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Introduction Developing prognostic markers can be useful for clinical decision‐making. Peripheral blood (PB) examination is simple and basic that can be performed in any facility. We aimed to investigate whether PB examination can predict prognosis in coronavirus disease (COVID‐19). Methods Complete blood count (CBC) and PB cell morphology were examined in 38 healthy controls (HCs) and 40 patients with COVID‐19. Patients with COVID‐19, including 26 mild and 14 severe cases, were hospitalized in Juntendo University Hospital (Tokyo, Japan) between April 1 and August 6, 2020. PB examinations were performed using Sysmex XN‐3000 automated hematology analyzer and Sysmex DI‐60 employing the convolutional neural network‐based automatic image‐recognition system. Results Compared with mild cases, severe cases showed a significantly higher incidence of anemia, lymphopenia, and leukocytosis (P

Article, International journal of laboratory hematology. 43(2): 281-289(2021)

Genome-wide association studies have revealed several susceptibility genes among patients with autoimmune thyroid disease (AITD), including CTLA4, PTPN22, FCRL3, and ZFAT. However, any possible association between these genes and AITD prognosis remains unknown. The objective of this study was to identify associations between polymorphisms of these genes and AITD prognosis. We genotyped functional polymorphisms, including CTLA4 CT60, CTLA4 +49A/G, CTLA4 -1147C/T, CTLA4 -318C/T, PTPN22 -1123C/G, PTPN22 SNP37, CD40 -1C/T, FCRL3 -169C/T, ZFAT Ex9b-SNP10, and ZFAT Ex9b-SNP2, in 197 AITD patients carefully selected from 456 registered AITD patients, and 86 control subjects. The restriction fragment length polymorphism method was used for genotyping. The CD40 -1CC genotype and C allele were significantly more frequent in patients with Graves’ disease (GD) in remission than in those with intractable GD (P = 0.041 and P = 0.031, respectively). The FCRL3 -169TT genotype was significantly less frequent in patients with intractable GD than in those with GD in remission (P = 0.0324). For a ZFAT Ex9b-SNP10 polymorphism, the TT genotype and T allele were significantly more frequent in patients with severe Hashimoto’s disease (HD) than in those with mild HD (P = 0.0029 and P = 0.0049, respectively). For a CTLA4 CT60 polymorphism, the antithyrotropin receptor antibody levels at the onset of GD were significantly higher in those with the GG genotype than in those with other genotypes (P = 0.0117). CD40 and FCRL3 gene polymorphisms were associated with GD intractability, and ZFAT polymorphism was associated with HD severity but not its development.

Respiratory afferent stimulation can elicit increases in respiratory motor output that outlast the period of stimulation by seconds to minutes [short-term potentiation (STP)]. This study examined the potential contribution of spinal mechanisms to STP in anesthetized, vagotomized, paralyzed rats. After C1 spinal cord transection, stimulus trains (100 Hz, 5–60 s) of the C1-C2 lateral funiculus elicited STP of phrenic nerve activity that peaked several seconds poststimulation. Intracellular recording revealed that individual phrenic motoneurons exhibited one of three different responses to stimulation: 1) depolarization that peaked several seconds poststimulation, 2) depolarization during stimulation and then exponential repolarization after stimulation, and 3) bistable behavior in which motoneurons depolarized to a new, relatively stable level that was maintained after stimulus termination. During the STP, excitatory postsynaptic potentials elicited by single-stimulus pulses were larger and longer. In conclusion, repetitive activation of the descending inputs to phrenic motoneurons causes a short-lasting depolarization of phrenic motoneurons, and augmentation of excitatory postsynaptic potentials, consistent with a contribution to STP.

Inhalation of furosemide, a loop diuretic, has shown favorable effects on experimentally induced cough, bronchoconstriction, and dyspnea. The effect of inhaled furosemide on tracheobronchial receptors was studied in anesthetized, spontaneously breathing rats. Single unit or pauci unit activity was recorded from the right vagus nerve. Tracheobronchial receptors were classified into slowly and rapidly adapting receptors (SARs and RARs, respectively), based on their adaptation index (AI), which was derived from the decrease in spike frequency (sf) over 2 s, expressed as a percentage of the peak firing rate. There were 43 SARs (AI/= 25%) and eight RARs (AI/= 50%). Inhalation of furosemide (n = 29) increased the slope of airway pressure (Paw) versus sf of SARs from 8.6 to 14.8 Hz/cm H(2)O with an increase in sf at Paw = 0 cm H(2)O from 18.0 to 49.5 Hz, resulting in an upward shift of the line. Neither inhalation of vehicle (n = 9) nor intravenous injection of furosemide (n = 5) changed this relationship. In addition, inhalation of furosemide attenuated the activity of RARs. These findings indicate that SARs are sensitized and RARs desensitized by inhalation of furosemide. We discuss possible mechanisms for this, and its relevance to clinical problems of dyspnea, bronchoconstriction, and cough.

The characteristics of GABAergic inhibitory modulation of respiratory bulbospinal neuronal activity and short-term potentiation (STP) of phrenic motoneuronal activity were studied. Extracellular unit recording and picoejection techniques in anesthetized dogs showed that both the spontaneous rhythmic and reflexly induced discharge patterns of inspiratory (I) and expiratory (E) premotor neurons were proportionately amplified by the localized application of picomole amounts of bicuculline (Bic), a competitive GABAA antagonist. Intracellular recording and paired-pulse stimulation techniques in anesthetized rats demonstrated an STP of phrenic motor output that appears to be mediated by NMDA receptors and is associated with facilitation of EPSPs and prolonged depolarization of individual phrenic motoneurons. We speculate that both GABAergic gain modulation of premotor neuronal activity and NMDA-mediated STP of phrenic activity may be neural substrates which are involved with the optimization of respiratory and non-respiratory behaviors, via adaptive and/or differential control of breathing.

Afferent input from pulmonary stretch receptors is important in the control of the timing of inspiratory and expiratory phases of the respiratory cycle. The current study was undertaken to identify neurons within a column of respiratory neurons in the ventrolateral medulla (termed the ventral respiratory group, VRG) that, when activated by lung inflation, produce the Breuer–Hering (BH) reflex in which lung inflation causes inspiratory termination and expiratory prolongation. Intracellular recordings of VRG neurons revealed three groups of inspiratory (I) and two groups of expiratory (E) neurons similar to previous descriptions: I-augmenting (I-Aug), I-decrementing (I-Dec), I-plateau (I-All), E-augmenting (E-Aug), and E-decrementing (E-Dec) neurons. Low-intensity, low-frequency stimulation of a vagus nerve elicited paucisynaptic EPSPs in E-Dec, I-Aug, and I-All neurons that could be divided into two groups on the basis of latency (2.8 ± 0.1 msec,n = 10; 4.0 ± 0.1 msec,n = 17). IPSPs were elicited in I-Aug and I-All neurons (4.8 ± 0.1 msec,n = 12). However, only E-Dec neurons were depolarized when the BH reflex was activated by lung inflation (7.5 cm H2O) or mimicked by vagus nerve stimulation (50 Hz). All other neurons were hyperpolarized and ceased firing during BH reflex-mediated expiratory prolongation. A subset of E-Dec neurons (termed E-Decearly) discharged before inspiratory termination and could contribute to inspiratory termination. The findings are consistent with the hypothesis that a group of E-Dec neurons receives a paucisynaptic (probably disynaptic) input from pulmonary afferents and, in turn, inhibits inspiratory neurons, thereby lengthening expiration.

It was hypothesized that, because rats appear to lack a prominent disynaptic projection from the dorsal respiratory group to phrenic motoneurons (Phr), they would lack the short-latency excitation of Phr output seen in cats in response to stimulation of some cranial nerve afferents. Single-pulse superior laryngeal nerve (SLN) stimulation elicited a short-latency bilateral excitation of glossopharyngeal (IX) and hypoglossal (XII) nerves and an ipsilateral excitation of pharyngeal branch of vagus (PhX) in 67% of rats, but no excitation of Phr. Vagus (X) stimulation elicited a bilateral excitation of Phr and a predominantly ipsilateral excitation of IX and PhX. Single-pulse stimulation of SLN or X also elicited longer-latency, bilateral decreases in activity of all recorded nerves. Repetitive stimulation (50 Hz) of SLN or X suppressed inspiratory activity and prolonged expiration. Lung inflation (7.5 cmH2O) inhibited Phr and PhX activity; X stimulation inhibited Phr but prolonged PhX activity. In conclusion, rats predictably lack the SLN-induced short latency Phr excitation but exhibit other short latency reflexes for which the underlying circuitry is not clear.

The detailed morphology of rat phrenic motoneurons (PMs) was studied in 40 electrophysiologically identified cells with intracellular injection of Neurobiotin. In 15 cells, the dendritic trees were fully analyzed by using path-distance analysis, and total surface area and volume were estimated. Based on their relative onset times (ROT; i.e., the time of firing onset relative to the onset of whole phrenic activity), PMs were classified into three types; early recruited (type E; ROT10%), late recruited (type L; ROT12.5%), and quiescent (type Q; not recruited under normal conditions). Dendrites constituted 93.3% of the surface area of cells and 38.9% of the cell volumes. The number of primary dendrites (nPD) averaged 10.1, and the mean number of terminations was 38.8. The combined diameters of primary dendrites of PMs correlated well with the total dendritic surface area and the number of dendritic terminations. Comparisons among cell types revealed that type Q cells had greater dendritic surface areas and volumes than type E or type L cells. With path-distance analysis, this difference was found to be due to differences between the cell types in the numbers of their dendrites, their combined dendritic lengths, and the number of their branches. The differences between these data and those available for cat motoneurons are discussed. The input resistance of PMs correlated with their total surface area but did not correlate with their somal surface area, indicating that, in rat, PM input resistance is a function of the entire neuronal membrane rather than of the somal surface alone.

A novel SAAF was isolated from the title ascidian. The structure was elucidated using the entire sample of 4 nmol, suggesting that the position of the OH group confers genus-specificity to sperm chemotaxis in ascidians. This study not only provides insight into the chemical tactics in sperm chemotaxis but demonstrates that the innovative techniques allow structure determination of natural products in trace amounts.

Electrophysiological properties of phrenic motoneurons (PMs) were studied by intracellular recordings in anesthetized, paralyzed, and artificially ventilated adult rats. Our results revealed that rat PMs, as compared to cat PMs, had a shorter afterhyperpolarization duration (55 +/- 13 ms; mean +/- SD), a narrower half-width of action potential, a larger membrane input resistance (Rm; 2.0 +/- 0.6 M omega), a smaller rheobase (Irh) and a shorter minimum paired pulse interval to provoke the second spike (1.9 +/- 0.6 ms). These features indicate that the rat PMs possess higher frequency responsiveness than cat PMs. Based on the time of firing onset relative to the onset of whole phrenic nerve activity (relative onset time; ROT) or on the absence of discharge during inspiration, the PMs could be classified into four types: early recruited with ROT10.0%; late recruited with 12.5%ROT37.5%; very late recruited with ROT45%, and quiescent which was not recruited during normal experimental conditions. A number of differences in the membrane properties such as end-expiratory membrane potential, Rm, and Irh among the four cell types are discussed in relation to the recruitment order. Inhibitory postsynaptic potentials (IPSPs) were present during the late expiratory phase (stage II expiration) in all PMs tested.

Cyanate derivatives such as NaOCN have been known to increase the hypoxia tolerance of animals by increasing the affinity of hemoglobin (Hb) to O(2). To clarify the mechanism of this increase in hypoxia tolerance, we examined changes in metabolic rate and cardiovascular parameters during a hypoxia test in halothane-anesthetized, NaOCN-treated and spontaneously breathing rats (50 mg/kg/d S.C., 10 d). Control animals received saline. The capillary density in the skeletal muscle (sternocleidomastoid muscle), cardiac papillary muscle and medulla oblongata was also examined histologically. The Hb-O(2) affinity index, P(50), decreased from 38 (control rat) to 24 mmHg in NaOCN-treated rats. During hyperoxic gas breathing, the rat treated with NaOCN showed a significantly lower metabolic rate (V(.)O(2), V(.)CO(2)), higher cardiac stroke volume, slower heart rate, lower PvO(2), and lower O(2) extraction ratio than those in control rats. The NaOCN-treated rats exhibited well-maintained arterial blood pressure and a larger cardiac output response to reduction in FIO(2) to 0.10-0.08. The increase in O(2) extraction ratio with reduction in FIO(2) was larger in NaOCN-treated than in control rats. The circulatory and metabolic depressions at FIO(2) 0.05 were effectively attenuated in NaOCN-treated rats. The capillary density of the cardiac muscle and medulla oblongata but not the skeletal muscle was significantly higher in NaOCN-treated rats than in control rats. The greater hypoxia tolerance in NaOCN-treated rats is ascribed to the combined effects of left shift of Hb-O(2) dissociation curve, lower basal V(. )O(2), higher capillary density in the heart, and brain, and other adaptive mechanisms induced probably by prolonged tissue hypoxia.

We studied the patterns of membrane potential changes in laryngeal motoneurons (LMs) during vocalization, coughing, swallowing, sneezing, and the aspiration reflex in decerebrate paralyzed cats. LMs, identified by antidromic activation from the recurrent laryngeal nerve, were expiratory (ELMs) or inspiratory (ILMs) cells that depolarized during their respective phases in eupnea. During vocalization, most ELMs depolarized and most ILMs hyperpolarized. Some ILMs depolarized slightly during vocalization. During coughing, ELMs depolarized abruptly at the transition from the inspiratory to the expiratory phase. In one-third of ELMs, this depolarization persisted throughout the abdominal burst. In the remainder (“type A”), it was interrupted by a transient repolarization. ILMs exhibited a membrane potential trajectory opposite to that of type A ELMs during coughing. During swallowing, the membrane potential of ELMs decreased transiently at the onset of the hypoglossal burst and then depolarized strongly during the burst. ILMs hyperpolarized sharply at the onset of the burst and depolarized as hypoglossal activity ceased. During sneezing, ELMs and ILMs exhibited membrane potential changes similar to those of type A ELMs and ILMs during coughing. During the aspiration reflex, ELMs and ILMs exhibited bell-shaped hyperpolarization and depolarization trajectories, respectively. We conclude that central drives to LMs, consisting of complex combinations of excitation and inhibition, vary during vocalization and upper airway defensive reflexes. This study provides data for analysis of the neuronal networks that produce these various behaviors and analysis of network reorganization caused by changes in dynamic connections between the respiratory and nonrespiratory neuronal networks.

To clarify the control mechanism of ventilation during posture change, ventilatory parameters, PETCO2, and ventilatory response to CO2 were examined in 11 healthy male subjects at supine (0 degrees) and 75 degrees head-up tilt positions. Minute expiratory ventilation (V.E), tidal volume (VT), respiratory frequency (f), end-tidal and transcutaneous PCO2 and CO2 output (V.CO2), and ventilatory response to CO2 were measured during a steady state condition. V.E (V.A) and VT increased significantly at 75 degrees tilt with significant decrease in PETCO2 from 40.1 mmHg (0 degrees) to about 36.1 mmHg (75 degrees). Transcutaneous PCO2 also decreased during tilt, by 3.3 mmHg. Physiological dead space (VD/VT) and V.CO2, however, remained unchanged, and ventilatory equivalent (V.E/V.CO2, V.A/V.CO2) increased significantly. The CO2-ventilatory response curve shifted upward (or leftward) without significant change in the response slope. At 75 degrees tilt, EMG activity of gastro-cnemius muscle increased. These findings suggested that PETCO2 decreased because of increased V.E (V.A) with a leftward shift of CO2-ventilatory response curve. Various signals such as afferents from lower extremities might have net stimulatory effects on a CO2-ventilation control system to reset the controlled level of PETCO2 to a lower range, but without significant change in CO2-ventilatory response during upright position.

Whether or not stimulation of the peripheral chemoreceptors by hypercapnic-hypoxic exposure results in a long-lasting increase in ventilatory activities was studied using the steady state CO2 response test on 12 human subjects. The degree of hypercapnic hypoxia was end-tidal PCO2 (PETCO2) 42.1 +/- 3.0 and PO2 (PETO2) 39.8 +/- 4.7 mmHg, lasting for 5 min. Minute ventilation values at PETCO2 45 mmHg (V45) and PETCO2 at minute volume 15 liter . min-1 (P15) were calculated from the respective CO2 response curves. The differences in V45 and P15 between the control and the 30 min test group were found to be significant (p less than 0.05). These results suggested the left- and upward-shift of the CO2 response curve of the 30 min test group. On the other hand, in 5 of the 12 subjects, three successive CO2 response tests conducted at 0, 30, and 90 min without hypercapnic-hypoxic exposure showed fairly reproducible results, and no statistically significant differences were found between any of the above trials with the parameters S, B, V45, and P15. These results indicated that the CO2 response curve obtained by using the steady state method can be effected for at least 30 min even if the stimulation of the peripheral chemoreceptors is only for brief periods.

Overall gain of the O2-ventilation feedback control system (GO2) was determined in 9 male and one female healthy subjects. GO2 progressively increased with decreasing end-tidal PO2 (PETO2). This value did not exceed the overall gain of the CO2-ventilation feedback system (GCO2) even at a PETO2 level of 40 mmHg, suggesting that hypoxic stimulation did not become predominant in the present experimental condition. With addition of 250 ml of external dead space, PETO2 decrement (delta PETO2 X actual) was experimentally observed. The delta PETO2 X actual thus obtained was found to be in good agreement with the PETO2 decrement deduced from GO2 (delta PETO2 X expected). This result was similar to that found in the PETCO2 change previously seen in normoxia.

The steady-state ventilatory responses to hypercapnia and hypoxia in 7 assisted breath-hold divers (Funado) were compared with those in 7 normal sedentary controls. Ventilatory response to hypercapnia was measured from the slope of the hyperoxic VN-PETCO2 line, where VN was normalized minute ventilation using the allometric coefficient and PETCO2 end-Tidal PCO2. The slope of this line in the Funado (1.48 +/- 0.54 liters . min-1 . Torr-1) was significantly less than in the control (2.70 +/- 1.08 liters . min-1 . Torr-1) (p less than 0.025). On the other hand, hypoxic sensitivity estimated by hyperbolic and exponential mathematical equations was not found to be significantly different between the two groups, although estimated increments in ventilation using the hyperbolic equation exhibited significantly lower response in the Funado than in the control only when PETO2 decreased lower than 50 Torr (p less than 0.05). These findings in the Funado were different from our previous observations obtained in unassisted breath-hold divers (Kachido), in whom no obvious attenuations in CO2 sensitivity were seen. This difference was assumed to be derived from more hypercapnic and hypoxic conditions produced in the Funado than in the Kachido during diving activities.

The ventilatory response to CO2 in rats under sodium pentobarbital anesthesia has been measured using the rebreathing technique. The animal rebreathed through a tracheal cannula for a period of 4 min from an apparatus of 200–400 ml capacity, containing 5–6% CO2 in O2.\(P_{{\text{CO}}_{\text{2}} } \) in the rebreathing apparatus (PappCO2), instantaneousVT,f, and\(\dot V_{\text{E}}\) were monitored before, during, and after rebreathing. During the rebreathing run,PappCO2 andPaCO2 rose linearly from 35–40 to 65–70 mm Hg; there was no significant difference betweenPappCO2 andPaCO2 at any time during rebeathing.VT and\(\dot V_{\text{E}}\) increased almost linearly with the rise inPappCO2, whilef increased to a maximum within 2 min of rebreathing. In the rat,VT regulation seemed to operate exclusively as a proportional control system in response to linearly increasing CO2 stimulus. The slopes ofPappCO2,VT or\(\dot V_{\text{E}}\) response curves varied considerably during the time course of the experiment, depending upon the level of anesthesia, even though there was no large change in\(\dot V_{\text{E}}\) in the control periods which were under hyperoxic conditions. However, a significant linear relationship was seen betweenf in the respective control period and the slope ofPappCO2-VT response at various levels of anesthesia. We concluded that the rebreathing technique can be applied in small experimental animals and that changes in the sensitivity of the respiratory control system to a CO2 stimulus by anesthesia can be easily monitored by repeating the rebreathing test.

Fifty-two active Judo athletes were examined using an isocapnic progressive hypoxia test. The results were analyzed by the hyperbola ventilation equation V = VO + A/(PETO2--C), where V is observed ventilation, VO the horizontal asymptote in ventilation for infinite end-tidal PO2(PETO2), A the slope constant indicating magnitude of hypoxic sensitivity, and C the vertical asymptote in PETO2 for infinite ventilation. Hypoxic sensitivity, A, was positively correlated with body weight (BW). Such correlation in the light and middleweight groups (BW less than 95 kg) and the heavyweight group (BW greater than 95 kg) with Röhrer's index being less than 200 became insignificant when the A value was recalculated after normalization of ventilation for 70 kg body mass. However, the heavyweight group with Röhrer index of higher than 200 still exhibited a significantly higher A value than the light and middleweight groups after normalization of ventilation. These results indicated that body weight plus obesity were determining factors in the increase of hypoxic sensitivity in our subjects.

The hypoxic ventilatory response of the anesthetized rat was measured using a progressive hypoxia test whilst end-tidal Pco2 was maintained at a constant level. The ventilatory response to hypoxia was expressed by the equation, VE = Vo + A/(Pao2-C)(VE, total ventilation in l BTPS . min-1; Pao2, arterial Po2 in mm Hg). The hypoxic ventilatory drive, A, averaged 4.1 +/- 2.5 1 . min-1 . mm Hg (mean +/- SD), from which a value of 252 1 . min-1 . mm Hg was calculated on the basis of appropriate allometric relationships, for a 70 kg body mass. This value is higher than those reported for the anesthetized dog and for human subjects. When end-tidal Po2 was gradually decreased from hyperoxia to normoxia, a significant increased in VE due to an increase in breathing frequency was observed, suggesting that the ventilation of the rat is maintained by a considerable 'hypoxic drive' even in normoxia. Furthermore, hypoxic ventilatory depression occurred at a relatively higher Pao2 level (45-60 mm Hg) than in other species. Thus, in the rat, the ventilation vs. end-tidal Po2 curve is shifted to the right compared to other species. After section of the carotid sinus nerve, the hypoxic drive (A) was reduced to 11%, indicating that almost all the ventilatory drive of hypoxia was mediated by the carotid chemoreceptors.

In 12 normal healthy males, the effect of preventing augmentation in tidal volume (VT) on the heart rate (HR) was examined during isocapnic progressive hypoxia. The amount of diminished tidal volume (delta VT) was 0.61 +/- 0.36 liters from the maximal VT value attained in the free breathing hypoxia. Hypoxic HR response in terms of arterial oxygen saturation (SaO2)/HR response slope (delta HR/delta SaO2) was significantly decreased from the free to controlled breathing (p less than 0.05). The effective VT range for eliciting such a HR change appeared to be more than 1,000 ml as has been demonstrated in the Hering-Breuer reflex on ventilation in humans. However, the magnitude of delta HR/delta SaO2 decrement was not significantly correlated with delta VT, suggesting that the command signal from the higher nervous center interfered with the expected response. Contrary to the HR response, the hypoxic ventilatory and occlusion pressure responses were not significantly influenced by the controlled breathing. We conclude that the hypoxic HR response is significantly depressed by the diminished VT breathing.

Relative contributions of chemical and non-chemical respiratory stimulations to breath-holding time (BHT) were examined in assisted (Funado) and unassisted (Kachido) breath-hold divers (Ama). In the Funado the magnitude of the chemical contribution was reduced, though statistically not significantly. On the other hand, in the Kachido no difference in chemical contribution was seen from the control. This was considered to be due to the fact that ventilatory response to CO2 was reduced in the Funado, but not in the Kachido. Despite the decreased contribution of CO2 drive to BHT, absolute BHT in the Funado was no prolonged. This may be related to sensitization of the respiratory centers to non-chemical stimulation. Such adaptation would be effective for preventing the danger of losing consciousness in the Funado who face extreme hypoxia on returning to the surface from a dive.

SASAKI, K., INOUE, S., YOSHIDA, A., HAYASHI, F., MASUDA, Y. and HONDA, Y. Ventilatory Response and Drive Due to Carbon Dioxide Stimulation in Idiopathic Scoliosis. Tohoku J. exp. Med., 1982, 137 (2), 145-151-Ten patients with idiopathic scoliosis and seven controls were studied for the purpose of investigating the ventilatory response and drive due to CO2 inhalation by the steady state CO2 response test. To evaluate the ventilatory drive for the respiratory output mouth occlusion pressure (P0.1) was used. The ventilatory response to CO2 of the patients was not significantly different from that of the controls. P0.1 for a given PCO2 stimulation or tidal volume in the patients was significantly higher than the control. Ventilatory output against P0.1, however, was not different in the two groups. The small tidal volume of the scoliotic patients seemed to be compensated by the high respiratory frequency with a large ventilatory drive in order to maintain adequate ventilation.

Twenty-four active judo athletes were examined by an isocapnic progressive hypoxia test. The results of ventilatory and heart rate responses to hypoxia were analyzed by the hyperbolic equations, $$\dot V$$ E= $$\dot V$$ o+A VE /( $$P_{ETO_2 }$$ −C VE ) andHR=HR O+A HR /( $$P_{ETO_2 }$$ −C HR ), respectively, where $$\dot V$$ Eand HR are observed ventilation and heart rate, $$\dot V$$ O andHR O, the horizontal asymptote in ventilation and heart rate for infinite endtidal $$P_{O2} \left( {P_{ETO_2 } } \right)$$ ,A VE andA HR the slope constant indicating the magnitude of hypoxic sensitivity, andC VE andC HR the vertical asymptote in $$P_{ETO_2 }$$ for infinite ventilation and heart rate.A VE was further re-calculated after inlineE was normalized for a 70 kg body mass, using an allometric coefficient, and was defined asA VEN . 1)A VE andA VEN significantly increased with increasing body weight (BW) as has been reported previously, but no such correlation was found betweenA HR and BW. 2) $$\dot V_{{\text{O}}_{\text{2}} }$$ at rest was found to be positively correlated withA VE andA VEN but not withA HR . 3) The relationship betweenA VE andA HR was not significant. Thus, the characteristic feature seen in hypoxic ventilatory activity was not accompanied by a similar trend in heart rate response.

With the addition of external dead space in normoxia, PCO2-ventilation response and CO2 production were determined in 10 healthy male subjects. Overall “gain” (G) of the respiratory control system was calculated from the slope of the CO2-response curve (S) and that of the metabolic hyperbola (SL) at alveolar partial pressure of CO2 (PACO2) of the respective experimental run. We found that 1) despite the depression of ventilation during non-rapid-eye-movement (NREM) sleep, G was generally not changed due to decreased SL, although considerable individual variations were seen; 2) effects of external dead space on PACO2 change during sleep and wakefulness were similar in magnitude; and 3) the above PACO2 changes experimentally induced agreed well with the predicted values estimated from G. Contrary to general opinion, these results demonstrated that overall gain of the respiratory control system is generally not depressed during NREM sleep in normal healthy subjects.

The objectives were to determine 1) respiratory responses to carotid chemoreceptor inputs in anesthetized rats and 2) whether the cerebellar vermis plays a role in these responses. A carotid sinus nerve was stimulated (20 Hz) with five 2-min trains, each separated by approximately 3 min. During stimulation, respiratory frequency (f), peak amplitude of integrated phrenic nerve activity (integral of Phr), and their product (f x integral of Phr) immediately increased. As stimulation continued, integral of Phr progressively increased to a plateau [short-term potentiation (STP)], but f and f x integral of Phr decreased [short-term depression (STD)] to a value still above control. Upon stimulus termination, integral of Phr progressively decreased but remained above control; f and f x integral of Phr transiently decreased below baseline. After the final stimulation, integral of Phr remained above control for at least 30 min [long-term facilitation (LTF)]. Repeated 5-min episodes of isocapnic hypoxia also elicited STP, STD, and LTF. Vermalectomy lowered the CO2-apneic threshold and eliminated LTF. In conclusion, carotid chemoreceptor activation in rats elicits STP and LTF similar to that in cats; the vermis may play a role in LTF. A new response, STD, was observed.