Extracellular acidification attenuates bronchial contraction via an autocrine activation of EP receptor: Its diminishment in murine experimental asthma.

Purpose: Extracellular acidification is a major component of tissue inflammation, including airway inflammation in asthmatics. However, its physiological/pathophysiological significance in bronchial function is not fully understood. Currently, the functional role of extracellular acidification on bronchial contraction was explored.

Altered renin-angiotensin system gene expression in airways of antigen-challenged mice: ACE2 downregulation and unexpected increase in angiotensin 1-7.

Objective: Evidence suggest that the renin-angiotensin system (RAS) is activated in people with asthma, although its pathophysiological role is unclear. Angiotensin-converting enzyme 2 (ACE2) is the major enzyme that converts angiotensin II to angiotensin 1-7 (Ang-1-7), and is also known as a receptor of SARS-CoV-2. The current study was conducted to identify the change in RAS-related gene expression in airways of a murine asthma model.

Hyperresponsiveness to Extracellular Acidification-Mediated Contraction in Isolated Bronchial Smooth Muscles of Murine Experimental Asthma.

Purpose: Extracellular acidification is a major component of tissue inflammation, including airway inflammation. The extracellular proton-sensing mechanisms are inherent in various cells including airway structural cells, although their physiological and pathophysiological roles in bronchial smooth muscles (BSMs) are not fully understood. In the present study, to explore the functional role of extracellular acidification on the BSM contraction, the isolated mouse BSMs were exposed to acidic pH under contractile stimulation.

Increased Gene expression of CCL2/CCR2 axis in bronchial smooth muscles of allergen-challenged mice.

Purpose: Augmented bronchial smooth muscle (BSM) contraction is a cause of airway hyperresponsiveness (AHR) in asthma. Increasing evidence suggest that C-C motif chemokine 2 (CCL2) modulates smooth muscle contractility by activating its binding partner C-C chemokine receptor type 2 (CCR2). In the present study, changes in the gene expression of CCL2/CCR2 axis were determined in the BSMs of a murine model of allergic asthma.

Down-regulation of miR-140-3p is a cause of the interlukin-13-induced up-regulation of RhoA protein in bronchial smooth muscle cells.

The current study aimed to determine the role of a microRNA (miRNA), miR-140-3p, in the control of RhoA expression in bronchial smooth muscle cells (BSMCs). In cultured human BSMCs, incubation with interleukin-13 (IL-13) caused an up-regulation of RhoA protein concurrently with a down-regulation of miR-140-3p. Transfection of the cells with a miR-140-3p inhibitor caused an increase in basal RhoA protein level.

Downregulation of miR-140-3p Contributes to Upregulation of CD38 Protein in Bronchial Smooth Muscle Cells.

In allergic bronchial asthma, an increased smooth muscle contractility of the airways is one of the causes of the airway hyperresponsiveness (AHR). Increasing evidence also suggests a possible involvement of microRNAs (miRNAs) in airway diseases, including asthma, although their roles in function and pathology largely unknown. The current study aimed to determine the role of a miRNA, miR-140-3p, in the control of protein expression of CD38, which is believed to regulate the contraction of smooth muscles, including the airways.

Intranasal administration of recombinant progranulin inhibits bronchial smooth muscle hyperresponsiveness in mouse allergic asthma.

Progranulin (PGRN) is a growth factor with multiple biological functions and has been suggested as an endogenous inhibitor of Tumor necrosis factor-α (TNF-α)-mediated signaling. TNF-α is believed to be one of the important mediators of the pathogenesis of asthma, including airway hyperresponsiveness (AHR). In the present study, effects of recombinant PGRN on TNF-α-mediated signaling and antigen-induced hypercontractility were examined in bronchial smooth muscles (BSMs) both in vitro and in vivo.

Interleukin-17A directly acts on bronchial smooth muscle cells and augments the contractility.

Background: Although interleukin-17 (IL-17) contributes to the induction of airway hyperresponsiveness in asthma, its effect on bronchial smooth muscle (BSM) remains largely unknown. Evidence support an involvement of RhoA/Rho-kinase in BSM contraction, and the pathway has now been proposed as a novel target for asthma therapy. To clarify the role of IL-17 on the development of BSM hyperresponsiveness, effects of IL-17A on BSM contractility and RhoA expression were investigated.

[Anesthetic Management of the Patient with an Anterior Mediastinal Tumor].

Perioperative management of the patient with anterior mediastinal tumor is challenging and should not be underestimated. The clinical presentation of the patient is variable because it depends on the size and localiza- tion of the tumor. Therefore, it is difficult to establish a structured protocol for anesthetic management of ante- rior mediastinal tumor.

Effect of sugammadex on bronchial smooth muscle function in rats.

Sugammadex can encapsulate the steroid-based neuromuscular blocker molecule and results in rapid reversal of neuromuscular blockade induced by rocuronium and vecuronium. However, several cases of bronchospasm after the administration of sugammadex have been reported. The current study was carried out to determine whether sugammadex directly affects smooth muscle function of the airways.

[The postoperative management of patients after pluropneumonectomy--influence of the mode of the operation].

Background: In our hospital, a new mode of operation was introduced in pleuropneumonectomy from 2004. We studied how these changes had affected postoperative management of patients after pleuropneumonectomy.

Methods: We retrospectively reviewed 22 patients who had undergone pleuropneumonectomy for malignant pleural mesothelioma from 2001 to 2008.

Angiotensin II induces hyperresponsiveness of bronchial smooth muscle via an activation of p42/44 ERK in rats.

Angiotensin II (Ang II) might be an important mediator in the pathogenesis of bronchial asthma, although the mechanisms of airway hyperresponsiveness caused by Ang II are not yet clear. Whether p42/44 ERK contributes to the Ang II-elicited bronchial smooth muscle (BSM) hyperresponsiveness in rats was presently examined. The RT-PCR analyses revealed that Ang II AT(1A), AT(1B), and AT(2) receptors, angiotensinogen, angiotensin-converting enzyme, but not renin, were expressed in the lungs, trachea, and main bronchi of rats.

Inhibition of geranylgeranyltransferase inhibits bronchial smooth muscle hyperresponsiveness in mice.

Recent studies revealed an involvement of RhoA/Rho-kinase in the contraction of bronchial smooth muscle (BSM), and this pathway has now been proposed as a new target for asthma therapy. A posttranslational geranylgeranylation of RhoA is required for its activation. Thus selective inhibition of geranylgeranyltransferase may be a novel strategy for treatment of the BSM hyperresponsiveness in asthmatics.

Anesthetic management of a patient with Alport-leiomyomatosis syndrome.

We report the anesthetic management of esophagectomy for a patient with Alport-leiomyomatosis syndrome. A 23-year-old woman complained of dysphagia and severe chest pain. Her chest X-ray, computed tomography (CT), and magnetic resonance imaging (MRI) showed an enlarged esophagus, in contact with the trachea, heart, aorta, and large vessels.

Y-27632 augments the isoflurane-induced relaxation of bronchial smooth muscle in rats.

Recent studies revealed an involvement of RhoA/Rho-kinase signaling in the agonist-induced Ca(2+) sensitization of bronchial smooth muscle contraction, and the pathway has now been proposed as a new target for the treatment of airway obstructive diseases, such as asthma. On the other hand, volatile anesthetics such as isoflurane are traditionally used to treat status asthmaticus. In the present study, the effect of inhibition of Rho-kinase on the isoflurane-induced relaxation of bronchial smooth muscle was investigated.

Favorable outcomes after living-donor lobar lung transplantation in ventilator-dependent patients.

Purpose: Living-donor lobar lung transplantation (LDLLT) is performed in critically ill patients, although the outcome is generally expected to be poor for those who are ventilator dependent. The aim of this study was to compare the outcomes of LDLLT in ventilator-dependent patients compared with those in ventilator-independent patients.

Methods: We reviewed 31 consecutive patients who received LDLLT between October 1998 and May 2004.

Rho-kinase inhibitors augment the inhibitory effect of propofol on rat bronchial smooth muscle contraction.

Background: Airway smooth muscle contraction is not caused by the increase in intracellular Ca(2+) ([Ca(2+)](i)) alone because agonist stimulation increases tension at the same [Ca(2+)](i) (increase in Ca(2+) sensitivity). The small G protein Rho A and Rho-kinase (ROCK) play important roles in the regulation of Ca(2+) sensitivity. In this study, we investigated the effects of three ROCK inhibitors (fasudil, Y-27632, and H-1152) on rat airway smooth muscle contraction and the effects of ROCK inhibitors on propofol-induced bronchodilatory effects.

Living-donor lobar lung transplantation for pulmonary arterial hypertension after failure of epoprostenol therapy.

Objectives: The aim of this study was to evaluate the long-term effects of living-donor lobar lung transplantation (LDLLT) for critically ill patients with pulmonary arterial hypertension (PAH) who failed in epoprostenol treatment.

Background: Although continuous epoprostenol infusion has markedly improved survival in patients with PAH, some patients do not benefit from this therapy.

Methods: From July 1998 to December 2003, 28 consecutive PAH patients who were treated with epoprostenol and accepted as candidates for lung transplantation were enrolled.

Effects of a novel palatinose based enteral formula (MHN-01) carbohydrate-adjusted fluid diet in improving the metabolism of carbohydrates and lipids in patients with esophageal cancer complicated by diabetes mellitus.

Background: During perioperative management of patients with gastrointestinal cancer complicated by diabetes mellitus, adequate alimentation is required, but we often face difficulties associated with hyperglycemia and other accompanying complications. Recently, we investigated the effects of a novel palatinose based enteral formula (MHN-01) in suppressing post-prandial hyperglycemia and improving lipid metabolism in experimental animals and perioperative management of patients with esophageal cancer complicated by diabetes mellitus.

Materials And Methods: We gave normal rats and rats with type 2 diabetes mellitus a single oral dose of fluid diet, and analyzed comparatively the time course of blood glucose level in each group until 3 h after the dose.

Colonic interposition and supercharge for esophageal reconstruction.

Aims: We evaluated the techniques of colonic interposition and supercharge for esophageal reconstruction and discussed the main considerations related to these procedures.

Patients And Methods: In this study, we performed 51 esophageal reconstructions using colonic interposition. Twenty-eight of the 51 patients had synchronous or allochronic gastric malignancy.

Peripheral N-methyl-D-aspartate receptors modulate nonadrenergic noncholinergic lower esophageal sphincter relaxation in rabbits.

We investigated the role of peripheral N-methyl-D-aspartate (NMDA) receptors in the myenteric plexus in mediating nonadrenergic noncholinergic (NANC) nitrergic relaxation of the lower esophageal sphincter (LES). Isometric contraction of LES strips from Japanese White rabbits was measured. NANC relaxation was induced by KCl (30 mM) in the presence of atropine and guanethidine.