The influence ofPa O2 on the effects of sinus nerve stimulation with intact and inactivated vagi

Summary In anesthetized rabbits inhaling successively pure oxygen, air, and certain hypoxic O₂/N₂ mixtures, one cut carotid sinus nerve was stimulated under each of these conditions electrically with stimuli of constant intensity both before and after inactivation of the vagi by cold blocking and finally sectioning. In one group of these animals the contralateral sinus nurve was left intact, in the other it was cut. In the first group in which hypoxia produced a moderate hyperpnea with concomitant lowering of thePA _CO2, the augmentation of ventilation by the nerve stimulation decreased markedly with thePa _O2. In the latter group, where hypoxia caused no significant increase or even a slight diminution of ventilation, the respiratory effects of the nerve stimulating were not, or only inconsiderably influenced by the lowering of thePa _O2, while the decrease of blood pressure induced normally by the stimulation was reversed into a distinct increase. After vagal inactivation the stimulatory effects on tidal volume were markedly greater, on respiratory frequency smaller, and on minute volume of ventilation (though only slightly and not always significantly) greater than before.Supported by grant Wi 165 from the Deutsche Forschungsgemeinschaft.     

Chemosensitivity of sympathoexcitatory neurones in the rostroventrolateral medulla of the cat

The hypothesis that sympathoexcitatory neurones within the rostroventrolateral medulla (RVLM) may be chemosensitive was tested in chloralose-anaesthetized cats by artificial perfusion of the RVLM via the left vertebral artery. The baroreceptors and peripheral chemoreceptors were denervated by bilaterally dissecting the carotid sinus and vagus nerves. Either white ramus T₃ (WR-T₃) or the renal nerve was recorded to monitor sympathetic activity. Perfusion with saline or Ringer solution bubbled with CO₂ (10%–100%) produced a rapid and pronounced increase in sympathetic activity and blood pressure. Solutions adjusted to the same pH (pH 5.2 for 100% CO₂) with HCl resulted in a much weaker excitation. A linear relationship between PCO₂ and sympathetic activity was demonstrated. During prolonged perfusion (90 s) sympathetic activity returned to the control level after initial excitation and fell below control levels when perfusion ceased. The sympathetic activity response to CO₂-bubbled solutions was unaffected by blockade of synaptic input by microinjection of CoCl₂ into the RVLM, whereas spontaneous sympathetic activity and the supraspinal somato-sympathetic reflex from intercostal nerve T₄ to WR-T₃ were markedly reduced. It is therefore concluded that sympathoexcitatory bulbospinal neurones in the RVLM are directly chemosensitive to changes in arterial PCO₂ and pH.This paper is dedicated to Prof. Dr. H. P. Koepchen on the occasion of his 65th birthday     

Der Einfluß desP A CO 2 auf die Wirkung der Sinusnervenreizung bei intakten und ausgeschalteten Nn. vagi

Summary In rabbits rebreathing oxygen one carotid sinus nerve was stimulated repeatedly by electrical stimuli of constant intensity, both before and after inactivation of vagi by cold blocking or sectioning. In animals with intact vagi the reflex hyperpnea elicited by the nerve stimulation decreased only slightly with increasing hypercapnia. After inactivation of the vagi the stimulatory effect was, at normalP _{A CO 2}, mostly greater than in the intact condition. But with increasing hypercapnia the decrease of the reflex hyperpnea was generally steeper than in the intact preparation, sometimes reaching even lower values than before inactivation. The depressant effects of the stimulation on systemic blood pressure and heart rate were not distinctly changed by the increase ofP _{A CO 2}, neither with intact nor with inactivated vagi. It is concluded that the ventilatory effect of chemoreceptor afferents is modified both by centralP _{CO 2} and by vagal afferents.

Mit Unterstützung der Deutschen Forschungsgemeinschaft (Wi 165).     

Breath-by-breath determinations of airway occlusion pressure in the developing lamb

The ventilatory effects of breath-by-breath measurements of airway occlusion pressure, i.e., airway pressure determined 100 ms after initiation of inspiration (P _{0. 1}) were evaluated in seven lambs studied sequentially between 7 and 28 days after birth. P _0.1 was determined by computer-aided, on-line regression analysis of the inspiratory pressure versus time (dP/dt) by means of a pneumatic occlusion valve that allowed occlusion times to vary in proportion to respiratory rate. No significant changes were found in minute ventilation, tidal volume, respiratory rate or end-tidal CO₂ concentration when the valve was operating as a one-way valve (opening pressure 0.02 kPa or 0.2 cm H₂0) compared to when in occlusion mode [opening pressure 0.18–0.2 kPa or 1.8–2.0 cmH₂0, mean occlusion time 44 (25) ms]. The calculated P _0.1 values correlated well with those obtained from manual occlusions (r = 0.87, P < 0.0001). This new technique, which detects and discards irregular or non-linear (r < 0.95) inspiratory pressure profiles, enables breath-by-breath determinations of inspiratory drive in rapidly breathing lambs with minimal impact on respiratory pattern and ventilation.These results were presented in part at the annual meetings of the American Pediatric Society and the Society for Pediatric Research 1992     

Effects of severe arterial hypocapnia on regional blood flow regulation,tissuePO2 and metabolism in the brain cortex of cats

The effect of a stepwise decrease inPaCO₂ from 3.9–1.6 kPa on rCBF, rCMRO₂, tissuePO₂ and concentrations of glucose, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine in the brain cortex was studied in cats lightly anaesthetized with sodium pentobarbital. 1. Moderate lowering ofPaCO₂ to 2.5 kPa induced in all animals a homogeneous decrease of rCBF in corresponding areas of the right and left hemisphere. Mean rCBF fell from 129.2 to 103.1 ml · 100 g^–1 · min^–1, while rCMRO₂ remained unchanged (12.7–12.9 ml · 100 g^–1 · min^–1). The tissuePO₂ frequency histograms showed a shift to lower values without indicating the presence of brain tissue hypoxia. 2. Severe arterial hypocapnia (PaCO₂=1.6 kPa) caused an inhomogeneous blood flow reaction. Both further decreased as well as increased rCBF values were measured simultaneously in the brain cortex of individual animals (mean rCBF=97.6 ml · 100 g^–1 · min^–1). At the same time tissuePO₂ measurements and metabolite assays indicated the presence of pronounced brain tissue hypoxia. The tissue concentrations of lactate and pyruvate and the lactate/pyruvate ratio were significantly increased, while the phosphocreatine concentration was significantly reduced. In addition, rCMRO₂ decreased to 11.3 ml · 100 g^–1 · min^–1. The results provide conclusive evidence that severe arterial hypocapnia leads to an insufficient O₂ supply of the brain cortex, which in turn seems to counteract the influence of hypocapnia on cortical blood flow regulation.Preliminary reports of these investigations were presented at the International Symposium on Oxygen Transport to Tissue, July 9–11, 1980 in Budapest and at the Second International Symposium on Pathophysiology and Pharmacotherapy of Cerebrovascular Disorders, July 22–25, 1980 in Tübingen, FRG     

Ammonia as a stimulant to ventilation in rainbow trout Oncorhynchus mykiss

Ammonia is the third most important respiratory gas in ammoniotelic fish after oxygen and carbon dioxide. We here investigated the effects of elevated plasma ammonia on ventilation in freshwater rainbow trout. Intact trout fitted with indwelling dorsal aortic catheters were given injections (over 5 min) of Cortland saline, isotonic high ammonia solutions (NH₄HCO₃, (NH₄)₂SO₄, NH₄OH at pH 8.0, and NH₄OH at pH 9.0), and other solutions as controls for acid–base effects, while ventilatory rate (VR) and buccal pressure amplitude (ΔP_buccal) were recorded. All high ammonia solutions resulted in immediate elevations of plasma Tamm_a, Pa_NH3, and [NH₄⁺]_a, and increases in ventilatory ΔP_buccal and VR to different degrees. However, while Pa_O2 remained constant, in every case there was a confounding change in one or more components of acid–base status (decreases in pH_a or increases in [HCO₃⁻]_a or Pa_CO2 in different treatments), although the ventilatory responses to ammonia injections were generally larger than could be explained by changes in acid–base status. Therefore a series was performed in which normal blood perfusion of the gills was replaced by ventral aortic perfusion with either Cortland saline or Cortland saline plus high ammonia in which pH, [HCO₃⁻], P_CO2, and P_O2 remained unchanged. Although ventilation was depressed in these anaesthetized, spontaneously ventilating preparations, perfusion with high ammonia saline increased ΔP_buccal. In a final series, trout were infused for 24 h with Cortland saline, isotonic NH₄HCO₃, or isotonic (NH₄)₂SO₄ solutions. The two ammonia solutions both caused persistent elevations in VR and ΔP_buccal, together with similar large increases in plasma Tamm_a, Pa_NH3, and [NH₄⁺]_a. As there was no changes in Pa_O2, pH_a, Pa_CO2, or [HCO₃⁻]_a in the (NH₄)₂SO₄ infusion series, this, together with the ventral aortic perfusion experiment, provides the most convincing evidence that ammonia stimulates ventilation. We suggest several circumstances (post-feeding, post-exercise) where the role of ammonia as a ventilatory stimulant may have adaptive benefits for O₂ uptake, and propose that ammonia-induced hyperventilation may also facilitate ammonia excretion in rainbow trout.     

Does the threshold of transcutaneous partial pressure of carbon dioxide represent the respiratory compensation point or anaerobic threshold?

On reaching the respiratory compensation point (RCP) during rapidly increasing incremental exercise, the ratio of minute ventilation (V_E) to CO₂ output (VCO₂) rises, which coincides with changes of arterial partial pressure of carbon dioxide (P _aCO₂). Since P _aCO₂ changes can be monitored by transcutaneous partial pressure of carbon dioxide (PCO_2,tc) RCP may be estimated by PCO_2,tc measurement. Few available studies, however, have dealt with comparisons between PCO_2,tc threshold (T _AT) and lactic, ventilatory or gas exchange threshold (V _AT), and the results have been conflicting. This study was designed to examine whether this threshold represents RCP rather than V _AT. A group of 11 male athletes performed incremental excercise (25 W · min^–1) on a cycle ergometer. The PCO_2,tc at (44°C) was continuously measured. Gas exchange was computed breath-by-breath, and hyperaemized capillary blood for lactate concentration ([la^–]_b) and P _aCO₂ measurements was sampled each 2 min. The T _AT was determined at the deflection point of PCO_2,tc curve where PCO_2,tc began to decrease continuously. The V _AT and RCP were evaluated with VCO₂ compared with oxygen uptake (VO₂) and V_E compared with the VCO₂ method, respectively. The PCO_2,tc correlated with P _aCO₂ and end-tidal PCO₂. At T _AT, power output [P, 294 (SD 40) W], VO₂ [4.18 (SD 0.57)l · min^–1] and [la^–] [4.40 (SD 0.64) mmol · l^–1] were significantly higher than those at V _AT[P 242 (SD 26) W, VO₂ 3.56 (SD 0.53) l · min^–1 and [la^–]_b 3.52 (SD 0.75), mmol · l^–1 respectively], but close to those at RCP [P 289 (SD 37) W; VO₂ 3.97 (SD 0.43) l · min^– and [la^–]_b 4.19 (SD 0.62) mmol · l^–1, respectively]. Accordingly, linear correlation and regression analyses showed that P, VO₂ and [la^–]_b at T _AT were closer to those at RCP than at V _AT. In conclusion, the T _AT reflected the RCP rather than V _AT during rapidly increasing incremental exercise.     

A feedback controller for ventilatory therapy

A computerized system that uses feedback of end-tidal CO₂ fraction (FET CO ₂) to adjust minute volume of a ventilator has been developed and tested. The effectiveness and robustness of the controller were evaluated in five anesthetized dogs. The controlled responded to step-changes in the set-point for FET CO ₂ by adjusting minute volume so that the FET CO ₂ settled to the new set-point in less than 60 sec with less than 20% overshoot. The system exhibited suitable dynamic response to step-changes in set-point with loop gains as large as two times and as small as one-half the optimal value. The breath-to-breath variation in FET CO ₂ values during prolonged periods of closed-loop controlled ventilation was smaller than the variation during periods of constant minute volume ventilation in three of five experiments. The controller generally maintained FET CO ₂ within ±0.1 vol% of the set-point. A disturbance to the controlled system was produced by releasing an occlusion of a branch of the pulmonary artery. The controller always responded to this disturbance in a stable manner, returning the FET CO ₂ to its desired value within 30 sec. Accurate control of arterial partial pressure of CO₂(PaCO ₂) will require modifications enabling the system to determine the relationship between FET CO ₂ and PaCO ₂.     

Extracorporeal CO2-removal: pulmonary and extracorporeal equilibria in dogs and sheep

Summary Extracorporeal CO₂-removal promises to be an efficient alternative to the conservative treatment of advanced lung diseases. Extracorporeal CO₂-removal is achieved in a veno-venous bypass in combination with low frequency ventilation. Positive clinical results in the treatment of adult respiratory distress syndrome (ARDS) are encouraging. In order to prove the applicability of this method to different kinds of respiratory insufficiency, physiological studies using animal models are necessary. We report here on experiments with dogs and sheep undergoing a veno-venous bypass employing a CO₂-eliminator. The experimental results are compared with theoretical values which predict the important relationships between blood flow rate of the extracorporeal circulation (ECC), the CO₂-elimination capacity of the CO₂-eliminator and the low ventilation rate (down to apnea for 5 h) of the natural lung. It was shown that the blood gas data as well as acid base status could be maintained within physiological ranges:Reported in part at the 4th International Symposium on Aktuelle Probleme der Notfallmedizin und Intensivtherapie, Münster, 1983     

Some aspects of determination of the cardiac output by the rebreathing method

It is shown that the rebreathing method can be used to study the cardiac output even when the ventilation does not correlate with the pulmonary blood flow. pCO₂ was measured in mixed venous blood by equilibrating it with pCO₂ in the alveolar air by the rebreathing method. A gas mixture with a CO₂ concentration close to that in venous blood was produced by the subject himself during rebreathing into a bag with a capacity of 2–3 liters, filled with oxygen. Irregularity of distribution of ventilation relative to blood flow was judged from the shape of the CO₂ concentration versus time curve. If signs of irregularity are present, it is impossible to make p_etCO₂ equal to p_ACO₂ and for that reason pCO₂ of arterialized blood was determined. By means of this correction it is possible to determine the cardiac output of patients with cardiac and pulmonary diseases. The possibility of using standard nomograms for calculating the CO₂ concentration in the arterial and venous blood in the presence of appreciable disturbances of the acid-base balance is discussed.Department of Experimental and Clinical Physiology, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician V. N. Chernigovskii). Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 2, pp. 245–247, February, 1977.     

Carbon dioxide sensitivity of the central chemosensitive mechanisms

Summary In urethane-anaesthetised adult albino rats ventral surface of the brainstem was stimulated chemically by increasing the local CO₂ concentration and electrically. Two areas were demarcated on the ventral surface of the brainstem, one which showed an increase in pulmonary ventilation on chemical and electrical stimulation, and another which showed a decrease in pulmonary ventilation and sometimes even respiratory arrest. EEG activity recorded from the area from where increased pulmonary ventilation was obtained showed a synchronous slow wave activity during chemical stimulation and inhalation of a CO₂-air mixture. This area is situated 0.5–1 mm lateral to the mid-line extending up to the rootlets of the VIIth to IXth cranial nerves. The response increased proportionately on increasing the strength of the chemical stimulus, till it reached a plateau. In carotid body denervated and chronic hypoxic animals, the magnitude of the responses was shown to be increased, probably due to increased sensitivity of the central chemosensitive mechanisms.     

Über die Wirkung der Pressoreceptoren des Carotisgebiets der narkotisierten Katze auf die Atmung nach isolierter Ausschaltung der Chemoreceptoren

1. In 5 cats ligthly anesthetized with chloralose-urethane all chemoreceptor response was abolished by cutting the vagosympathetic trunks including depressor nerves and by embolization of the carotid bodies by lycopodium powder. By means of a pressurized bottle attached to the femoral arteries mean arterial pressure was regulated to three different levels (160, 120 and 80 Torr consecutively) and was kept constant at each of these levels. Transients and steady state values of ventilation were recorded during this stepwise change of blood pressure. The effect on ventilation of severing sinus nerves at constant blood pressure was observed.After severing sinus nerves recording of the effect of blood pressure changes on ventilation was repeated.2. In this preparation (chemoreceptors denervated, carotid pressoreceptors intact) severing sinus nerves is followed by a diminution of ventilation in the same order of magnitude as described in the preceding papers, even if blood pressure is kept constant.3. Following stepwise diminution of mean arterial pressure in the chemodenervated cat, ventilation returns to its initial value after a transient increase. This confirms the conclusion of the preceding paper that during steady state no tonic influence of pressoreceptors on ventilation can be observed.4. The transient increase of ventilation following diminution of blood pressure is less pronounced, but not abolished, after severing the sinus nerves. It is therefore considered to be only partly due to the release of an inhibition by pressoreceptor impulses. The remaining effect must be due to other causes, possibly transient change of cerebral circulation.5. From this evidence and that from the preceding papers it must be concluded that the steady state decrease of ventilation observed after severing sinus nerves in cats inhaling gas mixtures containing 35 or 99% O₂ can not be attributed either to chemoreceptor drive by O₂ deficiency or to blood pressure effects on chemo—or pressoreceptors. Effects of CO₂ or H⁺ on chemoreceptors can be excluded as well since in the experiments of this paper all chemoreceptor drive is abolished.It must therefore be concluded that an unknown respiratory drive is depending upon the integrity of the sinus nerves.

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Acid base status in unanesthetized,unrestrained guinea pigs

Acid-base status of arterial blood was measured in chronically cannulated, unanesthetized, unrestrained guinea pigs. Normal values were: pH=7.444±0.032,PaCO₂=35.7±4.4; HCO ₃ ^– =24.4±2.8; BE=+0.4±2.1 (n=69) andPaO₂=91.9±7.3 (n=25) (Values are mean±S.D.).Induction of light anesthesia with thiopentone caused a respiratory depression (decrease inPaO₂) accompanied by respiratory acidosis (increase inPaCO₂ and decrease in pH) and a development of slight metabolic acidosis (decrease in base excess and standard bicarbonate). Acid base parameters of guinea pigs are compared to those obtained from rats under identical experimental conditions.     

The cholinergic pathway to cerebral blood vessels

Summary The effect of stimulating the greater superficial petrosal nerve (g.s.p.n.) upon retroglenoid venous blood flow has been tested in anaesthetized, paralysed and artificially ventilated rats. In 11 out of 15 tests, blood flow increased by an average of 25% with a time to peak response of 28 s. This response was abolished with the injection of atropine 0.1 mg kg^–1 injected intra-arterially. With both petrosal nerves intact, the administration of 6–7% CO₂ in air or 15% O₂ in N₂ caused average increases in blood flow of 105% and 45% respectively. These responses were not affected by bilateral section of the g.s.p.n. Similar experiments were carried out in 5 anaesthetized, spontaneously breathing rabbits in which, in addition toPaCO₂ andPaO₂,PO₂,PCO₂ and blood flow in the caudate nucleus were measured continuously using chronically implanted mass spectrometer catheters and heated thermistors. Caudate nucleus blood flow increased in response to hypoxia and hypercapnia and this response was not significantly affected by section of one or both g.s.p.n., sinus or vagus nerves. With section of sinus and vagus nerves, blood flow changed passively with arterial pressure.     

Effect of H+ and elevated PCO 2on membrane electrical properties of rat cerebral arteries

Some membrane electrical properties of muscle cells from the middle cerebral artery of the rat were recorded with intracellular microelectrodes. The resting membrane potential (E _m) of this preparation was –63 mV. Reduction of extracellular pH to 7.0 in the face of a constantP _{CO 2}of 40 mm Hg had no significant effect onE _m. Similarly the slope of the steady-state voltage/current curves was not different at pH 7.0 compared to control at pH 7.4. In marked contrast, whenP _{CO 2}was elevated to around 60 to 70 mm Hg there was a rapid hyperpolarization and reduction in the slope of the voltage current curve suggesting an increased conductance for one or more ionic species. In addition elevation ofP _{CO 2}increased the slope of theE _m vs. log[K]₀ curve from 46 mV/decade to 59 m V/decade which is in good agreement with a Nernstian potential for a K⁺ selective membrane. These data suggest that while the smooth muscle cells of rat cerebral arteries are relatively insensitive to a small reduction in extracellular pH; reduction of intracellular pH by elevatingP _{CO 2}induces hyperpolarization by increasing K⁺ conductance (g _k). However, it is not clear from these experiments if theP _{CO 2}effects are mediated entirely by changes in pH or if there is a direct membrane action of CO₂.This work is supported by Grant no. HL27862     

Effect of acceleration on distribution of lung perfusion and on respiratory gas exchange

Summary Application of new technical and methodological development as respiratory mass spectrometry and double nuclide perfusion scintigraphy results in more detailed knowledge of the effect of accelerational forces on lung perfusion and respiratory gas exchange.For evaluation of some details of lung perfusion and respiratory gas exchange 20 healthy male subjects were exposed to prolonged hypergravitational stress (2 min,+G _z,+G _x or–G _y). Distribution of lung perfusion was measured by means of double nuclide perfusion scintigraphy using^99mTechnetium- and¹³¹Iodinemicrospheres allowing the registration of 2 phases of pulmonary perfusion in the same subject.PAO₂ andPACO₂ were measured by continuous mass spectrometrical registration andPaO₂,PaCO₂ and pHa were determined from arterial blood samples polarographically and electrometrically, respectively. Measurements were performed in the pre-run, in the run and partly in the post-run period, too.Depending on the magnitude and direction of the gravitational vector blood volume shifts within the lungs. Using computer evaluation of the scintiscans, it is possible to determine the magnitude of the normal-, hypo- and hyperperfused lung regions: for the extreme case of –4G _y only 3% of the 47% left lung perfusion at rest persists.During+G _z-acceleration thePaO₂ decreases linearily for approximately 10 Torr/+1G _z,PAO₂ increases by about 5 to 7 Torr/+1G _z andAaDO₂ increases correspondingly from 10.4 Torr at rest to 60.1 Torr at+3G _z. ForPaCO₂ no significant change could be observed during acceleration up to+3G _z, whereasPACO₂ decreased significantly from 36.5 to 25.0 Torr in the same time;aADCO₂ increased correspondingly. No significant pHa change was observed during all +G _z runs up to+3G _z.Prolonged expiration during+G _z-acceleration reveals an amplification of the amplitude of the cardiogenic oscillations in the alveolar plateau of expiratoryPO₂ andPCO₂-curves. Furthermore the alveolar plateau slopes down depending on the gravitational stress and indicating large disturbances of the ventilation/perfusion ratio.     

Effect of prostaglandin B1 on the systemic and regional hemodynamics

The effect of prostaglandin B₁ (PGB₁) on the cardiovascular system was studied in experiments on anesthetized dogs. After intravenous injection of PGB₁ (40 g/kg in a single dose) arterial hypotension tachycardia, increased myocardial contractility, an increased cardiac output, and a rise of pressure in the pulmonary artery were observed. The total peripheral resistance and total pulmonary resistance were reduced. The work of the right and left ventricles was increased. The coronary blood flow was increased by 29%. The mean velocity of the volume blood flow in the renal and femoral arteries was appreciably increased after administration of PGB₁, but in the common carotid and superior mesenteric arteries the increase was not significant. Changes in the systemic and regional hemodynamics were of short duration.Department of Pharmacology, I. M. Sechenov First Moscow Medical Institute. Department of Anesthesiology, Institute of Clinical and Experimental Surgery, Ministry of Health of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 2, pp. 131–133, February, 1977.     

Der Effekt der Durchtrennung der Sinusnerven auf die Atmung der narkotisierten Katze bei konstant gehaltenem arteriellem Druck und seine Abhängigkeit vom CO2-Druck

1. In 18 cats lightly anesthetized with chloralose-urethane in which vago-sympathetic trunks including depressor nerves had been denervated beforehand the sinus nerves were severed while mean arterial pressure was being kept constant at about 150 torr using a pressurized vessel attached to the femoral arteries. Sinus nerves were cut in a first group of 9 cats during inhalation of 35% O₂ in N₂ and in a second group of 9 cats during inhalation of 4% CO₂, 35% O₂ in N₂. Lung ventilation and arterial pressure were recorded, arterial O₂ pressure was determined in blood samples.2. The average decrease of respiratory minute volume was 134,1 ml min^–1 in the first and 569,1 ml min^–1 in the second group, this is 22±3 and 27±4% of the control values respectively.3. It is concluded that the distinct decrease of ventilation which is observed after cutting sinus nerves at elevated inspiratory pO₂ cannot be explained either by a preexistent drive of ventilation by low oxygen pressure in the chemoreceptors or by the change of blood pressure.

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Diese Veröffentlichung ist ein Teil der der Medizinischen Fakultät Göttingen vorgelegten Habilitationsschrift.     

Ventilatory response of prepubertal boys and adults to carbon dioxide at rest and during exercise

Summary The aim of this study was to determine whether the greater ventilation in children at rest and during exercise is related to a greater CO₂ ventilatory response. The CO₂ ventilatory response was measured in nine prepubertal boys [10.3 years (SD 0.1)] and in 10 adults [24.9 years (SD 0.8)] at rest and during moderate exercise ( CO₂ = 20 ml·kg^–1·min^–1) using the CO₂-rebreathing method. Three criteria were measured in all subjects to assess the ventilatory response to CO₂: the CO₂ sensitivity threshold (Th), which was defined as the value of end titalPCO₂ (P _ETCO₂) where the ventilation increased above its steady-state level; the reactivity slope expressed per unit of body mass (SBM), which was the slope of the linear relation between minute ventilation ( _E) andP _ETCO₂ above Th; and the slope of the relationship between the quotient of tidal volume (V _T) and inspiration time (t _I) andP _ETCO₂ (V _T ·t _I ^–1 ·P _ETCO₂ ^–1) values above Th. The _E,V _T, breathing frequency (f _R), oxygen uptake ( O₂), and CO₂ production ( CO₂) were also measured before the CO₂-rebreathing test. The following results were obtained. First, children had greater ventilation per unit body weight than adults at rest (P<0.001) and during exercise (P<0.01). Second, at rest, onlyV _T ·t _I ^–1 ·P _ETCO₂ ^–1 was greater in children than in adults (P<0.001). Third, during exercise, children had a higher S_BM (P < 0.02) andV _T ·t _I ^–1 ·P _ETCO₂ ^–1 (P<0.001) while Th was lower (P<0.02). Finally, no correlation was found between _E/ CO₂ and Th while a significant correlation existed between _E/ CO₂ and S_BM (adults,r=0.79,P<0.01; children,r=0.73,P<0.05). We conclude that children have, mainly during exercise, a greater sensitivity of the respiratory centres than adult. This greater CO₂ sensitivity could partly explain their higher ventilation during exercise, though greater CO₂ production probably plays a role at rest.     

Ventilatory response of the panting dog to hypoxia

Summary The ventilatory response to isocapnic hypoxia was studied in anesthetized dogs during normothermia and thermally induced panting. In the normothermic dog, minute ventilation (_E), tidal volume (V _T) and respiratory frequency (f) did not vary significantly with changes ofPaO₂ above 80–90 mm Hg. Below this value, these three parameters increased substantially with progressively decreasingPaO₂. During panting the ventilatory response was triphasic: 1. withPaO₂ values above 90 mm Hg ventilation remained unaffected; 2. whenPaO₂ progressively decreased from 90 to 45 mm Hg, ventilation increased significantly over the levels of ventilation reached in response to heat alone; 3. withPaO₂ under 45 mm Hg ventilation abruptly decreased as compared to the second phase of the response.V _T increased significantly during the second and third segments as compared to the first. Respiratory frequency progressively decreased whenPaO₂ was under 60 mm Hg Isocapnic hypoxia suppressed thermally induced panting (tachypnea) but led to reduction of evaporative heat loss only at the lowest values ofPaO₂.Apparently, in the panting animal chemical control of respiration is set aside by the thermoregulatory control. However, chemical regulation of respiration may set aside the normal respiratory pattern of thermal polypnea in response to acute chemical stimuli, such as arterial hypoxia.