Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Laitinen, Lauri A.; Laitinen, Maria; Widdicombe, J. G.

doi:10.1111/j.1476-5381.1987.tb11374.x

Cited by 50 publications

(32 citation statements)

References 13 publications

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“…In another study fatal asthma was characterized by an increase in both numbers of large vessels and total vessel area in the cartilaginous airways, suggesting enlargement of existing vessels [6]. The authors have not assessed large airway vessel size and area, because such measurements may be artificially distorted by tangential cutting of vessels and vasodilatation induced by b 2 -agonists [19] or vasoactive mediators [20]. Furthermore, results from animal studies have shown that most of the airway narrowing is due to extravasation of plasma fluid rather than vascular congestion [21].…”

Section: Discussionmentioning

confidence: 99%

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Vrugt¹,

Wilson²,

Bron³

et al. 2000

Eur Respir J

131

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To examine the role of the bronchial microvasculature and adhesion molecule expression in severe asthma, the authors have performed an immunohistochemical study on bronchial biopsies comparing 15 glucocorticoid-dependent asthmatics, 15 mild asthmatics and eight control subjects.Serially cut glycol methacrylate-embedded sections were stained with monoclonal antibodies identifying the vessel marker EN-4, intercellular adhesion molecule (I-CAM)-1, vascular cell adhesion molecule (VCAM)-1, E-and P-selectin. Sections were also stained for lymphocyte function associated antigen (LFA)-1 and very late antigen (VLA)-4.By comparison with mild asthma and nonasthma, severe asthma was characterized by increased numbers of submucosal vessels (p=0.009) which was associated with increased numbers of vessels expressing ICAM-1 (p=0.005). A highly significant correlation was found between the total number of EN-4+ vessels and the vessels expressing ICAM-1 (r=0.85, p=0.01). In contrast, E-selectin expression was lower in severe as compared with mild asthma (p=0.01) but not different from normal. No differences were found between the three groups in the expression of VCAM-1 and Pselectin nor in numbers of LFA-1+ and VLA-4+ cells.The results of this study support the notion that mucosal neovascularization is an important feature of airways remodelling in severe asthma. This is associated with a relatively higher density of vessels expressing intercellular adhesion molecule-1, although the expression of this adhesion molecule per vessel was not raised.

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Section: Discussionmentioning

confidence: 99%

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Vrugt¹,

Wilson²,

Bron³

et al. 2000

Eur Respir J

131

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“…These include histamine, methacholine, 5-HT, peptides and prostaglandins (Laitinen et al, 1987;Salonen et al, 1988;Corfield et al, 1991). Here PAF has been shown to be one of the most potent vasodilators yet studied in this system, second only to the other inflammatory mediator bradykinin which is also notable for its extremely long duration of action (Corfield et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

“…The tracheobronchial circulation will have an important role in modulating these actions. However, the actions of PAF on airways blood flow has been little studied (Laitinen et al, 1987) and its mode of action is unknown. PAF induces microvascular leakage in the airways which may be due to a direct rather than indirect action on the vasculature since in guinea-pigs it is independent of cyclo-oxygenase or lipoxygenase products (Evans et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of platelet activating factor‐induced changes in sheep tracheal blood flow

Corfield

Webber

Widdicombe

1991

British J Pharmacology

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1 The effects of platelet activating factor (PAF) have been studied on the cervical tracheal vasculature and smooth muscle of anaesthetized sheep. 2 The predominant action of PAF (2 pmol-2 nmol) was a dose-dependent fall in tracheal vascular resistance. The maximum fall in resistance was -41.6% (-38.5 to -44.7%, 95% confidence interval) and the ED50 was 17 pmol (12-28 pmol). Lyso-PAF (200 pmol) did not change vascular resistance.3 PAF had no effect on tracheal smooth muscle tone assessed by measuring changes in the external diameter of the trachea. 4 The fall in vascular resistance produced with PAF was unaffected by the anti-asthma drug nedocromil sodium (1 mg, i.a.), the cyclo-oxygenase inhibitor indomethacin (5mg kg-, i.v.), the leukotriene receptor antagonist FPL55712 (2mgkg-1, i.v.), or a combination of the histamine H1-and H2-antagonists mepyramine (2 mg kg-1, i.v.) with cimetidine (5 mg kg-1, i.v.). The PAF antagonist WEB 2086 (300,ug kg-1, i.v.) significantly reduced the vasodilatation produced by PAF (before, -40.8 + 4.2%; after -16.5 + 5.9%, P <0.05). 5 Thus in this model, PAF is a potent vasodilator of the tracheal circulation but has no action on tracheal smooth muscle. The vasodilatation is mediated by specific PAF receptors and is not due to the release of prostanoids, leukotrienes or histamine.

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“…On the other hand, stimulation of the central end of a vagus nerve causes tracheal vasoconstriction, systemic hypertension and smooth muscle contraction via impulses came from the cardiac nerves not the pulmonary or abdominal branches of the vagus (Ş ahin et al 1987a). Whether or not parasympathetic cholinergic fibers to the laryngeal vasculature can cause relaxation is more controversial, and in general histological studies do not support a close cholinergic innervation of the vessels (Laitinen et al 1987b). Furthermore, the exact motor pathways have not been identified.…”

Section: Yelmen Nk şAhin G and Oruç T The Effects Of Vagal Stmentioning

confidence: 99%

“…Although the role of parasympathetic and sympathetic nerves to the laryngeal vascular bed are not well established, the stimulation of superior laryngeal nerve causes nasal and tracheal vasodilatation (Laitinen et al 1987a;Dylewska et al 1993). This response can be blocked by muscarinic agents such as atropine and may be caused by acetylcholine and metacholine (Laitinen et al 1987b). On the other hand, Laitinen et al (1987a) suggested that vasodilatation caused by parasympathetic nerve stimulation in nose and trachea after atropine administration, may be mediated by the release of neuropeptides such as VIP.…”

Section: Yelmen Nk şAhin G and Oruç T The Effects Of Vagal Stmentioning

confidence: 99%

The Effects of Vagal Stimulation on Laryngeal Vascular Resistance and Intraluminal Pressure in the Dog

Yelmen

Şahin

Oruc

2004

Tohoku J. Exp. Med.

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In anaesthetized dogs (sodium pentobarbitone 30 mg/kg, i.v.) laryngeal vascular resistance was measured by unilateral perfusion at constant flow of the branch of the cranial superior thyroid artery that supplies the larynx. Arterial perfusion was at constant flow and inflow pressure was divided by flow to give laryngeal vascular resistance (R LV ). Intraluminal laryngeal pressure (P L ) and systemic arterial blood pressure (BP) were also measured. Stimulation (20 V, 20 Hz, 0.2 milliseconds) of the central end of cervical vagus caused an increase in R LV (+22.9±6.1%) and a decrease in P L (−12.1±4.4%). Stimulation (10 V, 10 Hz, 0.2 milliseconds) of the central end of the recurrent laryngeal nerve (RLN) reduced R LV (−3.4±0.8%) and P L (−7.5±4.1%). Stimulation of the peripheral end of the RLN decreased R LV (−7.1±1.9%) and increased P L (+21.6±7.7%). Stimulation of the central end of the superior laryngeal nerve (SLN) increased R LV (+17.9±3.2%) and P L (+59.8±2.7%), whereas stimulation of the peripheral end of the SLN decreased R LV (-4.8±1.6%) and P L (−4.1±2.4%). After treatment with α -adrenoreceptor antagonist phentolamine (0.5 mg/kg, i.v.), stimulation of the central end of cervical vagus nerve reduced R LV by 25% and decreased BP. Phentolamine caused a decrease in BP and reduced the magnitude of increase in R LV in response to stimulation of central end of SLN. After atropine sulphate (0.5-2.0 mg/kg, i.v.), the stimulation of both central and peripheral ends of RLN reduced R LV . The decrease in R LV during stimulation of peripheral end of SLN was reduced by atropine. Thereafter, pancuronium bromide (0.06-0.1 mg/kg, i.v.) was given and dogs were artifically ventilated. After paralyzed, stimulation of the central end of the SLN decreased R LV (+26.0±4.5%) but produced no change in P L . It is concluded that parasympathetic motor fibers in the RLN and SLN are effective for the laryngeal vascularity and non-adrenergic system may be responsible for laryngeal vasoconstriction. laryngeal vasculature; vagal stimulation; phentolamine; atropine

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Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Cited by 50 publications

References 13 publications

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Mechanisms of platelet activating factor‐induced changes in sheep tracheal blood flow

The Effects of Vagal Stimulation on Laryngeal Vascular Resistance and Intraluminal Pressure in the Dog

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