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Biomedical subjects

A Berkenbosch

Publications and source records attributed to A Berkenbosch.

71 records · Page 4Linked to original sources
PubMed1983

Influence of peripheral O2 tension on the ventilatory response to CO2 in cats.

The effects of peripheral hypoxia on ventilation were investigated in 18 cats anaesthetized with chloralose urethane. The ponto-medullary region of the brain was artificially perfused via a cannulated vertebral artery, using an extracorporeal circuit fed from a femoral artery. In this way the carbon dioxide tension (PacCO2) and the oxygen tension in the blood supplying the brainstem could be imposed independently from the peripheral PCO2 (PapCO2) and PO2 (PapO2) in the systemic circulation. In all experiments the brainstem was kept hyperoxic. The steady-state ventilation VE could be described by (formula; see text) where Sp and Sc represent the peripheral and central sensitivity to carbon dioxide and K is a constant. Sc and K were independent of the PapO2. In general, peripheral hypoxia increased and peripheral hyperoxia decreased Sp, compared to normoxia. It is concluded that: (1) there is no interaction in the ventilatory response between peripheral O2-CO2 and central CO2 stimuli; and (2) a positive interaction in the ventilatory response between peripheral hypoxia and CO2 originates from the arterial chemoreceptors.

Animals↗
PubMed1982

Effect of temperature on the ventilatory response curve to carbon dioxide in anaesthetized cats.

Effects of body temperature on the ventilatory control system were studied in 17 anaesthetized cats. At different body temperatures (stabilized within 0.1 degrees C) CO2 response curves were measured in each cat. In with chloralose-urethan anaesthetized cats it was found that in the body temperature range of 34-40 degrees C, in which neither shivering nor panting occurred, no statistically significant trend with temperature was found in the slope (S) and the extrapolated intercept on the PaCO2-axis (B) of the linear CO2 response curve during hyperoxia as well as hypoxia. In two with pentobarbital anaesthetized cats similar results were obtained. The resting ventilation (at FICO2 = 0) did not change significantly, while the resting PaCO2 during hyperoxia showed a trend to increase with temperature just reaching the level of significance (P less than 0.05). Breathing frequency increased significantly with temperature (P less than 0.0005). When body temperature was elevated above 41 degrees C both the slope (S) and the intercept of the CO2 response curve (B) decreased. In three cats ventriculo-cisternal perfusion was performed and no apparent influence of body temperature was found on the relation between the PCSFCO2 and PETCO2 and on the VE-PCSFCO2 response curves. These findings show that body temperature has no important modifying effect on the ventilatory response to CO2 in anaesthetized cats in the temperature range of 34-40 degrees C.

Anesthesia, General↗
PubMed1982

Sites of action of halothane on respiratory pattern and ventilatory response to CO2 in cats.

To assess the major sites of action of halothane on the control of breathing, the ventilatory response to CO2 was studied in 11 cats and partitioned into tidal volume and frequency response. In these cats artificial perfusion of the ponto-medullary region was applied. In essence, this technique allows one to deliver to the brainstem blood-gas tensions and anesthetic concentrations at predetermined levels which are independent from those in the systemic circulation; thus the central and peripheral effects of halothane and CO2 can be determined separately. In cats exposed both centrally and peripherally to halothane (1.0-1.6%) tachypnea was observed which disappeared when the blood perfusing the brainstem was purged of halothane. From these results is follows that the tachypnea is exclusively due to an action of halothane on structures in the brainstem. In these cats the extrapolated Paco2 at zero ventilation was significantly lower during general halothane anesthesia than during light chloralose-urethane anesthesia (P less than 0.05). In cats lightly anesthetized with chloralose-urethane, halothane (0.5-1.5%) was either administered centrally or peripherally. In these experiments the "overall" ventilatory CO2 sensitivity of both the peripheral and central chemorereflex pathways decreased significantly (P less than 0.01). However, the ratio between these two sensitivities remained the same (P less than 0.5). The extrapolated Paco2 at zero ventilation was not affected by halothane provided its concentration was below 1% (P less than 0.7). From these results we conclude that the depressant effect of halothane on ventilation originates centrally as well as peripherally. Furthermore, from the findings that the ratio of the CO2 sensitivities and the extrapolated Paco2 at zero ventilation remained constant, the authors argue that halothane acts on the processing part of the neural respiratory drive (integrating centers) rather than on the neural activity of the peripheral and central chemoreceptors per se. The peripheral effect is mainly on the neuromechanical link between integrating centers and respiratory movements.

Animals↗
PubMed1981

Ventilatory response to carbon dioxide and apnoeic thresholds.

In 11 cats anaesthetized with chloralose-urethane, the steady state ventilation during hyperoxia was measured as a function of the central PaCO2 (PacCO2) and peripheral PaCO2 (PapCO2) using the technique of artificial ponto-medullary perfusion. The ventilatory response was described by VE = Sc . PacCO2 + Sp . PapCO2 - K where Sc and Sp represent the overall central and peripheral sensitivity to carbon dioxide. The post-hyperventilation apnoeic threshold values of PapCO2 for several fixed values of PacCO2 were also assessed. It was found that down to PaCCO2's and PapCO2's of about 3.5 kPa (26 mm Hg) the response surface for spontaneous ventilation could be used to satisfactorily predict the PapCO2 as a function of PacCO2 at apnoea. In 4 cats the ventilatory response to changes in central PCO2 was measured after carotid body denervation. These response curves were linear down to the PCO2-axis. We conclude that in anaesthetized cats during hyperoxia: (1) the above equation for the ventilation appears to be valid down to CO2 tensions of about 3.5 kPa (26 mm Hg); (2) the peripheral and central chemoreceptors exhibit neural activity down to at least 2.0 kPa (15 mm Hg); (3) in non-artificially perfused cats the CO2 response curve is linear down to ventilation zero; (4) the PaCO2 at apnoea (apnoeic 'threshold') in non-artificially perfused cats does not constitute a neural threshold for the peripheral or for the central chemoreceptors. Using these results a respiratory controller equation is proposed and some possible implications for the neural organization of the respiratory controller are discussed.

Animals↗
PubMed1980

Influence of the depth of anaesthesia on the peripheral and central ventilatory CO2 sensitivity during hyperoxia.

The influence of the depth of anaesthesia on the contribution of central and peripheral chemoreceptors to the slope of the ventilatory response to CO2 during hyperoxia was studied in 12 cats anaesthetized with chloralose-urethane or pentobarbital. By artificial perfusion of the pontomedullary region of the brainstem it was possible to assess the peripheral (Sp) and central (Sc) ventilatory sensitivity to CO2, as well as to vary selectively the level of anaesthesia at the ponto-medullary region (central level) or the overall level. In each cat Sp and Sc were assessed at the initial and at one or two deeper anaesthetic levels. Going from the initial to deeper anaesthetic levels both Sp and Sc decreased. However, Sp/Sc did not change significantly, whether the overall or the central level of anaesthesia was increased. Also the B-value, i.e. the PaCO2 of the extrapolated ventilation-PaCO2 curve at zero ventilation, did not change significantly when going to deeper anaesthetic levels. It is concluded that the respiratory depression caused by the anaesthetics used is due to an influence on the respiratory integrating centres, central chemoreceptors, or both.

Anesthesia↗
PubMed1979

Artificial perfusion of the ponto-medullary region of cats. A method for separation of central and peripheral effects of chemical stimulation of ventilation.

A technique is described by which the ponto-medullary region of anaesthetized cats is artificially perfused with their own blood in which the blood gas tensions are varied independently from gas exchange in the lung. Blood from a femoral artery is fed into a foamer and defoamer. After alteration of the blood gas tensions in this equilibrator it is pumped via a cannulated vertebral artery into the medulla oblongata, pons and cerebellum. In this way two separately perfused areas are obtained in which the blood gas tensions can be changed independently. The peripheral chemoreceptors are supplied with blood of the systemic circulation while the central chemoreceptors and respiratory integrating centres are artificially perfused. With this technique the contribution of the peripheral and central chemoreceptors to the total ventilation and their interaction can be assessed. In addition the method is also suitable for studying the effects of drugs on the central regulation of respiration and circulation.

Animals↗
PubMed1979

Relative contribution of central and peripheral chemoreceptors to the ventilatory response to CO2 during hyperoxia.

Using the technique of artificial ponto-medullary perfusion, the steady state ventilation during hyperoxia was measured in 15 anaesthetized cats as a function of the central PaCO2 (PaCO2) and peripheral PaCO2 (PapCO2). To a first approximation the ventilatory response was linearly related to both the central and peripheral arterial carbon dioxide pressures, viz. VE=SC . PacCO2 + Sp . PapCO2 - K where Sc and Sp represent the overall central and peripheral sensitivity to carbon dioxide. The mean ratio Sp/Sc was 0.48 (range 0.21 to 1.08). In carotid sinus denervated cats Sp was zero, while the values of Sc in these cats were in the range of Sc of cats with intact carotid sinus nerves. It is concluded that the peripse to CO2 under steady-state conditions. Chemodenervation experiments revealed that the carotid bodies play an essential role in this contribution.

Animals↗
PubMed1978

In vivo measurement of carbon dioxide tension with a miniature electrode.

A commercially available catheter type electrode with which PCO2 can be continuously measured in vivo and in vitro gave progressively less accurate results the longer the measuring period was extended. This proved to be due to temperature effects and a change in sensitivity with time. A correction procedure for these effects was developed which was based on two observations. 1. The relationship between temperature and the logarithm of the sensitivity of the electrode-amplifier combination was linear and virtually identical for 9 electrodes: 8% change in sensitivity for a deviation of 1 degree C from the temperature during calibration. 2. The change in sensitivity due to drift of the electrode output is approximately a logarithmic function of time: 1 h after calibration all electrodes exhibited a decreased sensitivity, varying between 0.3 and 16.7%. The drift effect can be dealt with by repeated calibrations, preferably at 1 1/2 h intervals. The adequacy of the correction procedure was assessed in in vivo measurements in cats and dogs. The mean PCO2 difference between the in vivo measurement, corrected for temperature and drift, and samples analyzed with a conventional electrode, was 0.005 kPa (0.04 mm Hg) with a standard deviation of 0.187 kPa (1.39 mm Hg).

Animals↗
PubMed1978

Influence of the CSF bicarbonate concentration on the ventilatory response to CO2 in relation to the location of the central chemoreceptors.

In anaesthetized cats, in which the cerebrospinal fluid bicarbonate concentration was varied by a ventriculocisternal perfusion technique, the ventilatory response to CO2 during hyperoxia could be satisfactorily described by VE = S(PCSFCO2 -B). Both the slope S and the intercept B were positively and linearly related to the CSF bicarbonate concentration. Assuming that the PCSFCO2 is equal to the PCO2 in extracellular fluid, it can be shown that VE is a linear, but not a unique function of the [H+] at the site of the chemoreceptors; the slope of this relation varies with the bicarbonate concentration at that site, possibly due to chemical complex formation between HCO-3 and Ca2+ or Mg2+. Changes in the B-value were related to the location of the central chemoreceptors with the models of Pappenheimer and Berndt aand their coworkers. It was found that changes in the CSF bicarbonate concentration are reflected for 60 per cent at the site of the central chemoreceptors, and that this was independent of the cerebral perfusion. Using Berndt's model a distance between CSF and central chemoreceptors of approximately 100 micron was found; this calculated distance is relatively insensitive to relationship (logarithmic or not) between ventilation and H+ concentration and to changes in cerebral perfusion, owing to the approximate nature of the diffusion model.

Animals↗
PubMed1976

The influence of CSF calcium and magnesium on the ventilatory response to carbon dioxide during hyperoxia.

Respiratory responses to inhaled carbon dioxide were measured in anaesthetized cats during perfusion of the ventriculocisternal system with artificial cerebrospinal fluid. A study was performed to evaluate the effect of changes in the magnesium and/or calcium concentration of the CSF on the CO2 response curve which was described as VE = S (PCSF, CO2 -- B). A decrease of S was observed when the magnesium concentration of the perfusion fluid was increased; the B-value remaining the same. The reverse was true down to magnesium concentrations of 0.6 mmol-1-1. Below this concentration S remained the same or decreased; the B-value was lowered. When both the calcium and magnesium concentrations of the CSF were changed, the relation between S and these concentrations could be described as to be proportional to CCAa-CMgb. The effect of changes in the calcium concentration was much more pronounced than comparable changes of the magnesium concentration as reflected by the magnitude of the exponents a and b which were found to be -2.80 (S.D. 0.11) and -0.60 (S.D. 0.03) respectively.

Animals↗