Biomedical subjects

T Ohdaira

Publications and source records attributed to T Ohdaira.

5 recordsLinked to original sources

PubMed1992

Effect of verapamil on ventilatory and circulatory responses to hypoxia and hypercapnia in normal subjects.

Recent investigations have shown that the calcium channel blocker verapamil attenuated the hypoxic ventilatory chemosensitivity of carotid body in animals. To determine whether this is also the case in humans, transient physiological chemodenervation by O2 breaths (withdrawal test) during sustained hypoxia (N = 7), and ventilatory and circulatory responses to progressive hypoxia and hypercapnia (N = 8) were examined after oral administration of verapamil. During sustained hypoxia after verpamil, there was a significant reduction of withdrawal response from 5th to 25th min value (p < 0.01), but not after placebo. On the other hand, no significant difference in ventilatory responses to progressive hypoxia and hypercapnia was observed after verapamil. Verapamil run reveals similar features with placebo run in circulatory parameters except blood pressure response, which tended to be suppressed by verapamil. We conclude that verapamil attenuates peripheral chemoreceptor activity with time during sustained mild hypoxia in normal adult humans and this may be explained by delayed depletion in intracellular Ca2+ for chemotransduction of the peripheral chemoreceptors.

Administration, Oral↗

PubMed1992

Dependence of biphasic heart rate response to sustained hypoxia on magnitude of ventilation in man.

We studied the dynamic profile of respiratory and circulatory activities during sustained isocapnic hypoxia in healthy males. In response to end-tidal PO2 depression to about 55 Torr, minute ventilation first increased briskly and then depressed. Such biphasic response to hypoxia was also observed in the heart rate. A significantly positive correlation was found between the magnitudes of ventilatory and heart rate responses. No significant increases were found in arterial noradrenaline and potassium, but adrenaline significantly increased gradually with time. Furthermore, when VT and f were intentionally maintained constant so as to prevent the biphasic ventilatory change, the biphasic heart rate response previously seen in spontaneous hypoxic breathing disappeared. We suggest that the heart rate is mainly determined by the pulmonary vagal inflation reflex. Putative neurochemicals to elicit hypoxic ventilatory depression, and arterial catecholamine and potassium concentrations may not be directly related to the specific profile of the biphasic heart rate response during moderate hypoxia.

Adult↗

PubMed1992

[Respiratory control in diffuse interstitial lung disease].

Whether the change of lung volume affect ventilatory responsiveness to chemical stimuli has not been studied in patients with interstitial lung disease (ILD). We measured the responses of minute ventilation (VE), tidal volume (VT), and occlusion pressure (P0.1) to hypercapnia (HCVR) and hypoxia (HVR) in these patients. Breathing efficiency (delta VE/delta P0.1) and effective compliance (delta VT/delta P0.1) were also measured under the same stimuli. 1) HCVR and HVR were measured in one female patient with hypersensitivity pneumonitis. VE responses during low VC phase (VC; 71% of predicted value) were similar to that during increased VC phase (VC; normal level) in both HCVR and HVR. However, VT responses of low VC phase were lower than those of increased phase, and P0.1 responses of low VC phase were higher than those of increased VC phase. Both breathing efficiency and effective compliance of low VC phase were lower than those of increased VC phase. 2) Thirty one patients with ILD were divided into two groups: low VC group; VC < 80% of predicted value, and normal VC group; VC > 80% of predicted value. HCVR and HVR were compared between two groups. Mean values of VE response to hypercapnia and hypoxia in low VC group were lower than those of in normal group, although they were not significantly different. VT response to hypercapnia and hypoxia were significantly lower of low VC group than those of normal VC group. Mean values of P0.1 responses to hypercapnia and hypoxia of low VC group were higher than those of normal VC group, although they were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Dynamic profile of cardiovascular activity in relation to augmented ventilation and humoral agents during hypercapnic hypoxia.

A time course of cardiovascular activity in 8 healthy males in relation to augmented ventilatory activity and humoral factors was observed during step CO2 elevation with constant hypoxia. During the first step increase, by 3 Torr in end-tidal PCO2 (PETCO2), the heart rate (HR) initially tended to decrease, then slowly increased to slightly below that of the previous eucapnic level, whereas ventilation maintained a gradual rise throughout this period. On the other hand, during second step PETCO2 elevation, by a further 3 Torr, both HR and ventilation progressively increased. The plasma catecholamine (CA) concentration was also significantly elevated during this period, suggesting a concomitant enhancement in sympathetic activity. Blood pressure (Bp) was progressively augmented throughout the entire hypoxic challenge. We conclude that 1) the characteristic profile of HR change may be explained by the observation that initial HR depression by peripheral chemoreceptor stimulation is gradually overridden by delayed hyperventilation, CA elevation, and enhanced sympathetic activity; 2) Bp augmentation may be elicited by increased CA release and sympathetic activity; and 3) plasma K+ concentration does not change so as to affect cardiovascular and respiratory activity.

Adult↗

PubMed1990

Contribution of chemical and non-chemical drives to breath-holding determined by visual analog scale (VAS).

Chemical and non-chemical contributions to breath-holding time (BHT) were directly determined by using a visual analog scale (VAS). These values were compared with those indirectly calculated from the method proposed by Godfrey and Campbell (1968). The magnitude of non-chemical factor at low PCO2 in our study was substantially less than the one obtained by the above investigators. We conclude that Godfrey and Campbell's model postulating linear augmentation of non-chemical sensation is inappropriate to explain dyspnea profile during breath-holding.

Biometry↗