scholarly journals Reply to “Letter to the editor: Sympathetically mediated increases in cardiac output, or peripheral vasoconstriction as primary regulator of BP during hyperinsulinemia?”

2020 ◽  
Vol 319 (2) ◽  
pp. H394-H395
Author(s):  
Jacqueline K. Limberg ◽  
Jaume Padilla
Keyword(s):  
Cardiac Output ◽  
Peripheral Vasoconstriction ◽  
Letter To The Editor

Obstructive Sleep Apnea

PEDIATRICS ◽  
1983 ◽  
Vol 72 (2) ◽  
pp. 267-268
Author(s):  
D. P. Southall
Keyword(s):  
Blood Flow ◽  
Obstructive Sleep Apnea ◽  
Cardiac Output ◽  
Sleep Apnea ◽  
Obstructive Apnea ◽  
Peripheral Vasoconstriction ◽  
Obstructive Sleep ◽  
Transcutaneous Po2

Kahn and colleagues1 point out that their findings of a decrease in transcutaneous PO2 after episodes of obstructive apnea could be due to a "... redistribution of blood flow away from the skin... ." Their suggestion, however, that the latter is due to a decrease in cardiac output is unlikely. Studies using indwelling arterial catheters during apnea and bradycardia have suggested that, if anything, there is an increase in cardiac output.2,3 Moreover, blood flow measurements3 have shown that there is often a peripheral vasoconstriction during such episodes.

Letter to the Editor

PEDIATRICS ◽  
1974 ◽  
Vol 53 (2) ◽  
pp. 289-289
Author(s):  
John Kattwinkel ◽  
Avroy A. Fanaroff ◽  
Marshall H. Klaus
Keyword(s):  
Cardiac Output ◽  
Venous Return ◽  
Blood Gases ◽  
Lung Compliance ◽  
Nasal Cpap ◽  
Vascular Space ◽  
Letter To The Editor

Initially, our procedure in instituting nasal CPAP was to start with a pressure of 6 cm H2O and increase gradually as blood gases dictated. Our concern was that in some infants, higher pressures might impede venous return thus compromising cardiac output. However, experience shows that if the technique is reserved for only patients with severe RDS (i.e., PaO2 < 60 mm Hg in FiO2 ≥ 70%) their lung compliance is low and transmission of pressure to the vascular space is probably negligible.

Peripheral vasoconstriction shortly after onset of moderate exercise in humans

1994 ◽  
Vol 77 (3) ◽  
pp. 1519-1525 ◽  
Author(s):  
K. Toska ◽  
M. Eriksen
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Set Point ◽  
Peripheral Vasoconstriction ◽  
Cholinergic Blockade ◽  
Healthy Humans ◽  
Exercise Period

The immediate cardiovascular responses at the onset of supine dynamic leg exercise were studied by noninvasive methods in healthy humans. Total peripheral conductance (TPC), heart rate, and cardiac output increased very rapidly at the onset of exercise. Mean arterial pressure (MAP) showed a moderate anticipatory increase during a 10-s countdown to exercise and then decreased (but not below resting level) during the first 10 s of exercise. The TPC response was biphasic, and TPC started to fall from its peak value approximately 12 s after onset of exercise. This peripheral vasoconstriction increased MAP. After 25 s, the cardiovascular variables were stable for the rest of the 2-min exercise period. In the same subjects, cholinergic blockade was induced by atropine sulfate (0.035 mg/kg) and resting cardiac output, MAP, and TPC increased considerably. The exercise protocol was repeated after atropine, and the increase in heart rate at onset of exercise was slower and smaller. MAP decreased and remained depressed throughout the exercise period. A monophasic increase in TPC was seen. We suggest that, in the normal situation, the biphasic response in TPC reflects a baroreflex sympathetic vasoconstriction very shortly after onset of exercise and that this response is due to a rapid increase in set point for arterial pressure control at the onset of exercise. After cholinergic blockade, MAP was probably continuously well above the set point for arterial pressure control both before and during exercise and no reflex vasoconstriction was observed in this situation.

Muscle metaboreflex control of cardiac output and peripheral vasoconstriction exhibit different latencies

2000 ◽  
Vol 278 (2) ◽  
pp. H530-H537 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Donal S. O'Leary
Keyword(s):  
Cardiac Output ◽  
Vascular Occlusion ◽  
Systemic Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Pressor Responses ◽  
Vascular Beds ◽  
The Individual ◽  
Renal Vascular

Experiments were designed to determine 1) the mechanisms mediating metaboreflex-induced increases in systemic arterial pressure (SAP) in response to total vascular occlusion of hindlimb blood flow [e.g., increases in cardiac output (CO) vs. peripheral vasoconstriction] and 2) whether the individual mechanisms display differential latencies for the onset of the responses. Responses were observed in seven dogs performing steady-state treadmill exercise of mild and moderate workloads (3.2 km/h at 0% grade and 6.4 km/h at 10% grade). Differential latencies were exhibited among CO, nonischemic vascular conductance (NIVC; conductance to all nonischemic vascular beds), and renal vascular conductance (RVC), with peripheral vasoconstriction significantly preceding metaboreflex-mediated increases in CO. In addition, the latencies for SAP were not different from those for NIVC or RVC at either workload. During the lower workload there were small increases and then subsequent decreases in CO before the metaboreflex-induced increase in CO, which did contribute somewhat to the initial increases in SAP. However, the increases in CO mediated by the metaboreflex occurred significantly later than the initial increases in SAP. Therefore, we conclude that the substantial metaboreflex-mediated pressor responses that occur during the initial phase of total vascular occlusion during mild and moderate exercise are primarily caused by peripheral vasoconstriction.

scholarly journals Role of cardiac output versus peripheral vasoconstriction in mediating muscle metaboreflex pressor responses: dynamic exercise versus postexercise muscle ischemia

2013 ◽  
Vol 304 (8) ◽  
pp. R657-R663 ◽  
Author(s):  
Marty D. Spranger ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
Jasdeep Kaur ◽  
Doug Stayer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Muscle Ischemia ◽  
Normal Individuals ◽  
Pressor Responses ◽  
Sustained Increase

Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in normal individuals increases mean arterial pressure (MAP) via increases in cardiac output (CO) with little peripheral vasoconstriction. The rise in CO occurs primarily via increases in heart rate (HR) with maintained or slightly increased stroke volume. When the reflex is sustained during recovery (postexercise muscle ischemia, PEMI), HR declines yet MAP remains elevated. The role of CO in mediating the pressor response during PEMI is controversial. In seven chronically instrumented canines, steady-state values with MMA during mild exercise (3.2 km/h) were observed by reducing hindlimb blood flow by ∼60% for 3–5 min. MMA during exercise was followed by 60 s of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR, and CO by 55.3 ± 4.9 mmHg, 42.5 ± 6.9 beats/min, and 2.5 ± 0.4 l/min, respectively. During sustained MMA via PEMI, MAP remained elevated and CO remained well above the normal recovery levels. Neither MMA during dynamic exercise nor during PEMI significantly affected peripheral vascular conductance. We conclude that the sustained increase in MAP during PEMI is driven by a sustained increase in CO not peripheral vasoconstriction.

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