P < .01 for acetylcholine versus ATP and SNP; P > .1 for ATP versus SNP). In contrast to animal data, high dosages of intra-arterially infused ATP (up to 1000 micrograms.100 mL forearm-1.min-1) did not reveal a reduction in the forearm vasodilator response but appeared to be similar to the maximal forearm vasodilation as observed during postocclusive reactive hyperemia. CONCLUSIONS: These observations indicate that ATP induces a potent dose-dependent vasodilator response that is not mediated by P1-purinergic receptor stimulation or by the release of nitric oxide. Moreover, in healthy volunteers, the vasodilator response to high intra-arterial dosages of ATP is not reduced by the release of endothelium-derived contracting factors or by the stimulation of P2x-purinergic receptors on the smooth muscle cells.

Adenosine Triphosphate↗
PubMed1994

Role of nitric oxide in reactive hyperemia in human forearm vessels.

BACKGROUND: The role of nitric oxide (NO) in reactive hyperemia (RH) is not well known. We investigated whether NO plays a role in RH in human forearm vessels by examining the effects of NG-monomethyl-L-arginine (L-NMMA), a blocker of NO synthesis, on reactive hyperemic flow. METHODS AND RESULTS: Forearm blood flow (FBF) was measured by strain-gauge plethysmography with a venous occlusion technique. The left brachial artery was cannulated for drug infusion and direct measurement of arterial pressure. To produce RH, blood flow to the forearm was prevented by inflation of a cuff on the upper arm to suprasystolic pressure for intervals of 3 and 10 minutes. After the release of arterial occlusion (AO), FBF was measured every 15 seconds for 3 minutes. Resting FBF was 4.3 +/- 0.3 mL.min-1.100 mL-1 before 3 minutes of AO and 4.1 +/- 0.6 mL.min-1.100 mL-1 before 10 minutes of AO. FBF increased to 32.3 +/- 1.9 and 38.2 +/- 3.1 mL.min-1.100 mL-1 immediately after 3 and 10 minutes of AO, respectively, and gradually decayed (n = 13). Intra-arterial infusion of L-NMMA (4 mumol/min for 5 minutes) decreased baseline FBF (P < .01) without changes in arterial pressure. L-NMMA did not affect the peak reactive hyperemic FBF after 3 and 10 minutes of AO. L-NMMA significantly decreased total reactive hyperemic flow (flow debt repayment) by 20% to 30% after 3 and 10 minutes of AO. Simultaneous infusion of L-arginine (a precursor of NO) with L-NMMA reversed the effects of L-NMMA. CONCLUSIONS: Our results suggest that NO plays a minimal role in vasodilation at peak RH but plays a modest yet significant role in maintaining vasodilation after peak vasodilation. Our results also suggest that reactive hyperemia in human forearms is caused largely by mechanisms other than NO.

Adult↗
PubMed1997

Vitamin C improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia.

BACKGROUND: Endothelium-dependent vasodilation is impaired in humans with hypercholesterolemia. Oxidative degradation of endothelium-derived nitric oxide plays a major role in endothelial dysfunction in animal models of hypercholesterolemia. To assess whether this mechanism is relevant to humans, we studied the effect of vitamin C, an antioxidant, on vasodilator function in forearm resistance vessels of patients with hypercholesterolemia. METHODS AND RESULTS: We studied 11 hypercholesterolemic and 12 healthy control subjects. Forearm blood flow was determined by venous occlusion plethysmography. Endothelium-dependent vasodilation was assessed by intra-arterial infusion of methacholine (0.3 to 10 micrograms/min). Endothelium-independent vasodilation was measured by intra-arterial infusion of nitroprusside (0.3 to 10 micrograms/min) and verapamil (10 to 300 micrograms/min). Forearm blood flow dose-response curves were determined for each drug before and during coadministration of vitamin C (24 mg/min). In hypercholesterolemic subjects, endothelium-dependent vasodilation to methacholine was augmented by coinfusion of vitamin C (P = .001); in contrast, endothelium-independent vasodilation to nitroprusside and verapamil were not affected by coinfusion of vitamin C (P = .8 and P = .3, respectively). In control subjects, vitamin C administration did not alter endothelium-dependent vasodilation (P = .2). CONCLUSIONS: We conclude that vitamin C improves endothelium-dependent vasodilation in the forearm resistance vessels of patients with hypercholesterolemia. These findings suggest that nitric oxide degradation by oxygen-derived free radicals contributes to abnormal vascular reactivity in hypercholesterolemic humans.

Adult↗
PubMed2003

Smoking activates rho-kinase in smooth muscle cells of forearm vasculature in humans.

Previous studies have shown that smoking is strongly associated with atherosclerosis and coronary vascular disease. Rho-kinase plays an important role in various cellular functions associated with atherosclerosis and hypertension. However, there is no information on the relationship between smoking and Rho-kinase activity in humans. The purpose of this study was to determine the Rho-kinase activity in forearm vascular smooth muscle cells (VSMCs) in healthy young male smokers. We evaluated the forearm blood flow (FBF) responses to fasudil (3, 10, and 30 microg/min for 5 minutes), a Rho-kinase inhibitor, or sodium nitroprusside (0.75, 1.5, and 3.0 microg/min for 5 minutes) in current smokers (n=8) and nonsmokers (n=8). FBF was measured with a strain-gauge plethysmograph. The vasodilatory effect of fasudil was significantly greater in smokers than in nonsmokers (14.9+/-3.5 versus 10.5+/-3.6 mL/min per 100 mL tissue; P<0.01). The FBF responses to sodium nitroprusside were similar in the 2 groups (34.7+/-10.4 versus 33.2+/-10.2 mL/min per 100 mL tissue; P=0.78). These findings suggest that smoking activates Rho-kinase in forearm VSMCs but does not alter the vasodilatory effect induced by exogenous nitric oxide in forearm VSMCs in healthy young men.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2003

Role of endothelium-derived hyperpolarizing factor in human forearm circulation.

Endothelium-derived hyperpolarizing factor (EDHF) contributes to endothelium-dependent relaxation of isolated arteries, but it is not known whether this also occurs in the case of humans in vivo. The present study examined the role of EDHF in human forearm circulation. Forearm blood flow (FBF) was measured by strain-gauge plethysmography in 31 healthy, normal subjects (mean+/-SE age, 23+/-2 years; 24 men and 7 women). After oral administration of aspirin (486 mg), we infused NG-monomethyl-L-arginine (8 micromol/min for 5 minutes) into the brachial artery. We used tetraethylammonium chloride (TEA, 1 mg/min for 20 minutes), a KCa channel blocker, as an EDHF inhibitor, and nicorandil as a direct K+ channel opener. TEA significantly reduced FBF (P<0.05) but did not change systemic arterial blood pressure. Furthermore, TEA significantly inhibited the FBF increase in response to substance P (0.8, 1.6, 3.2, and 6.4 ng/min, n=8) and bradykinin (12.5, 25, 50, and 100 ng/min, n=8; both P<0.001), whereas it did not affect the FBF increase in response to acetylcholine (4, 8, 16, and 32 microg/min, n=8), sodium nitroprusside (0.4, 0.8, 1.6, and 3.2 microg/min, n=8), or nicorandil (0.128, 0.256, 0.512, and 1.024 mg/min, n=8). These results suggest that EDHF contributes substantially to basal forearm vascular resistance, as well as to forearm vasodilatation evoked by substance P and bradykinin in humans in vivo.

Acetylcholine↗
PubMed1993

Salt loads attenuate potassium-induced vasodilation of forearm vasculature in humans.

To evaluate the role of the sodium pump in resistance control in vivo, we studied vascular responses to potassium, which produces vasodilation by the activation of vascular Na+, K(+)-ATPase, in normotensive volunteers receiving a high salt diet compared with volume-depleted subjects receiving diuretic treatment. Forearm blood flow was measured by strain-gauge plethysmography during small increments in local concentrations of potassium with intrabrachial arterial infusions of KCl. Infusions of 0.12 and 0.24 mEq/min KCl increased forearm blood flow and decreased forearm vascular resistance in a dose-dependent fashion. But the simultaneous intrabrachial arterial infusion of 2 micrograms/min ouabain, a Na+,K(+)-ATPase inhibitor, could blunt the decremental response of vascular resistance to 0.12 mEq/min KCl. The decrements of vascular resistance with KCl infusions divided by the initial resistance were significantly less with ouabain compared with those without ouabain (43 +/- 4% versus 57 +/- 3%, p < 0.01). This suggests that potassium produces vasodilation by the activation of vascular Na+,K(+)-ATPase activity. Similarly, salt loading (180 mEq NaCl for 7 days) after treatment with diuretics could attenuate percent decrements of resistance with KCl infusions (39 +/- 3% versus 53 +/- 2%, p < 0.01), whereas vascular resistance responses to sodium nitroprusside, a nonspecific vasodilator, and to verapamil, a calcium antagonist, did not change with salt loading after volume depletion. Therefore, salt loading could attenuate forearm vascular response to potassium specifically, as did the administration of ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Tachyphylaxis of human forearm vascular responses does not occur rapidly after exposure to isoproterenol.

In vitro and limited in vivo data suggest that rapid desensitization of beta-adrenoceptor responses occurs after exposure to agonist. Tachyphylaxis to a beta-adrenoceptor agonist would represent a potentially important mechanism for the short-term regulation of vascular tone. The effects of a 4-hour infusion of 400 ng/min intra-arterial isoproterenol on forearm blood flow and presynaptic beta-adrenoceptor-mediated norepinephrine release were determined in eight healthy volunteers. Intra-arterial isoproterenol at 400 ng/min resulted in a significant increase in forearm blood flow in all eight subjects at all time points, with no evidence of tachyphylaxis. In fact, forearm blood flow after 4 hours of the isoproterenol infusion (22.8 +/- 3.3 mL/100 mL per minute) was significantly greater than after 7 minutes (14.6 +/- 2.8 mL/100 mL per minute), 15 minutes (15.4 +/- 2.4 mL/100 mL per minute), and 30 minutes (17.4 +/- 3.0 mL/100 mL per minute) of the infusion (P < .05). Similarly, presynaptic beta-adrenoceptor responses showed no evidence of tachyphylaxis, so forearm norepinephrine spillover values after 7 minutes (6.6 +/- 0.94 ng/min), 15 minutes (7.6 +/- 1.5 ng/min), and 4 hours (8.8 +/- 1.1 ng/min) of isoproterenol infusion were increased and similar. Minimal systemic effects were observed, and there was no evidence of tolerance, there being no difference in heart rate after 7 minutes (70.7 +/- 2.7 beats per minute) and 4 hours (72.2 +/- 3.6 beats per minute) of isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Angiotensin mediates forearm glucose uptake by hemodynamic rather than direct effects.

Insulin sensitivity may be improved with the angiotensin-converting enzyme inhibitor captopril, suggesting that inhibition of angiotensin II (Ang II) improves insulin resistance. However, the administration of systemic Ang II has also been associated with an improvement in rather than worsening of glucose utilization. Since both stimulating and antagonizing the renin-angiotensin system improve glucose uptake and both angiotensin-converting enzyme inhibitors and intravenous Ang II elicit skeletal muscle vasodilation, it is conceivable that hemodynamic factors rather than a direct effect of either Ang II or angiotensin-converting enzyme inhibitors on skeletal muscle metabolism modulate the increase in glucose utilization. The direct effects of Ang II on glucose extraction in intact human skeletal muscle have not been previously described. We investigated the effects of local infusion of Ang II on glucose uptake in the forearm of 20 healthy subjects. With the use of the isolated insulin-perfused forearm model, local plasma insulin values were raised to 100 mU/mL over fasting values and maintained there for a 90-minute infusion period. After the first 60 minutes of insulin alone, Ang II was infused into the brachial artery for the last 30 minutes. Intra-arterial Ang II infusion caused a 38% decrease in forearm blood flow (P <.05) and 59% increase in the arteriovenous glucose gradients (P <.05) to maintain a steady glucose utilization (a decrease of 4%, P=NS). Thus, local Ang II infusion does not impair insulin-stimulated glucose utilization. Furthermore, glucose extraction increases to compensate for the decrease in forearm blood flow (as the Fick principle would predict for freely diffusible substances). We conclude that the described increase in glucose utilization from systemic infusion of Ang II and during angiotensin-converting enzyme inhibitor treatment is mediated by hemodynamic factors rather than a direct effect of Ang II on skeletal muscle metabolism.

Adult↗
PubMedDate not supplied

Augmentation of cardiopulmonary baroreflex control of forearm vascular resistance in borderline hypertension.

Arterial baroreflex control of heart rate is impaired in young men with borderline or mild hypertension. Despite this impairment, these subjects often have exaggerated increases in vascular resistance during orthostatic stress. We considered the possibility that this exaggerated reflex vasoconstriction might reflect augmented cardiopulmonary baroreflex control of vascular resistance in borderline hypertension (BHT). Accordingly, we studied cardiopulmonary baroreflex control of forearm vascular resistance in nine BHT men with blood pressure intermittently above 150/90 mm Hg and in seven normotensive (NT) men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP-5 to-20 mm HG), which decreases cardiac filling pressures. Baseline mean arterial pressure was 99 /+- 3 mm Hg (mean /+- SE) in BHT vs 83 /+- 2 mm Hg in NT (p less than 0.05). Baseline forearm resistance was also higher in BHT than in NT: 19 /+- 2 vs 13 /+-1 mm Hg/ml/min/100 ml or units (p less than 0.05). Reflex increases in forearm resistance during LBNP were greater (p less than 0.05) in BHT than in NT 8.6 /+- 1.7 vs 4.5 /+- 1.1 units during LBNP-20). Increases in arterial pressure and forearm resistance during a cold pressor test were not significantly different in the two groups. Thus, the augmented response to LBNP could not be attributed to a nonspecific influence of increased baseline resistance or a generalized abnormality in reflex control. In summary, the results of this study suggest that there is augmentation of the tonic inhibitory influence of cardiopulmonary baroreceptors in humans with BHT.

Adult↗
PubMed1982

Limited maximal vasodilator capacity of forearm resistance vessels in normotensive young men with a familial predisposition to hypertension.

The study was performed to determine whether there is a structural vascular abnormality in normotensive subjects with hypertensive relatives. We examined maximal vasodilator capacity of forearm resistance vessels in 23 normotensive young men (mean blood pressure 94 +/- 0.4 mm Hg, mean +/- SE) with hypertensive relatives (age 24 +/- 0.1 years) and in 17 normotensive subjects (mean blood pressure 85 +/- 0.4 mm Hg) with no family history of hypertension (age 24 +/- 0.1 years). Maximal vasodilator capacity was examined by measuring minimal vascular resistance during peak reactive hyperemia after release from 10 minutes of arterial occlusion. Minimal forearm vascular resistance after release from 10 minutes of arterial occlusion was 25% higher (P less than 0.02) in subjects with hypertensive relatives (2.0 +/- 0.02 units) than that in subjects with no family history (1.5 +/- 0.01) units. We confirmed the previous findings that increasing metabolic vasodilator stimulus by performing intermittent handgrip exercise during 10 minutes of arterial occlusion did not augment peak dilation. This suggests that 10 minutes of arterial occlusion produced maximal vasodilation. Forearm vascular responses to ice on the forehead was greater in subjects with hypertensive relatives than those in subjects with no family history. These results suggest that there may be a structural abnormality in the forearm resistance vessels in normotensive subjects with family history of hypertension.

Adult↗
PubMed1997

Cardiopulmonary and arterial baroreflex-mediated control of forearm vasomotor tone is impaired after acute stroke.

BACKGROUND AND PURPOSE: Elevated blood pressure (BP) levels are well recognized after acute stroke and are associated with increased BP variability. The underlying mechanisms producing such changes are unclear but may include abnormalities of baroreceptor-mediated control of heart rate and vasomotor tone. Lower body negative pressure (LBNP) can be used to assess the integrity of "low-pressure" cardiopulmonary and "high-pressure" arterial baroreceptor-derived responses by inducing nonhypotensive and hypotensive stimuli. METHODS: Cardiovascular responses, including BP, heart rate, forearm blood flow, and forearm vascular resistance, to nonhypotensive and hypotensive LBNP were assessed in 13 consecutive stroke patients. Patients were studied within 72 hours of stroke (acute) and again at 10 to 14 days (subacute) and were compared with 13 control subjects individually matched for age, sex, and BP. RESULTS: At an LBNP of -10 mm Hg, BP was unchanged in all groups, but a significant increase in forearm vascular resistance occurred only in the control group (11 U [interquartile range, 7 to 15]; P < .05) compared with stroke patients in the acute (9 U [3 to 14]; P = NS) or subacute phases (7 U [2 to 12]; P = NS). After LBNP at -40 mm Hg, the reductions in systolic BP levels were similar in all groups (control: -9 mm Hg [-16 to -3]; acute stroke: -9 mm Hg [-22 to 3]; subacute stroke: -7 mm Hg [-35 to 20]), as was the associated increase in heart rate (control: 8 bpm ([4 to 11]; acute stroke: 6 bpm ([1 to 12]; subacute stroke: 9 bpm [2 to 19]). However, forearm vascular resistance increased significantly only in control subjects (20 U [9 to 30]; P < .01). CONCLUSIONS: The present study has identified abnormal vasomotor responses to LBNP after acute stroke, with an increase in FVR only being observed in control subjects in response to nonhypotensive and similar hypotensive levels of LBNP. In acute stroke patients, the stimulus of hypotensive LBNP appears to be compensated by an increase in cardiac output since there appears to be no increase in peripheral vascular resistance, unlike the changes seen in control subjects. However, the exact mechanisms for these changes are still unclear and are the subject of further study.

Acute Disease↗