Ichiro Kobayashi

A dynamic analysis of chest wall motions with MRI in healthy young subjects.

The objective of this study was to analyse respiratory‐related motion of the chest wall with non‐invasive method.

Differences in motor control in the bronchus and extrathoracic trachea

The motor control of the bronchus and extrathoracic trachea was evaluated by continuously measuring bronchial diameter and tracheal muscle tension as well as phrenic nerve activity in decerebrated, paralyzed, artificially ventilated dogs. Spontaneous rhythmic changes in bronchial diameter and tracheal muscle tension occurred in phase with phrenic burst during mechanical ventilation and during apnea induced by disconnecting the ventilator. There was a small but consistent difference in the timing of their rhythmic activities; bronchial constriction started at mid-inspiration, whereas tracheal contraction began just prior to the end of inspiration. Both were active in the post-inspiratory phase. Both hypercapnia and apnea caused an enhanced rhythmic constriction of the bronchus, while evoking a tonic contraction of the trachea. Intermittent electric stimulation of the efferent vagus nerves revealed that repetitive stimulation with a short intermission was necessary to evoke a sustained constriction of the bronchus, and that the bronchus could maintain the sustained constriction only transiently. These results indicate that the motor control of the bronchus and extrathoracic trachea are distinct. The central nervous system may contribute to the difference in timing of the contraction between tracheal and bronchial smooth muscle. However, the difference in response to electric stimulation of the nervus vagus may be attributed to the peripheral neuromuscular system.

The potential dermal irritating effect of residual (meth) acrylic monomers in pressure sensitive adhesive tapes

It is generally thought that residual unpolymerized (meth)acrylic monomers commonly found in pressure sensitive adhesive tapes for medical use may cause dermal irritation, but a systematic study has never been carried out. Therefore, we assessed the potential dermal irritating effect of residual (meth)acrylic monomers. We studied seven acrylic monomers, acrylic acid (AA), methyl acrylate (MA), ethyl acrylate (EA), n-butyl acrylate (n-BA), n-hexyl acrylate (n-HA), 2-ethylhexyl acrylate (2-EHA) and 2-hydroxyethyl acrylate (HEA), as well as three methacrylic monomers, methacrylic acid (MAA), methyl methacrylate (MMA) and 2-hydroxyethyl methacrylate (2-HEMA). We first examined their cytotoxic effect on a cultured dermis model using the MTT method to determine their EC50 and then performed a primary irritation test in rabbits using the monomers at three different concentrations (i.e., EC50 , one-tenth EC50 and 10 times EC50). Marked variations were found in cytotoxic and dermal irritating activities among the (meth)acrylic monomers tested. HEA exhibited the most potent dermal irritation having the lowest erythema dose (the concentration which gives a primary dermal irritation index of 1.00) of 460 ppm. But the other monomers exhibited less potent dermal irritation (lowest erythema doses ≥1000 ppm). For the monomers, significant correlation was found between cytotoxic activity and in vivo dermal irritating activity. Our results show that residual unpolymerized (meth)acrylic monomers in adhesive tapes are unlikely to induce skin irritation except for HEA. This study also suggests that cultured skin models are extremely useful as a screening method for chemical substances that could potentially cause dermal irritating activity.

Role of cholinergic neural transmission on airway resistance in the dog

The unique contractile profiles of bronchial smooth muscle (Kondo et al., 1995) and its neural control were investigated by comparing responses of the bronchus and trachea to acute hypercapnia, stimulation of vagus efferent fibers before and after intravenous atropine, and intravenous acetylcholine in decerebrated and paralyzed dogs. During acute hypercapnia, airway resistance represented by peak airway pressure (Pedley et al., 1970) significantly increased as well as tracheal tension (Ttr). During electric stimulation of the vagal efferent fibers, Ttr increased and was sustained throughout the simulation period while the peak airway pressure was not maintained at the peak level. The peak Ttr and the airway resistance (Raw) calculated from ventilatory flow and airway pressure increased with increases in intensity of electric stimulation. Ttr reached its maximal level at an intensity 16 times of the threshold (T), while Raw became maximal at 4T. Although both the Ttr-stimulus intensity and Raw-intensity curves were shifted to the right by administration of intravenous atropine, the Raw curve shifted more to the right than the Ttr curve with the same dose of atropine. When muscular muscarinic receptors were directly stimulated by intravenous acetylcholine, Ttr once increased and then decreased promptly while peak airway pressure remained at a high level for a few minutes. These findings suggested that the bronchus is more sensitive to vagal efferent stimulation and susceptible to competitive antagonist of actylcholine than the trachea. In conclusion, the contractile profiles of the fifth-order bronchus we have reported (Kondo et al., 1995) were reflected in airway resistance, and the neuromuscular junction may be the site of adaptation of bronchoconstrictor response to motor nerve adaptation.

A Case of Pulmonary Varix Associated with Superior Pulmonary Vein Occlusion

A pulmonary varix is a localized dilatation of a pulmonary vein, which is usually asymptomatic presented as a mass on a chest roentgenogram, and diagnosed with pulmonary angiography. We encountered a case of 55 year-old man, in whom incidentally identified was a dilated blood vessel that passed through the minor fissure and returned to the inferior pulmonary vein, which we diagnosed as pulmonary varix. This vascular anomaly was accompanied by the occluded superior pulmonary vein, highly suggestive of the developmental mechanism of this disease.

Effect of the respiratory-related bronchial rhythmic constriction on alveolar ventilation in the dog.

The middle-sized bronchus constricts during mid-inspiration through early-expiration. The purpose of this study was to elucidate the physiological role of this respiratory-related bronchial rhythmic constriction (RRBRC). The following parameters were measured in 12 decerebrated and paralyzed dogs: pressure from a balloon-tipped catheter in the fifth-generation bronchus (to reveal RRBRC), efferent neurogram from C(5) phrenic, and ventilatory flow and volume. We found a small but significant reduction of peak expiratory flow of mechanical ventilation during RRBRC. During bilateral vagal cold block, RRBRC was simulated by intermittent electric stimulation of vagal fibers distal to the cold block. This stimulus evoked a decrease in peak expiratory flow and in Pa(CO2) (approximately 1.5 mmHg). After vagal warming, mechanical ventilation was terminated, and blood gases were maintained normal by extracorporeal oxygenation. During each RRBRC ventilatory volume decreased by approximately 3 ml. The changes in gas volume and RRBRC disappeared after bilateral vagotomy. These findings support the concept that the physiological role of RRBRC is to facilitate alveolar gas exchange by reducing expiratory flow, anatomical dead space, or both.

Contribution of brainstem hypoperfusion to the tracheal and phrenic nerve responses to high-pressure lung inflation in the dog

Lung inflation to high airway pressure is known to produce tracheal constriction following an initial dilation. This is attributed to stimulation of various pulmonary receptors. In an attempt to find cause of this response, we investigated in 20 decerebrated, tracheostomized and paralyzed dogs changes in the tracheal smooth muscle tension, arterial pressure and the phrenic nerve activity to high-pressure lung inflation. A high-pressure lung inflation evoked a contraction of tracheal smooth muscle following its short-lasting relaxation, and a persistent hypotension. After hilar denervation which eliminated all pulmonary afferents, a high-pressure lung inflation still evoked contraction of tracheal smooth muscle (an increase of 3.7 times) and augmented amplitude and frequency of phrenic bursts. Bilateral transections of sympathetic fibers to the lung, or blockade of arterial perfusion to the carotid sinus and denervation of the carotid sinus bilaterally did not alter the tracheal muscle and phrenic responses to a high-pressure lung inflation. We further found that severe hypotension alone caused similar responses of the tracheal smooth muscle contraction and augmented phrenic activity. Finally, when blood supply to the brainstem was transiently obstructed by clamping both the vertebral and internal carotid arteries bilaterally, the same responses were observed. In contrast, when blood hypoperfusion to the brainstem was prevented by means of extracorporeal circulation, a high-pressure lung inflation failed to evoke such contraction of tracheal smooth muscle and or increased phrenic activity. After transection of the vagus nerves bilaterally at the cervical level the tracheal muscle response to lung inflation was abolished but that of phrenic nerve was preserved. We concluded that the tracheal smooth muscle contraction and phrenic responses induced by high-pressure lung inflation may be in part attributed to brainstem hypoperfusion.