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Biomedical subjects

F Kreuzer

Publications and source records attributed to F Kreuzer.

At least 55 records · Page 3Linked to original sources

Respiratory oscillations of the arterial PO2 and their effects on the ventilatory controlling system in the cat.

The respiratory oscillations of the arterial PO2 were measured in paralyzed, artificially ventilated cats by a small (1.2 mm) fast-responding catheter oxygen electrode. The amplitude of these oscillations could be changed independently of the mean PA,O2n by a specially designed respirator circuit. deltaPaO2 was shown to increase with increasing tidal volume or decreasing frequency of the respirator, and with increasing mean PaO2. The amplitude of the oscillations was attenuated considerably from the left atrium to the aorta. No attenuation occurred from the aorta to the carotid artery, provided that the blood flow in the carotid artery was not impeded. The measured attenuation of the oscillations was compared to that calculated by Yokota and Kreuzer (1973) and found to be quite different. The output of the ventilatory controlling system of the cat was measured from the quantified phrenic nerve activity. When only deltaPaO2 was changed at a constant level mean PaO2, the quantified phrenic nerve activity did not change, indicating that the amplitude of the oscillations does not influence the ventilatory controlling system. In vagotomized animals, the periodicities of the oscillations and the phrenic nerve activity were completely dissociated. From the fact that no Cheyne-Stokes type of breathing occurred, it was concluded that the effect of timing is negligible.

Animals↗

Effects of pulmonary gas emoblism on circulation and respiration in the dog. VI. Influence of body position on the effects of pulmonary gas embolism.

In the present study the influence of body position on the effects of venous gas infusion was examined. The body position of anesthetized dogs ventilated artifically varied between supine, right-side-down and left-side-down position. Without venous gas infusion the change of body position hardly affected pulmonary arterial pressure (Pap) and alveolar CO2 fractional concentration (FACO2). However, during venous gas infusion a change of body position immediately elicited a rapid increase Pap and a decrease in FACO2 completed within a few seconds. Thereafter both variables gradually returned to their initial levels as before the change of body position. The extent of change in Pap and FACO2 due to alteration of body position depended on the initial embolic level (determined by the rate of infusion and the nature of the gas used) and on the change of body position.

Animals↗

Effects of pulmonary gas embolism on circulation and respiration in the dog. III. Excretion of venous gas bubbles by the lung.

Intravenous injection of gas (10-60 ml) causes acute pulmonary embolism, which disappears completely within 10-20 min. Intravenous infusion of gas (1-5 ml min-1) can be continued for a long time. During these infusions a steady state is reached in which pulmonary arterial pressure is increased and cardiac output remains unaltered. This indicates that the degree of embolization has reached a constant level despite the continuous gas infusion. These findings can be explained by a gradual disappearance of the bubbles from the pulmonary circulation. The purpose of this study was to measure the possible excretion of gas from the intravascular gas bubbles into the alveolar air after venous administration. Neon was used as a test gas since its fractional concentration in ambient air is low (0.00018) and it can be detected by gas chromatography with sufficient accuracy. It could be demonstrated that after injection neon was present in the expiration gas. During the steady state of infusion the rate of excretion in the expiration gas appeared to be equal to the rate of infusion. Changes in the pulmonary arterial pressure curve were reflected in the neon wash-out curve. It may be concluded that during pulmonary gas embolism the administered gas is excreted into the alveolar air and that the excretion rate largely depends on the increased pulmonary arterial pressure due to the obstructing bubbles themselves.

Animals↗

Effects of pulmonary gas embolism on circulation and respiration in the dog. I. Effects on circulation.

Mongrel dogs weighing 15-25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid were used to investigate the effects of pulmonary gas embolism on pulmonary arterial pressure (Pap), systemic arterial pressure (Pa) and cardiac output (Q). Pulmonary gas embolism was produced either by venous injecton or by venous infusion. The most marked effect of pulmonary gas embolism on circulation was an increase in Pap which returned to the original level after stopping the gas administration. 1. After gas injection Pap rose to a maximum within 30--60 s. The extent of this rise in Pap showed a positive correlation with the volume of the injected gas. The kind of gas (oxygen, helium, neon, nitrogen, air), however, did not influence the extent of the rise in Pap, but did influence the time of return of Pap to the original level. Carbon dioxide showed an exceptional behavior in that it had almost no effect on Pap at all. P a hardly changed with the volume of the gas injections (20--60 ml injected within 1 s); Q was not measured after gas injection (the direct Fick method is not usable in this situation). 2. Gas infusion caused a slow rise of Pap, its steepness and extent depending on the rate of infusion and on the physical properties of the infused gas. When the right ventricle was able to maintain its output, a constant level of Pap was reached after 10--15 min. In this circulatory steady state Pap appeared to be a measure of the degree of embolization. However, this relationship no longer held when the right ventricle failed as evidenced by a fall in Pap, Pa and Q. It may be concluded that pulmonary gas embolism produces a transient partial obstruction in the pulmonary circulation and that the performance of the right ventricle determines the maximum degree of embolization compatible with a sufficient circulation.

Animals↗

Effects of pulmonary gas embolism on circulation and respiration in the dog. II. Effects on respiration.

In mongrel dogs weighing 15--25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid the effects of venous gas infusion and injection on several respiratory variables were investigated. During spontaneous respiration pulmonary gas embolism caused an increase of the ventilatory minute volume depending on the degree of embolization. The contribution of breathing frequency and tidal volume to the increase of ventilatory minute volume varied from one animal to the other. During constant artificial ventilation pulmonary gas embolism impaired the pulmonary gas exchange depending on the degree of embolization. How far a steady-state phase in gas exchange can be reached during continuous venous gas infusion depended on the adaptation of the circulation. At severe degrees of embolization circulation as well as gas exchange became deficient. Increasing artificial ventilation during pulmonary gas embolism improved the wash-out of carbon dioxide, but hardly affected the uptake of oxygen. The most important origin of the disturbed gas exchange in pulmonary gas embolism seemed to be an increased inequality of the ventilation-perfusion ratio distribution.

Animals↗

Coronary blood flow in rats native to simulated high altitude and in rats exposed to it later in life.

In rats exposed to a simulated high altitude of 3500 m for their whole prenatal and postnatal life a severe cardiac hypertrophy develops. In rats born and first staying 5 weeks at sea level and then being exposed to simulated high altitude, only a unilateral right cardiac hypertrophy occurs. In both groups nutritional coronary blood flow was estimated in left ventricle, right ventricle, and septum and was compared with control animals of similar age. Coronary blood flow was measured at hypoxia in all groups. At first cardiac output was determined by the Fick principle, then 86Rb was applied and the animals were killed after 55 sec. Activity of 86Rb was measured in both cardiac ventricles and septum and the fractional uptake was calculated. According to Sapirstein (1956, 1958) the distribution of 86-RB follows the distribution of cardiac output and from both these data the nutritional blood flow to the parts of the heart may be estimated. Cardiac output was similar in rats exposed to simulated high altitude later in life ('newcomers') and in control animals, but it was significantly lower in rats born in the low pressure chamber ('natives'). Fractions of cardiac output supplying cardiac ventricles and septum in rats from both hypoxic groups were significantly higher than in control animals. In the 'natives' they were significantly higher than in the 'newcomers'. The fractions of cardiac output in both 'newcomers' and 'natives' remained significantly higher than those of the control animals, also when calculated per gram of heart tissue. Nutritional coronary blood flow (in ml/min) was higher in both ventricles and septum of the 'newcomers' and in the right ventricle of the 'natives', and lower in the septum of the 'natives', when compared with control animals. Coronary blood flow per gram of heart tissue (in ml/min.g) was significantly higher in all cardiac parts of the 'newcomers', but it was about the same in all cardiac parts of the 'natives' when compared with controls. The importance of observed changes concerning myocardial tissue oxygenation is analyzed by using Krogh's cylindrical tissue model.

Age Factors↗

The carbamate equilibrium of bovine hemoglobin at 37 degrees C.

emoglobin-bound CO2 was estimated by a procedure first described by Rossi-Bernardi et al. (1969) in which the carbamate compound is stabilized by rapid mixing with alkali and then separated from other CO2 constituents in solution by gel filtration and ion-exchange chromatography. Carbamate equilibrium of bovine hemoglobin was studied at constant PCO2 (44 mm Hg) and varying pH as well as at constant pH (7.4) and varying PCO2 (ionic strength 0.18, temperature 37.0 degrees C). The difference in Z (deltaZ) between hemoglobin and oxyhemoglobin appeared to be 0.11 plus or minus 0.04 (pH=7.40; PCO2=44 mm Hg) i.e. about half the value observed in human hemoglobin. DeltaZ was shown to account completely for the difference in CO2 content (CCO2) between hemoglobin and oxyhemoglobin when in total equilibrium with CO2. Carbamate determinations on bovine hemoglobin specifically modified at all terminal amino groups (double-blocked carbamylated derivative) did not show any CO2 binding at all, thus giving a final proof for the exclusive role of the terminal amino groups in CO2 binding under physiological conditions. Attempts to calculate the ionization constant (Kz) and the carbamate equilibrium constant (Kc) of the terminal amino groups failed, suggesting that both terminal groups are not equivalent in their CO2 binding properties. This was confirmed by the fact that carbamate data obtained at constant PCO2 and varying pH fitted binding curves derived from two sets of independent but non-equivalent binding sites. Association constants for both kinds of binding sites appeared to differ by a factor of at least 3 in hemoglobin and of about 10 in oxyhemoglobin. From determinations of hemoglobin-bound CO2 and CO2 content of hemoglobin and oxyhemoglobin solutions in total equilibrium with CO2, the apparent first dissociation constant of carbonic acid was calculated as 5.71 plus or minus 0.0061 pH and found to be independent of the oxygenation state of hemoglobin. In contrast with hemoglobin of other species bovine hemoglobin appeared to be not influenced by the presence of 2.3-diphosphoglycerate as far as its CO2-binding properties are concerned.

Animals↗

A single-unit carbon dioxide-oxygen sensing microelectrode system.

A membrane-covered CO2 microelectrode system is described; it consists of a platinum electrode surronded by a ring-shaped Ag-AgCl electrode, both in contact with an electrolyte layer composed 10 minus 3 M/l quinhydrone in 0.1 N KCl. The resulting oxidation-reduction potential is shown to vary linearly with the logarithm of the PCO2 of the medium. Response time for 95% deflection to a step change in PCO2 of 65 mm Hg is about 1 min i.e. considerably less than in the macroelectrode described previously, but stability is decreased at the same time. Since oxygen in concentrations up to about 21% (air) did not influence the CO2 response and the presence of both CO2 (10.33%) and quinhydrone (10 minus 3 M/l) did not alter the oxygen polarogran, this electorde may be used independently as an oxygen electrode as well. Stability and response time for oxygen were similar to those of the Clark electrode. Possibilities and limitations for in vivo estimation of PCO2 and PO2 are discussed.

Carbon Dioxide↗

The CO2 conductivity electrode, a fast-responding CO2 microelectrode.

A fast-responding CO2 microelectrode system is presented; it consists of a double-lumen polyethylene catheter provided with a stainless steel catheter tip covered by a CO2-permeable membrane, and connected with each lumen separately to a conductivity cell. The catheter is flushed with bidistilled water at constant flow rate and conductivity of inflowing and outflowing water is measured. The change of conductivity in the water leaving the catheter after exposure of the electrode to a medium containing CO2 is related to the PCO2 of the medium. High sensitivity and fast response, both depending on the flow rate of the carrier water, are shown to oppose each other. When cells are placed at a distance of 45 cm from the membrane, response time for 90% deflection is about 10 sec (at flow rates of 5 ml/min), but when located inside the electrode tip at a distance of within 10 mm from the membrane response time is reduced to about 4 sec. Hydrodynamical aspects concerning dispersion of CO2 in the carrier water and reaction kinetics of CO2 hydration are discussed.

Carbon Dioxide↗