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At least 1,279 records · Page 71Linked to original sources
PubMed1995

Dieulafoy's disease of the bronchus.

Dieulafoy's vascular malformation has not been described outside the gastrointestinal tract. Two cases are reported in which this vascular abnormality arose in right lower lobe bronchi, both of which presented with massive haemoptysis.

Adult↗
PubMed1999

Fatal haemorrhage from Dieulafoy's disease of the bronchus.

A 70 year old woman with a previous history of healed tuberculosis and suspected chronic obstructive pulmonary disease presented with recurrent haemoptysis and respiratory failure from a lobar pneumonia. Massive bleeding occurred when biopsy specimens were taken during bronchoscopy which was managed conservatively, but later there was a fatal rebleed from the same site. Two different Dieulafoy's vascular malformations were found in the bronchial tree at necropsy, one of which was the biopsied lesion in the left upper lobe. This report confirms the possibility that vascular lesions occur in the bronchial tree. It is suggested that, if such lesions are suspected at bronchoscopy, bronchial and pulmonary arteriography with possible embolotherapy should be performed.

Aged↗
PubMed2002

In vitro sensitization of human bronchus by beta2-adrenergic agonists.

Incubation of human distal bronchi from 48 patients for 15 h with 10(-7) M fenoterol induced sensitization characterized by an increase in maximal contraction to endothelin-1 (ET-1) and acetylcholine (ACh). Incubation of human bronchi with 10(-6), 3 x 10(-6), and 10(-5) M forskolin (an adenyl cyclase activator) reproduced sensitization to ET-1 and ACh. The sensitizing effect of fenoterol was inhibited by coincubation with gliotoxine (a nuclear factor-kappaB inhibitor), dexamethasone, indomethacin (a cyclooxygenase inhibitor), GR-32191 (a TP prostanoid receptor antagonist), MK-476 (a cysteinyl leukotriene type 1 receptor antagonist), SR-140333 + SR-48968 + SR-142801 (neurokinin types 1, 2, and 3 tachykinin receptor antagonists) with or without HOE-140 (a bradykinin B(2) receptor antagonist), SB-203580 (an inhibitor of the 38-kDa mitogen-activated protein kinase, p38(MAPK)), or calphostin C (a protein kinase C blocker). Our results suggest that chronic exposure to fenoterol induces proinflammatory effects mediated by nuclear factor-kappaB and pathways involving leukotrienes, prostanoids, bradykinin, tachykinins, protein kinase C, and p38(MAPK), leading to the regulation of smooth muscle contraction to ET-1 and ACh.

Acetylcholine↗
PubMed1989

Calcium channel currents in isolated smooth muscle cells from human bronchus.

An electrophysiological study was carried out on smooth muscle cells that were enzymatically dissociated from bundles of muscle fibers dissected out of human bronchi obtained at thoracotomy. These cells that retain the contractile properties of intact bundles were voltage-clamped by means of the whole-cell patch-clamp technique. Upon voltage steps from a holding potential of -60 mV to more positive levels, the initial inward current was followed by large outward currents that inactivated slowly. These were subsequently reduced by substituting Cs+ for K+ in the internal solution and by using Ba2+ instead of Ca2+ as a charge carrier in the external solution. Under these conditions, the inward current did not completely inactivate in the course of 300-ms voltage steps. Inward current measured after leak subtraction was activated at a membrane potential of -25.8 +/- 5 mV, was maximum at +18 +/- 4 mV, and had an apparent reversal potential of +52.5 +/- 5.5 mV (n = 5). The potential at which steady-state inactivation was half-maximum was -28 mV (n = 5). This inward current was identified as a calcium current on the following basis: 1) it was not altered by 10 microM tetrodotoxin (TTX) or by lowering to 10 mM external Na+ concentration; 2) it was blocked by 2.5 mM Co2+ or 1 microM PN 200-110; 3) it was enhanced by 1 microM BAY K 8644, which in addition suppressed the PN 200-110 blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchi↗
PubMed1998

Contractile responses to allergen and cholinergic stimulation in bronchus and trachea of cockroach allergen-sensitized guinea pigs.

Airway hyperreactivity is a hallmark of asthma. Yet, the role of allergic sensitization in the hyperreactivity remains controversial. This study examined the effects of airborne cockroach allergen (CRa) sensitization on the contractility of bronchial (BSM) and tracheal (TSM) smooth muscle rings to cholinergic stimulations, and to specific antigen, in vitro. Guinea pigs were actively immunized with CRa, 5 mg (high dose, HD), 0.5 mg (low dose, LD), or saline aerosols (2x/day, 5 days/week, for 4 weeks) and challenged by CRa inhalation 5 days after last exposure. Twenty-four hours postchallenge, the contractions of the TSM and BSM to electrical field stimulation (EFS), acetylcholine (ACh), and to CRa were measured in vitro. In addition, the contraction to these stimuli were also examined in the passively sensitized TSM with the sera of CRa-immunized guinea pigs. The contractile responses of actively immunized and passively sensitized tissues to EFS and ACh were very similar to those of control tissues. CRa induced dose-dependent contractions in both actively immunized and passively sensitized, but not in control, tissues. The CRa-induced contraction was stronger in the HD group than in the LD group (p<0.0001). Leukotriene C4/D4 receptor antagonist LY-171883 inhibited the CRa-induced contraction by 86% in actively immunized TSM, and by 9% in the passively sensitized TSM. Pyrilamine inhibited the contraction by 57% in actively immunized TSM and 70% in passively sensitized TSM. The results indicate that CRa sensitization does not cause increased airway smooth muscle contractility to cholinergic stimulations, but induces antigen-specific contractions in vitro. Leukotrienes appear to play a significant role in the CRa-specific contractions, more in the actively immunized than those in the passively sensitized tissues, while histamine exerts a moderate effect on the CRa-induced contractions.

Acetophenones↗
PubMed2000

Histamine-induced increase in isometric tension of smooth muscle is mediated by local vagus nerve in human bronchus.

BACKGROUND: The vagus nerve is reported to play an important role in the regulation of airway responsiveness. OBJECTIVE: In the present study, we investigated the role of the local vagus nerve in the changes in isometric tension of smooth muscle induced by histamine in the human airway. METHODS: Eight human lung tissue specimens were obtained at thoracic surgery, and 24 bronchial smooth muscle strips were used for isometric tension recording. The changes in isometric tension were induced by histamine in the presence or absence of physostigmine (10(-6) M), atropine (10(-6) M), and/or tetrodotoxin (10(-6) M). RESULTS: We found that: (1) histamine induced a dose-dependent increase in the isometric tension in human bronchial smooth muscle; (2) physostigmine (10(-6) M) significantly potentiated the amplitude of the histamine-induced increase in isometric tension; (3) atropine (10(-6) M) significantly suppressed the histamine-induced increase in isometric tension; (4) tetrodotoxin (10(-6) M), did not affect the histamine-induced increase in isometric tension of smooth muscle, and (5) in the presence of tetrodotoxin, atropine significantly suppressed the histamine-induced increase in isometric tension. CONCLUSION: These findings suggest that the histamine-induced increase in isometric tension is mediated partly by acetylcholine, presumably released by the direct action of histamine on the vagus efferent nerve terminals without the central reflex via vagus nerve.

Atropine↗