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Biomedical subjects

P Foëx

Publications and source records attributed to P Foëx.

15 recordsLinked to original sources
PubMed1979

Continuous measurement of blood gases in vivo by mass spectrometry.

Continuous analysis of oxygen and carbon dioxide tension in the blood phase, over periods of 4-5 h, was carried out in the pulmonary artery (93 determinations in six anesthetized dogs) and in the aorta (29 determinations in four anaesthetized dogs). Silastic-covered stainless steel catheters attached to a mass spectrometer were used. The mass spectrometer signals were linearly related to the blood-gas tensions measured by conventional analysis. The mass spectrometer signals were calibrated in vivo by exposing the animals to high and low oxygen and carbon dioxide tension. With such in vivo calibration the slopes of the straight line regressions for mass spectrometer PO2 or PCO2 on PO2 or PCO2 by conventional analysis were comprised between 0.944 and 1.031 while the standard error of the slopes were between 0.019 and 0.031. Deliberate reductions of cardiac output had little effect on the mass spectrometer readings.

Animals↗
PubMed1979

Effects of metoprolol on systemic haemodynamics, myocardial performance and the coronary circulation during halothane anaesthesia.

The effects of metoprolol 1 mg kg-1 i.v. on the systemic and coronary circulations and on myocardial performance were studied in nine open-chested dogs ventilated with halothane 0.8% in oxygen at normocarbia. In terms of the chronotropic effect, this dose of metoprolol produced a substantial shift to the right of the dose-response curve to isoprenaline; substantial reductions of arterial pressure (10%), cardiac output (21%), aortic blood acceleration (13%), left ventricular dP/dt max (13%) and left ventricular power (25%) were observed. Both preload, represented by left ventricular end diastolic pressure, and afterload, represented by systemic vascular resistance, increased. Left circumflex coronary blood flow and myocardial oxygen consumption decreased by approximately the same amount as peak ventricular power.

Anesthesia, Inhalation↗
PubMed1977

Properties of blood oxygen transport in the turtle Pseudemys scripta and the tortoise Testudo graeca: effects of temperature, CO2 and pH.

Properties of oxygen-haemoglobin binding have been investigated in the aquatic turtle Psuedemys scripta and the terrestrial tortoise Testudo graeca. Haematocrit (30-35%) and haemoglobin concentration (12-14 g/100 ml blood) were similar in both species. P50 at physiological levels of PCO2 (20-25 mm Hg) was 21 mm Hg in Pseudemys, compared with 23 mm Hg in Testudo. The Bohr shift of the blood of both the turtle and the tortoise was almost identical at -0.28. The heat of oxygenation, deltaH, reflecting the temperature sensitivity of O2-Hb affinity, was -10.55 in Pseudemys and -8.12 kcal/mol in Testudo. These data on whole blood do not support previous generalizations in the literature suggesting marked differences in oxygen-haemoglobin binding between aquatic and terrestrial chelonian reptiles.

Animals↗
PubMed1977

Haemodynamic responses to isoflurane anaesthesia and hypovolaemia in the dog, and their modification by propranolol.

In six dogs chronically implanted with flow and pressure transducers, equipotent inspired concentrations of halothane and isoflurane were determined as the minimum inspried concentration of each agent which would abolish an individual dog's response to paw clamping. In equipotent concentration, isoflurane (1.2%, SD 0.2%) caused less myocardial depression than halothane (1.0%, SD 0.1%). Dose-response studies were possible up to a mean inspired isoflurane concentration of 3.0%, both before and after propranolol 0.3 mg kg-1, i.v. After propranolol, sensitive indices of myocardial contractility were depressed at all concentrations of isoflurane, indicating a moderate degree of beta-receptor activation by isoflurane. The haemodynamic response to hypovolaemia during isoflurane anaesthesia was not modified by propranolol.

Anesthesia, Inhalation↗
PubMed1976

Interaction of anesthesia, beta-receptor blockade, and blood loss in dogs with induced myocardial infarction.

The cardiovascular effects of halothane-nitrous oxide anesthesia, and beta-receptor blockade with either propranolol or practolol, were studied in 15 dogs in which severe myocardial infarction had been induced ten days earlier. The hemodynamic responses to blood loss amounting to 25 per cent of estimated blood volume, and its subsequent replacement, were studied before and after induction of beta-receptor blockade. In terms of cardiac output and aortic blood flow acceleration, cardiac performance in the absence of beta-blockade was markedly impaired during steady-state anesthesia, compared with corresponding values in normal dogs. Practolol (2.0 mg/kg) administered during anesthesia induced no significant circulatory change other than a 14 per cent decrease in heart rate and a 25 per cent increase in strode volum. Propranolol (0.3 mg/kg) caused a comparable reduction of heart rate, but significantly reduced cardiac output (-27 per cent), aortic blood flow acceleration (-26 per cent), and peak LV power (-19 per cent), and increased systemic vascular resistance (+49 per cent). The two drugs caused comparable shifts of the isoproterenol dose-response curve during anesthesia. Graduated blood loss during anesthesia, to a total of 25 per cent of blood volume, caused consistent circulatory changes (decreased mean arterial pressure cardiac output, peak LV power, LV minute work) that were essentially similar before and after beta-receptor blockade with either propranolol or practolol. The positive inotropic effect of calcium gluconate during halothane anesthesia was significantly reduced following either propranolol or practolol, but the hemodynamic responses to changes of systemic vascular resistance induced with acetylcholine or phenylephrine were not modified by beta-receptor blockade.

Acetylcholine↗
PubMed1976

Cardiac responsiveness to beta-adrenergic stimulation in experimental anemia.

Cardiac reactivity of beta-adrenergic stimulation was assessed by isoproterenol dose-reponse curves (dose range 0.025-0.4 mug/kg) before and 1 h after the rapid induction of anemia in dogs anesthetized with halothane:N2O:O2. Anemai (hematocrit = 16 +/- 4%) was induced by an isovolumic exchange transfusion with Dextran 70, and was followed by significant increments in cardiac output (+57 +/- 9%), max dP/dt of the left ventricle (+37 +/- 7%), and in peak acceleration of blood flow in the ascending aorta (+46 +/- 13%). Anemia was associated with a significant reduction of the chronotropic responses to all but the lowest dose of isoproterenol. The simultaneously determined inotropic responses (max dP/dt) where the same before and after the induction of anemia. The responses in terms of peak acceleration of aortic blood flow tended to be greater in the anemic than in the control phase, at all dose levels used. These findings indicate that in rapidly induced experimental anemia the heart is capable of responding to marked degrees of beta-adrenergic stimulation, representing a more than two-fold increase in the dP/dt.

Adrenergic beta-Agonists↗
PubMed1976

A development of the oxyhemoglobin dissociation curve analyzer.

The development and improvement of an oxyhemoglobin dissociation curve analyzer is described. PO2 electrode performance was improved by electrochemical means and circuits are described for processing the PO2 and pH signals from the analyzer. A circuit for automatically correcting the curve for Bohr shifts from pH 7.40 is described, and the performance of the Bohr shift unit is verified by experiment. The analyzer produces curves under standard conditions of PCO2 40 mmHg, pH 7.40, and 37 degrees C.

Electrodes↗
PubMed1975

Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia.

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).

Anesthesia, Inhalation↗
PubMed1975

Effects of changes in PaCO2 on pulmonary input impedance.

Pulmonary arterial input impedance spectra were computed in goats in whom the appropriate pressure and flow transducers had been chronically implanted. In response to either hypocapnia or hypercapnia, under anesthesia (1% halothane in a 70% nitrous oxide--30% oxygen mixture) there were no significant modifications of impedance at zero frequency; no consistent or significant changes in the impedance moduli at frequencies between 2 and 14 Hz were observed; the position of the first impedance minimum or the subsequent maximum was not modified; however, pulmonary vascular resistance increased significantly with hypercapnia. Although the load opposing right ventricular ejection was not modified by variation of Paco2, right ventricular work was reduced in response to hypocapnia and augmented in response to hypercapnia.

Animals↗
PubMedDate not supplied

Oxygen availability during hypothermic cardiopulmonary bypass.

Oxygen availability during cardiopulmonary bypass was assessed in 22 patients under hypothermic and relatively normothermic conditions. The patients were divided into two groups, 17 of whom received ACD blood and 5, CPD blood. The mean P50 for all patients fell from a preoperative value of 25.9 +/- 2.4 (SD) to 15.6 +/- 2.1 during hypothermia confirming a leftward shift of the oxyhemoglobin dissociation curve. Oxygen uptake, calculated from a-v oxygen content differences (avDO2) and flow, was significantly lower during hypothermic bypass (65 +/- 27 ml/min) than during rewarming (121 +/- 41 ml/min). The increase in oxygen affinity during hypothermia was influenced also by changes in acid base and 2,3-DPG concentrations, the changes being similar in both the ACD and CPD groups of patients. During rewarming, however, oxygen availability was increased in the CPD group presumably from significantly increased 2,3-DPG concentrations. A "functional" value of hemoglobin, based upon the effects of the shift of the oxyhemoglobin dissociation curve and, therefore, reflecting the true capacity of hemoglobin to unload oxygen at the tissue level, was calculated. During the hypothermic phase of bypass, this functional hemoglobin was only 4.2 g/100 ml blood, suggesting that, in spite of reduced metabolic demands, oxygenation reserves are minimal.

Adult↗
PubMedDate not supplied

[CO2 "wash-out" : a factor contributing to increase myocardial performance in the face of hypoxia (author's transl)].

The cardiovascular system of the anaesthetized dog has been used as an experimental model for studying the mechanisms of the haemodynamic responses to hypoxia. Together with aortic and left circumflex coronary artery blood flow (electromagnetic flow transducers), aortic and left ventricular pressures have been recorded and blood has been sampled from the aorta and the coronary sinus (PO2, PCO2, pH). During short periods of hypoxia an improvement of myocardial performance has been observed both before and after administration of a beta-adrenergic receptor blocker and a marked reduction of coronary sinus PCO2 has been noted. When hypoxia was caused by a mixture of nitrogen (95%) and CO2 (5%) an improvement of performance was observed only before administration of the beta-blocker. The slope of the relationship between PCSCO2 and cardiac performance was found to be similar before and after administration of the beta-blocker and also similar to that observed in studies of the response of the isolated heart muscle to acute hypocapnia. Besides beta-adrenergic receptor stimulation, a reduction of coronary sinus PCO2 (CO2 wash-out due to an increase of coronary blood flow) could be a factor contributing to the maintenance of myocardial performance in the face of hypoxia.

Animals↗
PubMedDate not supplied

[Role of P50 in resuscitation (author's transl)].

The amount of oxygen made available to the tissues of the body depends essentially upon pulmonary gas exchanges, cardiac output and its regional distribution, haemoglobin concentration and also upon the oxygen affinity of the haemoglobin molecule. That a standard oxyhaemoglobin dissociation curve faithfully describes oxygen loading and unloading both in healthy subjects and in those suffering from pathological process has come under attack. Beside the effect of pH, PCO2 and temperature, the oxyhaemoglobin dissociation curve can be modified by alterations of other factors (concentration of 2,3-diphosphoglycerate, hormones, drugs). Although the shifts of the oxyhaemoglobin dissociation curve, expressed by variations of P50 may seem minute, the effect of these shifts, expressed in terms of the "functional value of haemoglobin" are very large. Assessment of the intensive care patient must take into account the effect of alterations of the oxyhaemoglobin dissociation curve which can either increase or diminish tissue oxygenation.

Blood↗
PubMedDate not supplied

Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions.

The responses to hypocapnia and to hypercapnia of both the systemic and the coronary circulations have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia. In the absence of significant variations of myocardial contractility, the reduction of cardiac output, because of hypocapnia, was determined by the increase of systemic vascular resistance, while the increase of cardiac output because of hypercapnia was determined by an increase of heart rate without change of stroke volume. The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption. Such disparity between oxygen supply and demand, together with the effect of pH and PCO2 on the oxyhaemoglobin dissociation curve led to a marked reduction of coronary sinus PO2 in response to hypocapnia and a marked increase of coronary sinus PO2 in response to hypercapnia. The data suggests that PCO2 (or respiratory alterations of pH) may have a direct effect on the regulation of coronary blood flow. The low coronary sinus PO2 observed at hypocapnia may suggest the risk of myocardial ischaemia.

Animals↗