Biomedical subjects

T Natsui

Publications and source records attributed to T Natsui.

At least 19 recordsLinked to original sources

PubMed1998

Effects of extracellular calcium and magnesium on central respiratory control in the brainstem-spinal cord of neonatal rat.

The influence of extracellular Ca2+ and Mg2+ concentrations ([Ca2+]ECF and [Mg2+]ECF, respectively) on central respiratory control was analyzed using the isolated brainstem-spinal cord of the neonatal rat. Central respiratory activity was recorded from the C4 ventral roots. The depth profile of [Ca2+]ECF below the ventral medullary surface was measured with ion-sensitive electrodes. The gradient in [Ca2+]ECF disappeared about 1 h after changing superfusate Ca2+ ([Ca2+]CSF) from 2 to 0.5 mM, but not even in 2 h after switching to Ca2+-free superfusate. High [Ca2+]CSF (4 mM) or high [Mg2+]CSF (4, 8 mM) decreased respiratory frequency (fR), whereas low [Ca2+]CSF (0.5 mM) increased fR and augmented the respiratory CO2 responsiveness. High [Ca2+]CSF as well as low [Mg2+]CSF (0.5 mM) disturbed respiratory rhythm and pattern, which were markedly restored by high CO2. The depressing effect of high [Ca2+]ECF and the stimulating effect of low [Ca2+]ECF on the medullary neuronal activity were confirmed by perforated patch recordings. These results suggest that [Ca2+]ECF and [Mg2+]ECF determine the excitability of the respiratory neuron network by modulating the neuronal surface potential, transmembrane Ca2+ influx, Ca2+-sensitive cation channel gating, and synaptic transmission. Furthermore, some of these actions appear to be antagonized by CO2/H+.

Animals↗

PubMed1994

Central hypoxic depression of respiration determined by perfusing a recipient cat's carotid bodies with blood from a donor cat.

The respiratory response to sustained hypoxia reflects the net effect of the peripheral chemoreceptor excitation and the central depression. To obtain a pure depressant effect of central hypoxia (alv. PO2, 35-75 mmHg) on respiration, the recipient cat's carotid bodies were vascularly isolated and bilaterally perfused with blood from a donor cat. Cats were anesthetized, vagotomized, paralyzed, and artificially ventilated. Alv. PCO2 was kept at a normal value (iso- and normocapnia) throughout the experiment. The minute integrated phrenic nerve activity (Min. PNA) was used as an indication of inspiratory activity. The Min. PNA at which the recipient and donor cats were both breathing room air (central normoxia and peripheral chemoreceptor normoxia) was taken as 100% (control), and Min. PNA expressed as a percentage of the control was measured in a series of three experiments (A, B, and C): experiment A (normoxia-hypoxia; central normoxia and peripheral chemoreceptor hypoxia), experiment B (hypoxia-hypoxia; central hypoxia and peripheral chemoreceptor hypoxia), and experiment C (hypoxia-normoxia; central hypoxia and peripheral chemoreceptor normoxia). At alv. PO2 of about 50 mmHg, Min. PNA was 169.7 +/- 23.6% (mean +/- SD) in experiment A, 127.3 +/- 22.0% in experiment B, and 71.6 +/- 17.3% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 50 mmHg) was 42.4% (= 169.7-127.3) or 28.4% (= 100-71.6). At alv. PO2 of about 40 mmHg, Min. PNA was 185.2 +/- 16.8% in experiment A, 146.2 +/- 19.0% in experiment B, and 54.8 +/- 15.2% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 40 mmHg) was 39.0% (= 185.2-146.2) or 45.2% (= 100-54.8). From these results, we concluded that a pure depressant effect of normocapnic central hypoxia (alv. PO2, 40-50 mmHg) was 28-45% and this was affected by a stimulating drive from the peripheral chemoreceptors.

Animals↗

PubMed1991

Characteristics of inspiratory inhibition by occlusion of both external carotid and basilar arteries in cats.

Effects of the occlusion of both the external carotid and basilar arteries on the inspiratory activity were studied in anesthetized, vagotomized, paralyzed, and artificially ventilated cats. Integrated phrenic nerve activity was used as an index of the inspiratory activity. Blood pressure in the lingual artery, located downstream from the occluded external carotid arteries, was measured as the arterial pressure of the upper brain stem during occlusion. The basilar artery was occluded at the boundary between the medulla and pons. Occlusions of the external carotid arteries and basilar artery suppressed the phrenic nerve activity to finally disappear within 1 min (phrenic nerve apnea, 45 out of 50 occlusions in 6 cats). The blood pressure in the upper brain stem was 16.6 +/- 5.7 mmHg (mean +/- S.D.) during occlusions. These effects of occlusion on the phrenic nerve activity were also observed during hypercapnia and hypoxia, although they were not so remarkable as those during normocapnia and normoxia. The results indicate that the upper part of the brain stem operates a profound facilitatory mechanism on the medullary inspiratory activity.

Animals↗

PubMed1990

Respiratory responses to occlusion or hypercapnic blood injection of the anterior inferior cerebellar artery in cats.

To examine whether the central chemoreceptors of respiration are located in the perfused area of the anterior inferior cerebellar artery (AICA), we occluded arteries or injected hypercapnic blood into arteries in the ventral surface of the medulla in anesthetized, paralyzed, and peripherally chemodenervated cats. Phrenic nerve activity, as an index of respiratory output, was augmented by an injection of hypercapnic blood into the vertebral artery. This vertebral-injection response decreased during bilateral occlusion of AICA. However, responses of phrenic nerve activity to the occlusion of AICA were complicated; activity increased in 19 cats, did not change in 10, and decreased in 9 during occlusion. In experiments with blood of various PCO2 levels being bilaterally injected into AICA, phrenic discharges increased with increases of PCO2. During the injection of constant PCO2 blood into AICA, phrenic response to alveolar PCO2 decreased by 80% compared with the original response. From these results, the blood flow and blood PCO2 level of AICA seemed to be related to the central chemosensitivity for respiration. To examine the perfused area, the ventral surface pH of the medulla was measured with a micro-combination pH electrode (2 mm diameter). During the injection into AICA, pH in the rostral medulla depended on the PCO2 of injected blood, and pH in other areas depended on the PCO2 of systemic blood. Also, histological study of India ink injection into AICA showed that ink-filled vessels were exclusively observed in the rostral medulla. Thus, we conclude that at least part of the central chemoreceptors of respiration are located in the perfused area of AICA, that is, in the rostral medulla.

Animals↗

PubMed1988

Inspiratory response to occlusion of arteries in the ventral surface of the medulla in anesthetized cats.

By the occlusion of arteries in the ventral surface of the medulla, the blood supply to the central chemoreceptor for respiration was examined in anesthetized, paralyzed and peripheral chemodenervated cats. Phrenic nerve activities (P.N.A.), as an index of the respiratory center output, increased with an injection (3 ml/min, 10 sec) of hypercapnic blood (PCO2 = 104.5 mmHg) into the vertebral artery (VA injection response). The VA injection responses during occlusion of arteries in the ventral surface of the medulla were classified into three groups: 1) The response disappeared by the bilateral occlusion of the anterior inferior cerebellar arteries (AICA) in 8 out of 29 cats. 2) The response disappeared by the occlusion of both AICA and the posterior inferior cerebellar arteries (PICA) in 9 cats. 3) The response did not disappear in spite of the additional occlusion of several branches from the basilar artery in 11 cats, although the response had diminished. These different results may be due to the complexity of the central chemosensitive structure or of the central vascular system. However, among arteries the AICA blood flow seemed to be most preferentially related to the VA injection response. Thus, at least a part of the central chemosensitive structure may be located in the area perfused by the AICA.

Animals↗

PubMed1987

Effect of hypercapnic blood injection into the vertebral artery on the phrenic nerve activity in cats.

Hypercapnic blood was injected into the vertebral artery in anesthetized and paralyzed cats. The stimulating effect on the phrenic nerve activity was dependent on the injection rate, duration, and PCO2 level of the injected blood. The time delay from the start of injection to the onset of increase in phrenic nerve activity was inversely proportional to both the injection rate and the PCO2 of injected blood.

Animals↗

PubMed1985

Effect of inactivation of carotid sinus nerve by cold block on phrenic nerve activity in cats.

The effect of the elimination of input via the carotid chemoreceptor on respiratory output was examined quantitatively in anesthetized, vagotomized, and paralyzed cats. The integrated phrenic nerve activity (PNA) was recorded as an indication of output of the respiratory center. Also, the elimination of the carotid chemoreflex drive was repeatedly done by a cold block of the carotid sinus nerve at various PCO2 levels during hyperoxia, normoxia, and hypoxia. The blockade induced a reduction in PNA at each PCO2 level in every PO2 group. If the highest PNA value recorded at a high PCO2 in each PO2 condition was assigned a value of 100%, the reduction of the PNA by the blockade, i.e., the respiratory effect of the carotid chemoreflex drive, would be slightly larger during normoxia (16%) than during hyperoxia (8.7%), but would be independent of PCO2. During hypoxia, this chemoreflex effect was about 40% of a low PCO2, and decreased with increments of PCO2, finally reaching about 20% of a high PCO2 level. Furthermore, the relative contribution of the carotid chemoreceptor to respiratory output, expressed as the ratio of the PNA reduction during blockade to the PNA before blockade, was inversely proportional to both PO2 and PCO2. It is concluded that the interaction of the peripheral and central chemoreceptor drive is hypoadditive at moderate and high PCO2 levels in anesthetized cats, and this interaction is emphasized by central hypoxia.

Animals↗

PubMed1981

Effect of arterial [H+] on threshold PCO2 of the respiratory system in vagotomized and carotid sinus nerve denervated cats.

Phrenic nerve discharges were recorded as an output of respiratory activity in anaesthetized, vagotomized cats immobilized by gallamine and artificially ventilated with room air. 2. With the carotid sinus nerve (c.s.n.) intact or denervated, PcO2 threshold levels (Pth, CO2) were determined at arterial pH, varied between 7.0 and 7.6 ([H+] 25-100 nM) by successive intravenous infusions of 0.5 N-HCl or 1.0 M-NaHCO3. Ventilation was increased stepwise to induce a successive decrease in end-tidal PCO2. Pth, CO2 was defined as the level of end-tidal PCO2 at which phrenic discharges ceased. 3. With the c.s.n. intact, Pth, CO2 decreased linearly upon increasing arterial [H+]. The mean regression line, calculated from seven cats, was Pth, CO2 =-0.37 [H+] + 34.33. A similar inverse relationship was observed with the c.s.n. denervated. However, the slope of the regression line was significantly smaller, the mean regression line/eleven cats) being Pth,CO2 =-0.18 [H+]+ 35.06. 4. The relative contributions of arterial [H+] and PCO2 in stimulating the peripheral and central chemoreceptors could be estimated quantitatively. Arterial [H+] appears to be almost equally effective on both peripheral and central chemoreceptors; PCO2 acts exclusively on the central chemoreceptors. 5. Thus, the additive theory regarding the induction of respiratory activity by arterial [H+] and PCO2 was confirmed. In addition, the H+ drive was shown to be able to affect respiratory activity even in the absence of the peripheral chemoreceptors.

Animals↗

PubMed1980

Analysis of dynamic change in phrenic nerve activity following a sudden decrease in alveolar carbon dioxide.

The effects of a sudden decrease in alveolar CO2 concentration (FCO2) on phrenic nerve activity (PNA) were studied in anesthetized and paralzyed cats. The vago-sympathetic and carotid sinus nerves were sectioned. The peak of integrated PNA was used as an index of the central inspiratory activity. 1) FCO2 decreased immediately and curvilinearly after hyperventilation. However, PNA did not change during the initial period of hyperventilation. After this time delay (Dt), the PNA began to decrease linearly over a certain period and finally disappeared. Toff, the time from the onset of hyperventilation to the disappearance of PNA, was in the range of 30-250 sec. This was related to both the level of FCO2 in a control period and the rate of decrease in FCO2 during hyperventilation, but Dt was mostly independent of these values. Mean (with SD) Dt was 10.68 +/- 7.01 sec (n = 68, from 6 cats). 2) VCO2, the quantity of CO2 eliminated through the lung during Toff, was measured in each experimental run. The VCO2 was directly proportional to the level of control FCO2 and, at a given level of control FCO2, was almost identical, irrespective of the different rates of decrease in FCO2. 3) We concluded that Dt is the time required for a change in the hydrogen ion concentration, [H+], in the brain interstitial fluids bathing the central chemosensitive structures, and that the central inspiratory activity, in the absence of the peripheral chemoreceptors, will be a single function of the [H+] in these fluids.

Animals↗

PubMed1975