B. Katsaros

Vergleich der Wirkung verschiedener Acidosen (NH4Cl, CaCl2, Acetazolamid) auf die Lungenbelüftung beim Menschen

SummaryIn seven healthy subjects acidosis was induced by NH4Cl, by CaCl2 or by acetazolamide (diamox). The response of respiratory minute volume to inhaled CO2 mixtures was studied in control and acidosis experiments. The arterial and endexpiratory CO2-tensions were determined simultaneously. The respiratory minute volumes were plotted against arterial or alveolar CO2 tensions (CO2 response curve). By interpolation in the CO2 response curves the lung ventilation in acidosis and in the control experiment could be compared at equal CO2 tensions.1. Conclusions obtained with endexpiratory and with arterial CO2 tension measurements were coinciding.2. The mean slope of the curves describing the dependance of lung ventilation upon arterial CO2 tension was not significantly altered in acidosis. The effect of acidosis is a parallel shift of the curve to higher ventilation or lower CO2 tension.3. No significant difference in the response of lung ventilation to acidosis could be detected between NH4Cl, CaCl2 or acetazolamide acidosis.4. If ventilations at equal CO2 tensions were compared, the effect of acidosis on lung ventilation was found to be in the average 2.01 min−1 per −0.01 ph change or 2.7 l min−1 per −1 meq l−1 change of whole blood buffer base.

Die Rolle der Chemoreceptoren des Carotisgebiets der narkotisierten Katze für die Antwort der Atmung auf isolierte Änderung der Wasserstoffionen-Konzentration und des CO2-Drucks des Blutes

Abstract1. In 16 vagotomized cats anesthetized with chloralose-urethane CO2 response curves [V=f (pCO2A)] were determined at elevated inspiratory O2 (35%) during normal acid base balance and in metabolic acidosis induced by i.v. infusion of HCl or in metabolic alcalosis induced by i.v. infusion of NaHCO3. The experiments were repeated after severing the sinus nerves. By a graphical method using the data in acidosis and normal state or alcalosis and normal state, the isolated drives of CO2 and H+ were determined.2. Cutting the vagosympathetic and depressor nerves caused the total CO2 sensitivity (slope of CO2 response curve) to increase. At the same time the intercept of the CO2 response curve with the abszissa (pCO2A) was shifted to the right. This was interpreted as suggesting the disappearance of a (possibly nonspecific) respiratory drive.3. Severing sinus nerves caused only minor changes of the isolated CO2 (0–13%) and H+ effects (< 33%). It must be stated, however, that an accurate determination is much hampered by scattering of data. According to the small effect on isolated H+ and CO2 drives the slope of the CO2 response curve was only slightly diminished (from 49 to 44 ml min−1 Torr−1).4. Additionally to the (small) decrease of slope, severing of the sinus nerves caused a shift of the CO2 response curve to the right (to higher pCO2) of 5,6 Torr in the average of the animals in normal acid base balance. The shift is possibly smaller during metabolic alcalosis and bigger during metabolic acidosis.5. It is concluded that in the presence of sufficiently high arterial pO2 the role in respiratory regulation of isolated CO2 and isolated H+ effects on the chemoreceptors of the carotid region is small compared to the more central effects. The role of a possibly nonspecific respiratory drive conducted in the sinus nerves, however, is considerable. The nature of this drive is not yet clear.

Wirkung der Bicarbonat-Alkalose auf die Lungenbelftung beim Menschen Bestimmung der Teilwirkungen vonph und CO2-Druck auf die Ventilation und Vergleich mit den Ergebnissen bei Acidose

Summary1. In human subjects metabolic alcalosis was induced by 0,5 g/kg NaHCO3. Gas mixtures of about 0, 2, 4, and 6% CO2, 35% O2 in N2 were inhaled, and the response of respiratory minute volume to variation of alveolar (arterial)pco2 was determined. Alveolarpco2 was read as endtidalpco2 from an infrared analyzer record. During inhalation of each gas mixture samples of arterial blood were taken from an indwelling needle in the femoral artery. CO2 content, O2 content, O2 capacity andph were determined with routine methods.pco2 and whole blood buffer base were calculated.2. In alcalosis the curve describing the dependance of respiratory minute volume upon alveolarpco2 was shifted to higherpco2 in comparison to the control experiments in an approximately parallel way. The shift perph unit, however, was smaller than was found in earlier experiments on acidosis with similar methods. This indicates that the partialph sensitivity of respiration is diminishing in the alcaline range.3. The data were used together with already published data on metabolic acidosis to draw isoventilatory lines in apco2-ph diagramm which allows to isolate the partialpco2 andph effects and gives a more general information on the dependance of lung ventilation upon the parameters of acid base equilibrium.

Differenzierung der Wirkungen von CO2-Druck und Wasserstoffionenkonzentration im Blut auf die Atmung beim Menschen

SummaryData published in the preceding paper on effects of augmented arterial CO2 tensions on lung ventilation before and after inducing acidosis by NH4Cl or CaCl2 or acetazolamide (diamox) were used to differentiate the partial effects of pH changes at constant CO2 tension and of CO2 tension changes at constant pH in arterial blood on lung ventilation.The total increase of lung ventilation caused by elevation of CO2 tension was found to be 3.2 l min−1 Torr−1. The partial pH effect was 1.4 l min−1 Torr−1 or 43% per cent of the total effect and the partial CO2 effect was 1.8 l min−1 Torr−1 or 57 per cent of the total effect. This is in agreement with the prediction of Gray and the experimental results of Lambertsen and Semple.

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

Abstract1. 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.

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

Abstract1. 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.

Der Effekt der Durchtrennung der Sinusnerven auf die Atmung der narkotisierten Katze bei konstant gehaltenem arteriellen Druck in tiefem Niveau und der Einfluß stufenweiser Änderung des arteriellen Drucks auf die Atmung vor und nach Durchtrennung der Sinusnerven

Abstract1. In 8 cats lightly anesthetized with chloralose-urethane in which vagosympathetic trunks including depressor nerves had been cut beforehand ventilation and arterial pressure were recorded. Arterial pressure was changed stepwise and kept at constant level between changes. Sinus nerves were severed and the effects of stepwise change of arterial pressure on ventilation again was recorded. Throughout the experiment inhaled oxygen fraction was 35%.2. Steady state ventilation at an arterial pressure of 80 torr is not significantly different from steady state ventilation at arterial pressure of 146 torr. Cutting the sinus nerves at low level (80 torr) of mean arterial pressure is followed by a decrease of ventilation which is not significantly different from the decrease found when cutting sinus nerves at an arterial pressure of 146 torr.3. If mean arterial pressure is diminished stepwise from 160 to 120 and 80 torr, ventilation each time returns to its initial value after a transient increase. If this experiment is repeated after cutting the sinus nerves, steady state ventilation again is not influenced by the mean arterial pressure. The transient increases of ventilation are still observed though they are possibly less pronounced and of shorter duration. The transient increases of ventilation after diminution of arterial pressure therefore must partly be considered as consequences of changes of the cerebral circulation rather than as being caused by diminution of pressoreceptor impulse traffic.

Antwort der Ventilation auf Perfusion der vom übrigen Kreislauf isolierten Chemoreceptoren des Carotisgebiets mit Lösungen, in denen CO2-Druck und Wasserstoffionen-Konzentration variiert wurden

Abstract1. After preliminary experiments in 5 cats, in 2 cats lightly anesthetized with chloralose-urethane both carotid regions were isolated from the circulation and perfused alternately with three solutions (A, B, C) in which pH and pCO2 were varied while perfusion pressure and systemic blood pressure were kept constant. Solution A was a mock protein-free blood plasma equilibrated with 6% CO2, 6% N2 in O2. Solution B was the same solution equilibrated with 12% CO2 in O2. Solution C was equilibrated with the same gas mixture as A but contained less bicarbonate. Ventilation and end-tidal pCO2 were measured. The changes of end-tidal pCO2 resulting from changes in ventilation were compensated for by adding CO2 to inspired air.2. Diminution of perfusate pH alone (at constant perfusion pCO2) by about 0,3 units was followed by an increase in ventilation of about 10% in the steady state if end-tidal pCO2 and systemic blood pressure were kept constant.3. Diminution of perfusion pH by about 0, 2 units, as caused by an increase of perfusion pCO2 of about 41 Torr (at constant perfusion buffer base) was followed by an increase in ventilation of about 25% in the steady state when end-tidal pCO2 and systemic blood pressure were kept constant.4. The transient changes of ventilation exceeded the steady state changes.1. After preliminary experiments in 5 cats, in 2 cats lightly anesthetized with chloralose-urethane both carotid regions were isolated from the circulation and perfused alternately with three solutions (A, B, C) in which pH and pCO2 were varied while perfusion pressure and systemic blood pressure were kept constant. Solution A was a mock protein-free blood plasma equilibrated with 6% CO2, 6% N2 in O2. Solution B was the same solution equilibrated with 12% CO2 in O2. Solution C was equilibrated with the same gas mixture as A but contained less bicarbonate. Ventilation and end-tidal pCO2 were measured. The changes of end-tidal pCO2 resulting from changes in ventilation were compensated for by adding CO2 to inspired air. 2. Diminution of perfusate pH alone (at constant perfusion pCO2) by about 0,3 units was followed by an increase in ventilation of about 10% in the steady state if end-tidal pCO2 and systemic blood pressure were kept constant. 3. Diminution of perfusion pH by about 0, 2 units, as caused by an increase of perfusion pCO2 of about 41 Torr (at constant perfusion buffer base) was followed by an increase in ventilation of about 25% in the steady state when end-tidal pCO2 and systemic blood pressure were kept constant. 4. The transient changes of ventilation exceeded the steady state changes.