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Biomedical subjects

Niki M Dietz

Publications and source records attributed to Niki M Dietz.

15 recordsLinked to original sources
PubMed2006

Excessive heart rate response to orthostatic stress in postural tachycardia syndrome is not caused by anxiety.

Postural tachycardia syndrome (POTS) is characterized by excessive increases in heart rate (HR) without hypotension during orthostasis. The relationship between the tachycardia and anxiety is uncertain. Therefore, we tested whether the HR response to orthostatic stress in POTS is primarily related to psychological factors. POTS patients (n = 14) and healthy controls (n = 10) underwent graded venous pooling with lower body negative pressure (LBNP) to -40 mmHg while wearing deflated antishock trousers. "Sham" venous pooling was performed by 1) trouser inflation to 5 mmHg during LBNP and 2) vacuum pump activation without LBNP. HR responses to mental stress were also measured in both groups, and a questionnaire was used to measure psychological parameters. During LBNP, HR in POTS patients increased 39 +/- 5 beats/min vs. 19 +/- 3 beats/min in control subjects at -40 mmHg (P < 0.01). LBNP with trouser inflation markedly blunted the HR responses in the patients (9 +/- 2 beats/min) and controls (2 +/- 1 beats/min), and there was no HR increase during vacuum application without LBNP in either group. HR responses during mental stress were not different in the patients and controls (18 +/- 2 vs. 19 +/- 1 beats/min; P > 0.6). Anxiety, somatic vigilance, and catastrophic cognitions were significantly higher in the patients (P < 0.05), but they were not related to the HR responses during LBNP or mental stress (P > 0.1). These results suggest that the HR response to orthostatic stress in POTS patients is not caused by anxiety but that it is a physiological response that maintains arterial pressure during venous pooling.

Adult↗
PubMed2006

Effects of combined inhibition of ATP-sensitive potassium channels, nitric oxide, and prostaglandins on hyperemia during moderate exercise.

ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg.dl(-1).min(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals.

Adenosine Triphosphate↗
PubMed2006

Influence of beta2-adrenergic receptor genotype on airway function during exercise in healthy adults.

BACKGROUND: In humans, beta(2)-adrenergic receptors (beta(2)ARs) influence airway tone. There are known functional polymorphisms of the beta(2)AR, such as substitution of glycine for arginine at codon 16. We sought to determine if this variation in genotype differentially influences airway function during exercise. METHODS: Healthy subjects without asthma who were either homozygous for Arg16 (n = 16; mean age, 29 +/- 2 years [+/- SD]; mean maximum oxygen uptake [Vo(2)], 32 +/- 2 mL/kg/min) or the Gly16 allele (n = 26; mean age, 30 +/- 1 years; mean maximum Vo(2), 33 +/- 1 mL/kg/min) participated in the study. Baseline testing included spirometry and maximal symptom-limited exercise. On a separate day, an arterial cannula was placed to measure catecholamine levels. Subjects then performed exercise at two work levels (40% and 75% of peak work) for 9 min each and performed spirometry at 3-min intervals for assessment of airway function. RESULTS: There were no statistically significant differences between groups in maximum Vo(2) or baseline spirometry (p > 0.05). With both light and heavy exercise, the groups had similar increases in the forced expiratory flow at 50% of vital capacity (FEF(50)). FEF(50) increased by 14 +/- 4% and 15 +/- 3% in arginine and glycine groups, respectively, by end exercise (p > 0.05). During recovery (5 min and 10 min after), the Gly16 homozygotes demonstrated persistent bronchodilation (10 min after FEF(50) = + 7 +/- 2% over pre-exercise) while the Arg16 subjects had a rapid return to baseline (10 min after FEF(50) = - 3 +/- 3%, p = 0.007 between groups). No differences were observed in the catecholamine responses between genotypes, although the increase in epinephrine in the arginine group tended to be higher (p = 0.07). CONCLUSIONS: These data suggest that the Arg16Gly polymorphism of the beta(2)AR does not influence airway function during short-duration low- and high-intensity exercise. However, during recovery, the Arg16 genotype is associated with a reduced bronchodilation, possibly due to increased catecholamine desensitization.

Adult↗
PubMed2005

Arg16Gly polymorphism of the beta2-adrenergic receptor is associated with differences in cardiovascular function at rest and during exercise in humans.

In humans, subjects homozygous for arginine (ArgArg) at codon 16 of the beta2-adrenergic receptor (beta2AR) have been shown to have greater agonist-mediated desensitization than subjects homozygous for glycine (GlyGly). We sought to determine if this substitution differentially influenced cardiovascular function during short duration (9 min) low and high intensity exercise (40 and 75% of peak work). Healthy Caucasian ArgArg (n = 16), GlyGly (n = 31) and ArgGly (n = 17) subjects matched for age, sex and peak oxygen uptake were studied. There were no differences in adrenaline (ADR) at rest or with heavy exercise, but the ArgArg group had lower ADR with light exercise (P = 0.04). Resting heart rate (HR) was higher in ArgArg (P < 0.01), while cardiac output (Q), stroke volume (SV), and mean arterial pressure (MAP) were lower than the other groups (HR = 86+/-2, 78+/-2, 80+/-1 beats min(-1); Q = 5.7+/-0.81, 6.1+/-0.18, 6.7+/-0.22 l min(-1); SV = 68+/-3, 82+/-3, 89+/-4 ml beat(-1); MAP = 92+/-1, 103+/-2, 98+/-1 mmHg-- for ArgArg, ArgGly and GlyGly, respectively, means +/-s.e.m., P < 0.01), however, no differences were observed in systemic vascular resistance (SVR). With low intensity exercise and high intensity exercise the ArgArg group continued to have a lower , SV and MAP compared to the other groups (P < 0.05), with no differences observed in SVR. During recovery, the ArgArg subjects continued to have a lower MAP but there were no differences in HR, , or SVR. These data suggest that subjects homozygous for Arg at codon 16 of the beta2AR have reduced and MAP at rest that persist during exercise with no evidence for differential changes over the course of exercise despite large changes in catecholamines. This may suggest possible genotype-related differences in baseline receptor function or density which causes phenotypic differences at rest that are sustained during short-term exercise.

Adult↗
PubMed2005

Arg16/Gly beta2-adrenergic receptor polymorphism alters the cardiac output response to isometric exercise.

Normotensive adults homozygous for glycine (Gly) of the Arg16/Gly beta2-adrenergic-receptor polymorphism have 1) greater forearm beta2-receptor mediated vasodilation and 2) a higher heart rate (HR) response to isometric handgrip than arginine (Arg) homozygotes. To test the hypothesis that the higher HR response in Gly16 subjects serves to maintain the pressor response [increased cardiac output (CO)] in the setting of augmented peripheral vasodilation to endogenous catecholamines, we measured continuous HR (ECG), arterial pressure (Finapres), and CO (transthoracic echocardiography) during isometric, 40% submaximal handgrip to fatigue in healthy subjects homozygous for Gly (n = 30; mean age +/- SE: 30 +/- 1.2, 13 women) and Arg (n = 17, age 30 +/- 1.6, 11 women). Resting data were similar between groups. Handgrip produced similar increases in arterial pressure and venous norepinephrine and epinephrine concentrations; however, HR increased more in the Gly group (60.1 +/- 4.3% increase from baseline vs. 45.5 +/- 3.9%, P = 0.03), and this caused CO to be higher (Gly: 7.6 +/- 0.3 l/m vs. Arg: 6.5 +/- 0.3 l/m, P = 0.03), whereas the decrease in systemic vascular resistance in the Gly group did not reach significance (P = 0.09). We conclude that Gly16 homozygotes generate a higher CO to maintain the pressor response to handgrip. The influence of polymorphic variants in the beta2-adrenergic receptor gene on the cardiovascular response to sympathoexcitation may have important implications in the development of hypertension and heart failure.

Adult↗
PubMed2005

A restrospective perspective.

Venous occlusion plethysmography is a simple but elegant technique that has contributed to almost every major area of vascular biology in humans. The general principles of plethysmography were appreciated by the late 1800s, and the application of these principles to measure limb blood flow occurred in the early 1900s. Plethysmography has been instrumental in studying the role of the autonomic nervous system in regulating limb blood flow in humans and important in studying the vasodilator responses to exercise, reactive hyperemia, body heating, and mental stress. It has also been the technique of choice to study how human blood vessels respond to a variety of exogenously administered vasodilators and vasoconstrictors, especially those that act on various autonomic and adrenergic receptors. In recent years, plethysmography has been exploited to study the role of the vascular endothelium in health and disease. Venous occlusion plethysmography is likely to continue to play an important role as investigators seek to understand the physiological significance of newly identified vasoactive factors and how genetic polymorphisms affect the cardiovascular system in humans.

Cardiovascular Diseases↗
PubMed2005

A comparison of peripheral skin blood flow and temperature during endoscopic thoracic sympathotomy.

The assessment of sympathetic denervation to the upper extremities during surgery for hyperhidrosis is essential in predicting postoperative outcome, particularly for endoscopic thoracic chain sympathotomy, a recently described, minimally destructive technique that minimizes postoperative compensatory hyperhidrosis. To test the hypothesis that skin blood flow (SkBF; laser Doppler flowmetry) provides a faster and more reliable indication of denervation than temperature (temp), we prospectively compared palmar SkBF and fingertip temp in 10 patients undergoing endoscopic thoracic chain sympathotomy for essential hyperhidrosis. From baseline to peak values, palmar SkBF (mean +/- SEM) increased 273.3 +/- 24.7 arbitrary units and 252.4 +/- 30.1 arbitrary units, whereas temp increased 0.9 degrees C +/- 0.3 degrees C and 1.5 degrees C +/- 0.6 degrees C on the right and left, respectively. Upon effective sympathotomy of the right thoracic chain, the time to peak SkBF was 43 +/- 13 s, whereas the time to peak temp was 277 +/- 53 s (P <0.001). On the left, the time to peak SkBF was 81 +/- 14 s, and time to peak temp was 305 +/- 34 s (P <0.001). All patients considered the sympathotomy successful. We conclude that laser Doppler SkBF is superior to temp in temporal resolution for assessment of denervation during sympathotomy and that it provides a superior qualitative and quantitative adjunct to monitoring denervation.

Adolescent↗
PubMed2004

Agonist-dependent variablity of contributions of nitric oxide and prostaglandins in human skeletal muscle.

The relative contributions of endothelium-dependent dilators [nitric oxide (NO), prostaglandins (PGs), and endothelium-derived hyperpolarizing factor (EDHF)] in human limbs are poorly understood. We tested the hypothesis that relative contributions of NO and PGs differ between endothelial agonists acetylcholine (ACh; 1, 2, and 4 microg.dl(-1).min(-1)) and bradykinin (BK; 6.25, 25, and 50 ng.dl(-1).min(-1)). We measured forearm blood flow (FBF) using venous occlusion plethysmography in 50 healthy volunteers (27 +/- 1 yr) in response to brachial artery infusion of ACh or BK in the absence and presence of inhibitors of NO synthase [NOS; with NG-monomethyl-L-arginine (L-NMMA)] and cyclooxygenase (COX; with ketorolac). Furthermore, we tested the idea that the NOS + COX-independent dilation (in the presence of L-NMMA + ketorolac, presumably EDHF) could be inhibited by exogenous NO administration, as reported in animal studies. FBF increased approximately 10-fold in the ACh control; L-NMMA reduced baseline FBF and ACh dilation, whereas addition of ketorolac had no further effect. Ketorolac alone did not alter ACh dilation, but addition of L-NMMA reduced ACh dilation significantly. For BK infusion, FBF increased approximately 10-fold in the control condition; L-NMMA tended to reduce BK dilation (P < 0.1), and addition of ketorolac significantly reduced BK dilation. Similar to ACh, ketorolac alone did not alter BK dilation, but addition of L-NMMA reduced BK dilation. To test the idea that NO can inhibit the NOS + COX-independent portion of dilation, we infused a dose of sodium nitroprusside (NO-clamp technique) during ACh or BK that restored the reduction in baseline blood flow due to L-NMMA. Regardless of treatment order, the NO clamp restored baseline FBF but did not reduce the NOS + COX-independent dilation to ACh or BK. We conclude that the contribution of NO and PGs differs between ACh and BK, with ACh being more dependent on NO and BK being mostly dependent on a NOS + COX-independent mechanism (EDHF) in healthy young adults. The NOS + COX-independent dilation does not appear sensitive to feedback inhibition from NO in the human forearm.

Acetylcholine↗
PubMed2004

Is physician anesthesia cost-effective?

UNLABELLED: One of the most controversial issues in anesthesia is whether nonmedically directed nurse anesthetists are relatively more cost-effective than anesthesiologists in the provision of anesthesia care. We electronically surveyed anesthesia practices throughout the United States to estimate the range in anesthesia professional costs from the payer perspective. Using this survey data on anesthesia reimbursement and published outcomes studies, we developed an ad hoc model to estimate the cost-effectiveness of physician-directed anesthesia relative to a nonmedically directed nurse anesthetist model of care from the payer perspective. Cost-effectiveness ratios were defined as the ratio of incremental costs associated with physician anesthesia relative to the estimated incremental life expectancy gains with this model of care (i.e., dollars per year of life saved [US dollars /YLS]). Reference case results suggest that physician anesthesia is cost saving with an estimated incremental cost-effectiveness ratio of -US dollars 2601/YLS for a younger privately insured patient and an estimated cost-effectiveness ratio of -US dollars 4410/YLS for an elderly Medicare insured patient. Cost-effectiveness ratios ranged from -US dollars 4410 to US dollars 38778/YLS in univariate and multivariate sensitivity analyses across payer types. Results were most sensitive to assumed differences in reimbursement (commercial conversion factors) and to mortality rate assumptions by provider type. This analysis offers economic evidence in support of the physician anesthesia model of care. IMPLICATIONS: Recent outcome studies suggest improved patient outcomes when physicians medically direct nurse anesthetists versus anesthesia care delivered with nonmedically directed nurses. The relative cost-effectiveness of this practice model is, however, unknown. This economic analysis suggests that outcome gains with physician anesthesia may be obtained at cost savings or, under conservative assumptions, at a cost deemed reasonable by society.

Age Factors↗
PubMed2003

Alpha-adrenergic vascular responsiveness during postexercise hypotension in humans.

In sedentary individuals, postexercise hypotension following a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. We tested the hypothesis that alpha-adrenergic responsiveness in the forearm and leg vasculatures is blunted during postexercise hypotension. We studied 12 men and two women before and 30 min after a 60 min bout of cycling at 60 % VO2,peak. In the first five subjects, arterial pressure (brachial artery catheter) and forearm blood flow (plethysmography) were measured and vascular conductance was calculated during intraarterial infusions of the alpha1-agonist phenylephrine and the alpha2-agonist clonidine. Exercise reduced mean arterial pressure (89 +/- 2 vs. 95 +/- 2 mmHg, P < 0.05) and increased forearm vascular conductance 77 +/- 33 % (P < 0.05). Despite these changes in baseline vascular conductance, vasoconstrictor responses in the forearm to phenylephrine and clonidine were similar (or enhanced) postexercise vs. preexercise. In the remaining nine subjects, arterial pressure (femoral artery catheter) and leg blood flow (Doppler ultrasound of the femoral artery) were measured and vascular conductance was calculated during intraarterial infusions of phenylephrine and clonidine. Exercise reduced mean arterial pressure (80 +/- 2 vs. 89 +/- 2 mmHg, P < 0.05) and increased leg vascular conductance 94 +/- 16 % (P < 0.05). Despite these changes in baseline vascular conductance, vasoconstrictor responses in the leg to phenylephrine and clonidine were similar (or enhanced) postexercise vs. preexercise. These results suggest that vascular responsiveness to alpha-adrenergic agonists is maintained during postexercise hypotension in humans. Thus, while postexercise hypotension is associated with increased vascular conductance in the forearm and leg, it does not appear that blunting of alpha-adrenergic responsiveness is the cause.

Adrenergic alpha-Agonists↗
PubMed2003

Beta(2)-adrenergic receptor polymorphism and nitric oxide-dependent forearm blood flow responses to isoproterenol in humans.

Polymorphisms in the gene encoding the beta(2)-adrenoceptor have been associated with interindividual differences in blood pressure and the diagnosis of hypertension. A common polymorphism resulting in a change from arginine to glycine at amino acid 16 (Arg16-->Gly) enhances agonist-promoted downregulation of receptor expression in vitro. It is unknown whether genotype-dependent differences in nitric oxide generation contribute to differences in vasodilator responses to beta(2)-agonists in vivo. To address this question, venous occlusion plethysmography was used to measure forearm blood flow responses to graded brachial artery infusions of the beta-agonist isoproterenol in 41 healthy normotensive Caucasian adults (mean age (+/- S.D.) = 29 +/- 6 years), who were either Arg16 (n = 18) or Gly16 (n = 23) homozygotes. Compared to Arg16 homozygotes, Gly16 homozygotes demonstrated significantly greater blood flow responses to isoproterenol (P = 0.02). After inhibition of nitric oxide synthase by N(gamma)-monomethyl-L-arginine, blood flow responses did not differ significantly between genotype groups (P = 0.27). Consequently, effects of the Arg16 Gly polymorphism on forearm blood flow responses to isoproterenol appear to be dependent on differences in endothelial generation of nitric oxide. In contrast to previous reports based on systemic infusions of beta(2)-agonists, our findings indicate that regional blood flow responses to locally infused isoproterenol are significantly greater in Gly16 than in Arg16 homozygotes.

Adrenergic beta-Agonists↗
PubMed2002

Aging and forearm postjunctional alpha-adrenergic vasoconstriction in healthy men.

BACKGROUND: Muscle sympathetic vasoconstrictor nerve activity increases with age in healthy humans but does not result in an augmented forearm vasoconstrictor tone. We tested the hypothesis that this is due to a reduction in postjunctional alpha-adrenergic responsiveness to endogenous norepinephrine (NE) release and determined whether this was specific to alpha1- or alpha2-adrenergic receptors. METHODS AND RESULTS: Forearm blood flow (FBF, by strain-gauge plethysmography) responses to local intra-arterial infusions of tyramine (which evokes endogenous NE release), phenylephrine (selective alpha1-agonist), and clonidine (alpha2-agonist) were determined in 10 young (aged 26+/-1 [mean+/-SEM] years) and 10 older (aged 65+/-1 years) healthy normotensive men after local beta-adrenergic blockade with propranolol. Basal forearm vascular tone was not different in young men and older men. The percentage reduction in FBF in response to the highest dose of tyramine was blunted in older men compared with young men (-37+/-3% versus -49+/-3%, respectively; P<0.01) despite a greater increase in deep venous NE concentration in older men (910+/-103 versus 565+/-69 pg/mL, respectively; P<0.001). Maximal reductions in FBF to phenylephrine were also blunted in older men (-47+/-2% versus -58+/-3% in young men, P<0.05). In contrast, the reductions in FBF (-36+/-7% versus -40+/-3% for older versus young men, respectively) and also in venous NE concentration (-79+/-24 versus -84+/-13 pg/mL for older versus young men, respectively) to clonidine were similar in the 2 groups. Finally, forearm sympathetic alpha-adrenergic vasoconstrictor tone (assessed via nonselective alpha-blockade with phentolamine) was significantly lower in older men. CONCLUSIONS: Our results indicate that human aging is associated with a reduction in forearm postjunctional alpha-adrenergic responsiveness to endogenous NE release and that this might be specific to alpha1-adrenergic receptors. Furthermore, the contribution of sympathetic alpha-adrenergic vasoconstriction to basal forearm vascular tone is reduced with age in healthy men.

Adrenergic Agonists↗
PubMed2002

Post-junctional alpha-adrenoceptors and basal limb vascular tone in healthy men.

Previous studies have demonstrated that post-junctional alpha(1)- and alpha(2)-adrenoceptors mediate vasoconstriction in the human forearm. However, the relative contributions of the alpha-adrenoceptor subtypes to basal limb vascular tone are unknown. In healthy young men, forearm blood flow (FBF; venous occlusion plethysmography) responses to brachial artery administration of prazosin (an alpha(1)-adrenoceptor antagonist), yohimbine (an alpha(2)-adrenoceptor antagonist) and phentolamine (a non-selective alpha-adrenoceptor antagonist) were determined after local beta-adrenoceptor blockade with propranolol. In 10 subjects, prazosin increased FBF from 2.4 +/- 0.3 to 5.8 +/- 1.0 ml (100 ml)(-1) min(-1) (approximately 140 %; P < 0.001 vs. baseline). Subsequently, phentolamine further increased FBF to 11.7 +/- 1.6 ml (100 ml)(-1) min(-1) (approximately 385 %; P < 0.001 vs. baseline). Thus, the average calculated increase in FBF due to removal of alpha(2)-vasoconstrictor tone was greater than that due to removal of alpha(1)-tone (5.9 +/- 0.8 vs. 3.4 +/- 0.8 ml (100 ml)(-1) min(-1); P < 0.01) and represented approximately 63 % of basal sympathetic tone. Complete alpha(1)-adrenoceptor blockade was confirmed by a minimal reduction in FBF in response to phenylephrine after prazosin (46 +/- 3 vs. 6 +/- 4 %; before vs. after blockade) and in a separate group of four subjects, increasing the dose of prazosin threefold did not evoke further forearm vasodilatation. Additionally, the reduction in FBF in response to tryamine (evokes endogenous noradrenaline release) was abolished after phentolamine (40 +/- 3 vs. 2 +/- 1 %; before vs. after blockade), documenting complete pharmacological sympathectomy. In another group of seven subjects, administering yohimbine prior to phentolamine resulted in similar findings. These observations indicate that vasoconstricting post-junctional alpha(2)-adrenoceptors contribute more to basal vascular tone than alpha(1)-adrenoceptors in the forearms of young healthy men. The potential physiological and pathophysiological implications of these findings are discussed.

Adrenergic alpha-Agonists↗
PubMed2002

Effects of chronic sympathectomy on vascular function in the human forearm.

To determine whether endothelial function is altered by chronic surgical sympathectomy, we infused ACh, isoproterenol, nitroprusside (NTP), and the nitric oxide synthase inhibitor NG-mono-methyl-L-arginine (L-NMMA) into the brachial arteries of nine patients 5-64 mo after thoracic sympathectomy for hyperhidrosis. Age- and gender-matched controls were also studied. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. Lower body negative pressure was used to assess reflex vasoconstrictor responses. Tyramine, which acts locally and causes norepinephrine release from sympathetic nerves, was also administered via the brachial artery. FBF at rest was 2.5 +/- 0.4 ml x dl-1 x min-1 in the patients and 2.5 +/- 0.3 ml x dl-1 x min-1 in the controls (P = 0.95). The normal vasoconstrictor responses to lower body negative pressure were abolished in the patients. By contrast, tyramine produced dose-dependent vasoconstriction in the patients that was identical to that of controls. The dose-response curves to ACh were similar in patients and controls, with maximum values of 19.3 +/- 4.4 vs. 25.5 +/- 2.8 ml x dl-1 x min-1, respectively. L-NMMA reduced baseline FBF similarly and reduced the maximal FBF response to ACh in both groups (patients 8.9 +/- 3.5 vs. controls 9.7 +/- 2.5 ml x dl-1 x min-1). The vasodilation to isoproterenol was similar and blunted to the same extent in both groups by L-NMMA. The responses to NTP in patients and controls were similar and not affected by L-NMMA. We conclude that, in humans, chronic surgical sympathectomy does not cause major disruptions in vascular function in the forearm. The normal vasoconstrictor responses to tyramine indicate that there were viable sympathetic nerves in the forearm that were not engaged by LBNP.

Adult↗