Adrenergic Modulation of the Pulmonary Circulation during Strenuous Exercise in Sheep

Kane, Douglas W.; Tesauro, Thomas; Newman, John H.

doi:10.1164/ajrccm/147.5.1233

Cited by 18 publications

(33 citation statements)

References 13 publications

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“…Animals were fitted with a padded leather collar that was attached at a comfortable level to side posts built into a standard treadmill (Quinton Instruments, Seattle, WA). Train-ing consisted of repeated trotting on the treadmill for 5-8 d until each animal was familiar with the procedure and was able to trot comfortably at 4mph for 5-10 min (13,21).…”

Section: Methodsmentioning

confidence: 99%

“…Flow probe and thermodilution values were recorded simultaneously, and a regression plot and equation were constructed for each animal. The derived formula was then used to correct each flow probe value during exercise to the thermodilution standard (13,22).…”

Section: Methodsmentioning

confidence: 99%

“…Resting vascular tone is also modulated by basal adrenergic output (9)(10)(11)(12). We recently observed that alpha and beta adrenergic activation occurs during exercise in sheep and that pulmonary vascular resistance (PVR) was most affected by alpha constriction when beta receptors were blocked ( 13). In addition to direct vasodilation, endothelium-derived relaxation factor (EDRF) may modulate vascular tone in part by interaction with the sympathetic nervous system, by reducing sympathetic nerve outflow (14)(15)(16)(17), or by reducing synaptic norepinephrine efflux ( 18).…”

Section: Introductionmentioning

confidence: 99%

“…Most of the decrease in PVR occurs within 20-40 s of onset ofexercise and is not affected by adrenergic blockade (13). This adrenergic-independent decrease may be due to passive vasodilation ( 13,23).…”

Section: Introductionmentioning

confidence: 99%

“…This adrenergic-independent decrease may be due to passive vasodilation ( 13,23). A second, slower decrease in PVR is modulated by adrenergic receptors and is blocked during the unopposed alpha-mediated constriction that occurs during beta blockade ( 13).…”

Section: Introductionmentioning

confidence: 99%

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Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

Kane¹,

Tesauro²,

Koizumi³

et al. 1994

J. Clin. Invest.

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We studied the effects of inhibition of nitric oxide (NO) (endothelium-derived relaxation factor) synthase in combination with alpha and beta adrenergic receptor blockade on pulmonary vascular tone during exercise. In paired studies, we exercised sheep on a treadmill at a speed of 4 mph, and measured blood flow and pressures across the pulmonary circulation with and without inhibition of NO synthase (Nw-nitro-L-arginine 20 mg/kg intravenous Ii.v.I), alpha receptor blockade (phentolamine 5 mg i.v.), beta receptor blockade (propranolol 1 mg i.v.), and combined alpha and beta receptor blockade. Activation of both types of adrenergic receptors occurs with exercise, and because increased release in NO is hypothesized to occur during exercise, these studies were designed to determine the magnitude of effect and interactions of these competing dilator and constrictor influences. We found that inhibition of NO synthase raised pulmonary vascular resistance (PVR) at rest and that, although a reduction in PVR occurred with exercise from this new baseline, vasoconstriction persisted. Combined beta blockade and NO synthase inhibition unmasked unopposed alpha vasoconstriction; PVR rose at rest and continued to rise with exercise; and mean pulmonary arterial pressures approached very high levels, 43.8±4.4 cmH20. Using a distal wedged pulmonary artery catheter technique, most of the vasoconstriction was found to be in vessels upstream from small pulmonary veins. During exercise in sheep there appears to be a high degree of alpha and beta adrenergic-mediated tone in the pulmonary circulation. Endogenous production of NO actively dilates pulmonary vessels at rest and opposes potent alpha-mediated pulmonary vasoconstriction during exercise. (J. Clin.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

Kane¹,

Tesauro²,

Koizumi³

et al. 1994

J. Clin. Invest.

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Peripheral Circulation

Laughlin

Davis

Secher

et al. 2012

Comprehensive Physiology

212

234

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Blood flow (BF) increases with increasing exercise intensity in skeletal, respiratory, and cardiac muscle. In humans during maximal exercise intensities, 85% to 90% of total cardiac output is distributed to skeletal and cardiac muscle. During exercise BF increases modestly and heterogeneously to brain and decreases in gastrointestinal, reproductive, and renal tissues and shows little to no change in skin. If the duration of exercise is sufficient to increase body/core temperature, skin BF is also increased in humans. Because blood pressure changes little during exercise, changes in distribution of BF with incremental exercise result from changes in vascular conductance. These changes in distribution of BF throughout the body contribute to decreases in mixed venous oxygen content, serve to supply adequate oxygen to the active skeletal muscles, and support metabolism of other tissues while maintaining homeostasis. This review discusses the response of the peripheral circulation of humans to acute and chronic dynamic exercise and mechanisms responsible for these responses. This is accomplished in the context of leading the reader on a tour through the peripheral circulation during dynamic exercise. During this tour, we consider what is known about how each vascular bed controls BF during exercise and how these control mechanisms are modified by chronic physical activity/exercise training. The tour ends by comparing responses of the systemic circulation to those of the pulmonary circulation relative to the effects of exercise on the regional distribution of BF and mechanisms responsible for control of resistance/conductance in the systemic and pulmonary circulations.

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Pulmonary Circulation at Exercise

Naeije¹,

Chesler

2012

Comprehensive Physiology

154

164

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The pulmonary circulation is a high flow and low pressure circuit, with an average resistance of 1 mmHg.min.L−1 in young adults, increasing to 2.5 mmHg.min.L−1 over 4–6 decades of life. Pulmonary vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary pressures, up to a 20–25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40–50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher pulmonary vascular pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of pulmonary vascular tone have little effect on pulmonary vascular pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with pulmonary hypertension is associated with sharp increases in pulmonary artery pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint pulmonary vascular pressures-flow relationships may uncover early stage pulmonary vascular disease.

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Adrenergic Modulation of the Pulmonary Circulation during Strenuous Exercise in Sheep

Cited by 18 publications

References 13 publications

Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

Exercise-induced pulmonary vasoconstriction during combined blockade of nitric oxide synthase and beta adrenergic receptors.

Peripheral Circulation

Pulmonary Circulation at Exercise

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