Yoshitaka Oku

Location and axonal projection of one type of swallowing interneurons in cat medulla

Extracellular recordings were made from a type of relay neurons of the superior laryngeal nerve (SLN) afferents in the vicinity of the retrofacial nucleus (RFN) in either pentobarbitone-anesthetized or unanesthetized and decerebrate cats, which were paralyzed and artificially ventilated. A total of 26 neurons that could be activated both orthodromically by electrical stimulation of the SLN and antidromically by stimulation of the brainstem were analyzed. All 26 neurons were activated from the ipsilateral SLN and 13 were activated from the contralateral SLN with mean latencies of 7.7 ms and 11.4 ms, respectively. The majority of these neurons were located in the parvocellular reticular formation dorsomedial to the RFN and to the rostral part of the nucleus ambiguus (AMB). Antidromic stimulation of the medulla showed that 22 of the 26 neurons projected to the hypoglossal nucleus (HYP) and 19 neurons tested projected to the AMB. Of these, 15 neurons projected to both the HYP and AMB and two projected to the lateral reticular nucleus as well. Seventeen neurons were tested for their behavior during fictive swallowing which was elicited by continual electrical stimulation of the SLN and monitored by the activity of the hypoglossal nerve. Twelve neurons showed brief (100-200 ms) burst firing at the onset of swallowing; the firing of the other 5 neurons were suppressed during swallowing. Both the swallowing-active and swallowing-inactive neurons projected to the HYP and AMB. Thus, the SLN relay neurons in the vicinity of the RFN might participate in the early stage of SLN-induced swallowing by integrating inputs from SLN afferents.

Age-related changes in the static and dynamic mechanical properties of mouse lungs.

To investigate the effects of aging on pulmonary mechanical properties in mice, we devised a new experimental apparatus to measure the respiratory impedance of excised lungs in mice and examined age-related changes in both static and dynamic properties. In an accelerated senescence-resistant strain of mice, SAMR1 (Takeda, T., Y. Fukuchi, Y. Uejima, K. Teramoto, T. Oka and H. Orino, J. Am. Geriatr. Soc. 39: 911-919, 1991), ranging from 3 to 24 months of age, static compliance (Cst) as well as total lung capacity increased significantly with age, whereas specific compliance and the K value, as determined by exponential analysis, showed no significant change. In the dynamic study, dynamic compliance (Cdyn) increased significantly with age, whereas the frequency dependence of Cdyn (Cdyn/Cst) did not vary with age. From these results we concluded that lung elasticity, normalized to lung volume, remained constant with age and that the effects of aging on pulmonary mechanics might be solely derived from increases in lung volume in the SAMR1 strain of mice.

Distorted Trachea in Patients with Chronic Obstructive Pulmonary Disease

Background and Objectives: We evaluated the size and configuration of the trachea in patients with chronic obstructive pulmonary disease (COPD; n = 35) on high-resolution computed tomography (HRCT) images and compared them with those of healthy volunteers (n = 24). Methods: Using a newly developed computed method for analyzing the digital data of HRCT, the size and configuration of the trachea were automatically evaluated. Results: The size of the trachea of the COPD subjects was the same as that of the control subjects; however, the configuration was more distorted in the COPD patients. There was no difference in the tracheal index (TI), which is the ratio of the coronal to the sagittal length, between these two groups; however, the ratio of the short to the long radius (SR/LR) was significantly smaller in the COPD group than in the control group. There was a significant correlation between SR/LR and airflow limitation as assessed by pulmonary function tests in the COPD group. Conclusions: The SR/LR is a better index of tracheal deformity than the classical TI. This deformity is not a consequence secondary to hyperinflation or emphysematous change of the lung, because the low attenuation area of the lung was not correlated with SR/LR.

Effects of Willful Ventilatory Control on Respiratory Sensation during Hypercapnia

Remarkable augmentation of breathing discomfort has been noted when ventilation is constrained to the steady state level during progressive hypercapnia. However, the effect of willful enhancement of ventilation on breathing discomfort remains to be evaluated. The present study examined the effects of moderate willful increases or decreases in ventilation during progressive hypercapnia on breathing discomfort in 12 subjects. There were a total of 5 rebreathing trials. In the first (F1) and the fifth trials the subjects rebreathed freely. In the other trials subjects breathed by tracking a target to achieve hypercapnic ventilatory responses that were the same (HCVR-S), 25% higher (HCVR-H) and 25% lower (HCVR-L) than in the F1 trial. Breathing discomfort was assessed every 30 s by a 150-mm visual analog scale (VAS). The sensational response (dVAS/dPCO2) during HCVR-S [3.8 +/- (SE) 0.8 mm/Torr] was significantly smaller (p < 0.01) than that during the F1 (6.3 +/- 0.8 mm/Torr) trial. HCVR-H resulted in a further decrease in dVAS/dPCO2 to 3.1 +/- 0.7 mm/Torr as compared to HCVR-S (p < 0.05). HCVR-L significantly increased dVAS/dPCO2 to 4.9 +/- 0.7 mm/Torr compared to HCVR-S (p < 0.05). The final free rebreathing ventilatory response was significantly larger than the initial free rebreathing response (2.7 +/- 0.5 as compared to 2.1 +/- 0.4 liters/min/Torr, p < 0.01). However, the sensational response did not change (6.3 +/- 0.8 vs. 5.8 +/- 0.7 mm/Torr). These rebreathing studies indicate that willful control of respiration decreases respiratory sensation even at comparable levels of ventilation. In particular, moderate willful increases in ventilation produce an ameliorating effect on the sensation of breathing discomfort.

Ondine’s Curse and its Inverse Syndrome

Breathing is controlled separately by the autonomic and voluntary pathways, which are, at least partially, anatomically different1,2. Rarely, a discrete lesion of the central nervous system may produce a selective paralysis of one type of respiration, but spare another. Recently, we encountered a patient with the paralysis of autonomic respiration (Ondine’s curse) of unknown etiology, in whom the voluntary respiration remained intact. Then, we encountered another patient with its inverse clinical feature, in whom a localized, traumatic damage of the cerebral peduncle had induced a complete loss of voluntary respiration, while the autonomic respiration remained intact.

The effect of the level of ventilatory assist on the level of respiratory drive in decerebrate cats

The present study was undertaken to investigate whether, independent of changes in PaCO2, ventilatory assist influences not only the pattern but also the level of the respiratory drive. The experiments were performed on decerebrate and paralyzed cats ventilated by a phrenic-driven servo respirator at three different FICO2 levels (0, 0.30, 0.05). The level of ventilatory assist was altered within the range where PaCO2 did not exceed 80 Torr. A higher FICO2 accompanied a higher level of ventilatory assist. The relationship between the minute phrenic activity and log10 PaCO2 at a given FICO2 was linear. No significant difference was found in the regression lines at different levels of FICO2. We conclude that ventilatory assist has little effect on the respiratory drive at a constant level of chemical feedback during hypercapnia.

Thoracoscopic Electrode Implantation for Diaphragm Pacing in Dogs

Background: Diaphragm pacing is an attractive method of ventilatory support; however, it requires electrode implantation to the phrenic nerve or diaphragm. The thoracic approach is favored for several reasons, and it usually accompanies invasive bilateral thoracotomy. Objectives: This study was conducted to develop a new electrode suitable for video-assisted thoracoscopic implantation, which is less invasive than the conventional thoracic approach. Methods: The feasibility of video-assisted thoracoscopic implantation was tested with newly designed electrodes using 5 mongrel dogs. Furthermore, diaphragm pacing was performed for 60 min to test whether or not the implanted electrodes were functional. Results: Video-assisted electrode implantation was successful in all 5 cases. No complications occurred during the implantation procedure. In acute-phase pacing trials, the electrodes stimulated the phrenic nerves for 60 min without any pacing failures. The mean value of PaCO2 increased gradually from 32.2 ± (SEM) 1.52 to 54.6 ± 4.58 mm Hg, and the value of tidal volume decreased gradually from 242.9 ± 31.3 to 147.5 ± 24.5 ml in 60 min pacing. Conclusions: The thoracoscopic implantation of new electrodes was less invasive, and was a safe procedure for diaphragm pacing. Meticulous care should be taken to avoid muscle fatigue.

Are the Respiratory Responses to Changes in Ventilatory Assist Optimized

The input-output relationship of the CO2 respiratory controller can be described in two different ways. The first method is to describe the output as a function of the inputs; this type of controller model may be called a reflex controller model. The other method is to describe the relationship by an operating principle. The operating principle is often the minimization of a certain criterion or parameter; in this case, the controller is called an optimal controller. Several investigators have proposed that the respiratory controller responds to various stimuli in order to minimize certain criteria, which represent the energetic cost of breathing (3,4,9,13). In the concept proposed by Poon (9), the maintenance of arterial blood gas tensions and mechanical work are competing priorities for the respiratory controller, and the controller functions to minimize the net operating cost of both work and deviations of the blood gas tensions from given set points.

The Application of ARX Modelling to Ventilatory Control

Instability of the respiratory control system causes periodic breathing, and life-threatening hypoxia may also occur during this time. Simple analysis of the steady-state ventilatory response to hypercapnia or hypoxia is not sufficient to evaluate the stability of this system, because the respiratory control system has a number of negative feedback loops, as shown in Figure 1.