Measurement of airway mucosal perfusion and water volume with an inert soluble gas

Wanner, Adam; Barker, James A.; Long, William M.; Mariassy, Andrew T.; Chediak, A. D.

doi:10.1152/jappl.1988.65.1.264

Cited by 23 publications

(5 citation statements)

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“…These findings are in agreement with those of Barker and colleagues (2), who demonstrated that local exposure of the tracheal mucosa to inhaled isoproterenol resulted in a dose-dependent increase in tracheal mucosal blood flow. However, Wanner et al (27) measured only the tracheal mucosal blood flow by the inert soluble gas technique using dimethyl ether, whereas we measured the total bronchial arterial blood flow directly with an ultrasonic flow probe, a technique that measures the total blood flow to the airway mucosa as well as that supplying the entire airway wall. Q br progressively increased with higher doses of isoetharine HCl and ultimately reached a plateau.…”

Section: Discussionmentioning

confidence: 99%

Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled β-agonists

Carvalho

Johnson

Charan

1998

Journal of Applied Physiology

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We studied the dose-dependent effects of inhaled isoetharine HCl, a beta-adrenergic bronchodilator (2.5, 5.0, 10.0, and 20.0 mg), on bronchial blood flow (Qbr) in anesthetized sheep. Isoetharine resulted in a dose-dependent increase in Qbr. With a total dose of 17.5 mg, Qbr increased from baseline values of 22 +/- 3.4 (SE) to 60 +/- 16 ml/min (P < 0.001), an effect independent of changes in cardiac output and systemic arterial pressure. To further study whether synthesis of endogenous nitric oxide (NO) affects beta-agonist-induced increases in Qbr, we administered isoetharine (20 mg) by inhalation before and after the NO-synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME). Intravenous L-NAME (30 mg/kg) rapidly decreased Qbr by approximately 80% of baseline, whereas L-NAME via inhalation (10 mg/kg) resulted in a delayed and smaller (approximately 22%) decrease. Pretreatment with L-NAME via both routes of administration attenuated bronchial arterial vasodilation after subsequent challenge with isoetharine. We conclude that isoetharine via inhalation increases Qbr in a dose-dependent manner and that beta-agonist-induced relaxation of vascular smooth muscle in the bronchial vasculature is partially mediated via synthesis of NO.

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Section: Discussionmentioning

confidence: 99%

Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled β-agonists

Carvalho

Johnson

Charan

1998

Journal of Applied Physiology

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“…The same principle was applied to measure the blood flow of the airways15 making use of dimethylether (DME), a soluble gas with a high affinity for haemoglobin. This method is based on the assumption that the uptake of an inert soluble gas in a tissue with capillaries and active flow of blood is determined by the volume of the tissue and by the blood flow 16.…”

Section: Measurement Of Bronchial Blood Flowmentioning

confidence: 99%

The airway vasculature: recent advances and clinical implications

Paredi¹,

Barnes

2009

Thorax

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It is increasingly recognised that the airway circulation plays an important role in airway diseases, either through a change in blood flow or through microvascular leakage. Most of the information available regarding the anatomy and physiology of bronchial blood flow and its regulation has necessarily derived from animal studies. However, there have recently been important advances in understanding airway blood flow in airway disease in humans through the development of non-invasive methods and in the quantification of microvascular leakage using plasma markers. These studies have shown that bronchial blood flow is increased in patients with asthma but not in those with chronic obstructive pulmonary disease, confirming previous pathology investigations. Changes in bronchial blood flow may in part reflect the generation of new vascular vessels, a process known as ''angiogenesis'' which is caused by airway inflammation. Angiogenesis and the resulting plasma leak affect airway physiology, drug clearance and its bioavailability. This review discusses the anatomy, physiology and regulation of bronchial blood flow in the normal and diseased lung, In addition, it analyses the effect of current medical treatment and discusses the potential use of new antiangiogenesis medications. The development of noninvasive assessment of bronchial blood flow and the study of angiogenesis have provided a tool to investigate airway physiology in vivo; these advances will contribute to a better understanding of inflammatory airway diseases as well as the implication of these findings to management.

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“…The effect of aerosolized phenylephrine on tracheal mucosal blood flow has been studied by Barker et al (1) in a sheep model. In their study, tracheal mucosal flow was measured by an inert soluble gas technique using dimethyl ether (15). Barker and colleagues found that phenylephrine administered as an aerosol reduced mucosal blood flow in a dose-dependent manner and that this response was partially blocked by phentolamine (1).…”

Section: Discussionmentioning

confidence: 99%

Comparative effects of α-receptor stimulation and nitrergic inhibition on bronchovascular tone

Carvalho

Thompson

Charan

2000

Journal of Applied Physiology

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Adrenergic agonists are known to influence bronchial blood flow and bronchovascular resistance. Recently, the nitrergic system has also been implicated in the control of bronchovascular tone. In this study, we compared the effects of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) and the alpha(1)-receptor agonist phenylephrine on bronchovascular resistance in anesthetized sheep (n = 9). Bronchial blood flow, cardiac output, and systemic and pulmonary arterial pressures were continuously monitored. Phenylephrine (1.2-3.4 microg. kg(-1). min(-1)) was infused intravenously to increase mean systemic arterial pressure above 95 Torr for 10 min and then was discontinued. When hemodynamic parameters returned to baseline, nebulized phenylephrine (10 mg) was given over 10 min. When parameters again normalized, L-NAME (30 mg/kg) was infused intravenously over 1 min. Intravenous phenylephrine increased systemic vascular resistance by 40% at 10 min with no concurrent increase in bronchovascular resistance, but inhaled phenylephrine increased bronchovascular resistance by 66% at 10 min. By comparison, intravenous L-NAME produced a rapid and sustained fivefold increase in bronchovascular resistance at 10 min. We conclude that, although alpha-agonist stimulation has some influence on bronchovascular resistance in sheep, the nitrergic system has predominant control of bronchovascular tone.

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Measurement of airway mucosal perfusion and water volume with an inert soluble gas

Cited by 23 publications

References 0 publications

Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled β-agonists

Non-cAMP-mediated bronchial arterial vasodilation in response to inhaled β-agonists

The airway vasculature: recent advances and clinical implications

Comparative effects of α-receptor stimulation and nitrergic inhibition on bronchovascular tone

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