PubMed Health⌕ Search

Biomedical subjects

J de Goede

Publications and source records attributed to J de Goede.

12 recordsLinked to original sources
PubMed1989

A model study of the regulation of gastric acid secretion.

A computer simulation model is presented of the gastric phase regulation of gastric acid secretion in humans. The model is based on experimental data from the literature and includes terms representing gastric pH and gastric volume-dependent gastrin secretion, gastrin-dependent acid secretion, food storage in the stomach, and gastric emptying. We have explored the predictive value of the model in assessing the relative importance of gastric pH-dependent and gastric volume-dependent acid secretion mechanisms under various conditions. Similarly we have studied the role of gastric acid deregulation in achlorhydria, the Zollinger-Ellison syndrome, and duodenal ulcer, and the influence of the antacid drugs cimetidine and ranitidine under duodenal ulcer conditions. Model analysis of normal gastric acid regulation suggests that gastric volume-controlled acid secretion is of major importance during eating and predicts that pH-dependent gastrin secretion is of major importance in preventing excessively low pH levels between meals and during the night.

Achlorhydria↗
PubMed1985

Effects of halothane on the ventilatory response to hypoxia and hypercapnia in cats.

The influence of halothane 0.8-1.2% inspired on the peripheral hypoxic chemoreflex was investigated in 13 cats subjected to artificial brain stem perfusion (ABP). This technique allows for an independent control of blood gas tensions and halothane concentration between blood perfusing the brain stem (central) and the systemic circulation (peripheral). In six cats the ventilatory response to isocapnic hypoxia was assessed during overall halothane anesthesia (HO) before and during ABP. Before ABP, systemic and brain stem circulations both were rendered hypoxic. During ABP, hypoxia was induced systemically while the brain stem was maintained hyperoxic. The ventilatory response in non-ABP cats (mean 698 ml . min-1 at PaO2 6.6 kPa; 50 mmHg) was about half the response in ABP cats (mean 1,194 ml . min-1 at PaO2 6.5 kPa; 49 mmHg), indicating that in the presence of halothane, central hypoxia depressed ventilation appreciably. Compared with chloralose-urethane anesthesia (CU), halothane reduced the ventilatory response to hypoxia in both perfusion conditions but never abolished it. To assess the influence of halothane on peripheral and central mediation of the CO2 response during hypoxia, each was assessed during CU anesthesia, during HO, and with halothane applied exclusively peripherally against a background of CU (CUHP). In all drug states, the periphery was kept hypoxic and brain stem hyperoxic. Compared with CU anesthesia, HO and CUHP anesthesia reduced both peripheral (Sp) and central (Sc) CO2 sensitivity but not the Sp/Sc ratio. Similarly, the extrapolated PaCO2 at zero ventilation was not detectably different among these three states.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1984

Effects of brain stem hypoxaemia on the regulation of breathing.

In 22 cats, anaesthetized with chloralose-urethane, the brain stem was artificially perfused with their own blood via a gas exchanger in which the central PaO2 and PaCO2 were imposed independently from the peripheral PaO2 and PaCO2 in the systemic arterial blood. The effects of brain stem hypoxaemia on ventilation and on the ventilatory responses to central and peripheral chemoreceptor stimulation were investigated. When the central PaO2 was lowered from 375 mm Hg to 100 and 50 mm Hg, keeping all other blood gas tensions constant, ventilation decreased on the average by 0.22 L X min-1 and 0.54 L X min-1, respectively. The increase in ventilation due to peripheral hypoxaemia and the sensitivities to central and peripheral CO2 (delta VE/delta PaCO2) were independent of the central PaO2, despite the depression of ventilation. The sensitivity to central CO2 was also not influenced when central hypoxaemia was combined with peripheral hypoxaemia. The linear VE-VT relation was not affected by central hypoxaemia. Our findings suggest that the functioning of respiratory neurons in the brain stem is unaltered during moderate central hypoxaemia.

Animals↗
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

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↗
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

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

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↗
PubMed1975

Conductance fluctuations in Ranvier nodes.

Voltage fluctuations associated with the sodium system were measured upon elimination of the potassium current in the nodal membrane by internal application of cesium-ions. The intensity of this noise reaches a maximal value at a membrane potential in the vicinity of --40 mV. Here the power spectrum consists of two additive components: a 1/f component and a Lorentzian. The Lorentzian is associated with h-gate kinetics and is consistent with the binary state conduction model. On the basis of this model the sodium-channel conductance is calculated to be 2 to 5-10(-12) S. The analysis is complicated by the existence of an incomplete slow sodium inactivation process.

Animals↗