Acute hypoxemia leads to activation of the sympathetic nervous system (SNS), yet adrenergic vasoconstriction does not occur and venous plasma norepinephrine (NE) fails to rise as expected. To examine whether this dissociation between SNS tone and plasma NE is due to altered metabolism of NE, we measured arterial NE kinetics ([3H]NE infusion technique) and sympathetic nervous outflow to muscle (peroneal microneurography) during 25-30 min of hypoxemia (spontaneous breathing, mean O2 saturation 74%) in six healthy young men. During hypoxemia, muscle sympathetic nervous activity (MSNA) rose significantly from 12.2 +/- 3.3 to 18.6 +/- 3.5 bursts/min, and the total amplitude increased from 123 +/- 36 to 255 +/- 50 mm/min. NE spillover, an index of NE release at the sympathetic nerve terminals, rose from 1.66 +/- 0.30 to 2.33 +/- 0.40 nmol.min-1.m-2 (P = 0.014). However, NE clearance increased also from 0.99 +/- 0.05 to 1.19 +/- 0.11 l.min-1.m-2 (P = 0.014), and arterial NE rose from 281 +/- 50 to 339 +/- 64 pg/ml (P = 0.023). Hypoxemia resulted in a significant rise in forearm blood flow and a decrease in forearm vascular resistance. The fact that skin blood flow and vascular resistance did not change implies that forearm vasodilation was localized to skeletal muscle. Our results suggest that during acute hypoxemia in humans the SNS is activated but the rise in plasma NE is attenuated because NE clearance is increased.

Adult↗

PubMed1990

Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans.

The total blood flow requirements of a large muscle mass can exceed the maximal cardiac output generated by the heart during exercise. Therefore, to maintain blood pressure, muscle vasodilation must be opposed by sympathetic vasoconstriction. The primary neural signal that increases sympathetic outflow is unclear. In an effort to isolate the vasoconstricting mechanism that opposes vasodilation, we measured the peak forearm vascular conductance response after the release of 10 minutes of forearm circulatory arrest under five separate study conditions: 1) no leg exercise, 2) low-level supine leg exercise, 3) low-level supine leg exercise with leg circulatory arrest after exercise, 4) high-level supine leg exercise, and 5) high-level supine leg exercise with leg circulatory arrest after exercise. We found that both high-workload conditions reduced peak forearm conductance below the no-leg exercise condition (a 34% reduction during leg exercise and a 52% reduction during leg exercise followed by leg circulatory arrest). In addition, at each workload, leg circulatory arrest after exercise, which isolated the skeletal muscle metaboreceptor contribution to vasoconstriction, reduced forearm conductance by approximately 20% below the values noted for leg exercise alone (combined central command and metaboreceptor stimulation). In a separate group of subjects, peak forearm blood flow was measured during lower-body negative pressure to levels up to -40 mm Hg, a maneuver that unloads high- and low-pressure baroreceptors. This intervention did not affect peak forearm blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Muscle acidosis during static exercise is associated with calf vasoconstriction.

In this study we measured (n = 6) the phosphocreatine-to-inorganic phosphate ratio (PCr/Pi), Pi, and pH with 31P-nuclear magnetic resonance (31P-NMR) in the human forearm during static work at 30% of maximal voluntary contraction (MVC) for 2 min followed immediately by 3 min of circulatory arrest (forearm arterial occlusion). Static exercise, with its central volitional and skeletal muscle metabolic and mechanical afferent components, caused a rise in heart rate (HR, 32%), blood pressure (BP, 29%), and calf vascular resistance (calf R, 30%). During forearm occlusion after static exercise, HR returned to base line, the increase in BP was attenuated by 30%, and calf R remained elevated and unchanged. The percent change in calf R was correlated with forearm cellular pH (R = 0.56, P less than 0.001) but only weakly associated with PCr/Pi (R = 0.33, P less than 0.042). 30% MVC for 1 min followed by arterial occlusion (3 min) reduced PCr/Pi by 65% and pH by 0.16 U (P less than 0.05). Calf R was unchanged. Circulatory arrest alone (20 min) caused no change in either pH or calf R but large changes in PCr/Pi (50% reduction). We conclude that 1) there is an association between forearm cellular acidosis and calf vasconstriction during static forearm exercise and 2) large changes in PCr/Pi without concomitant changes in pH are not associated with changes in calf R.

Acidosis↗

PubMed1989

Characteristics of flow-mediated brachial artery vasodilation in human subjects.

In an effort to determine whether arterial conductance vessels dilate in response to increased blood flow stimuli, brachial artery area (cm2) and diameter (cm) were derived by simultaneous measurement of forearm blood flow (ml/min.100 ml) and brachial artery blood flow velocity (cm/sec) following the release of arterial occlusion. Measurements were made at rest and at the time of maximal flow after the release of graded periods of forearm arterial occlusion (20 seconds to 10 minutes). These studies showed a graded large vessel dilation following occlusions of up to 1 minute (baseline diameter, 0.33 +/- 0.01; after 1 minute occlusion, 0.45 +/- 0.02 cm; p less than 0.05) after which time diameter plateaued (after 10 minutes of occlusion, 0.48 +/- 0.02 cm). In addition, the time course of diameter and flow changes after 3 minutes of arterial occlusion were examined. Flow was maximal at 5 seconds but diameter was maximal at 15-30 seconds after release. Furthermore, the half time for the return of diameter to baseline was longer than that for blood flow. We also measured the diameter after forearm heating (42 degrees C) and noted a substantial increase in diameter (before heating, 0.32 +/- 0.01; after heating, 0.39 +/- 0.02 cm; p less than 0.05). Finally, we applied pressure to the venous side of arteriovenous fistulae in five hemodialysis patients. This maneuver was associated with large reductions in forearm blood flow (baseline flow, 63.3 +/- 10.6; venous compression flow, 36.0 +/- 4.4 ml/min.100 ml; p less than 0.05) and a decrease in brachial artery size (baseline diameter, 0.63 +/- 0.07; venous compression diameter, 0.58 +/- 0.06 cm; p less than 0.05). We conclude that 1) the human brachial artery size changes in response to changes in blood flow, and 2) the maximal dilation occurs after maximal flow is noted. Although alternate explanations are possible for each of our observations, our results are most consistent with a flow-mediated, localized vasodilating process.

Adult↗

PubMedDate not supplied

Myocardial infarctions; frequently asked questions.

Explore the source record for details and available documents.

Abstracting and Indexing↗

PubMedDate not supplied

AHIMA provides testimony on coding/classification issues pertaining to HIPAA (Health Insurance Portability and Accountability Act of 1996) implementation.

In summary, AHIMA has identified the following key issues: Uniformity and consistency must be required of all health-care organization, payers, and other data users. A central authority, comprised of representatives from the public and private sector, should be created to ensure compliance with and enforcement of coding system rules and official coding guidelines. A realistic implementation plan for the introduction of any new coding system, including migration to a single procedural classification system, must be established. Since data quality is based on the data source, clinical vocabulary, and classification system, it is important not to focus on only one component. A standard data set must be established. It is important to maintain data comparability with other nations in order to conduct global research studies. AHIMA has had a long-standing relationship working with the department on coding and classification issues and is committed to providing assistance to carry out out the requirements of the law.

Abstracting and Indexing↗