Biomedical subjects
J Butler
Publications and source records attributed to J Butler.
A non-equilibrium state of deoxyhaemoglobin. Temperature-dependence and oxygen binding.
After reduction of human methaemoglobin by solvated electrons a non-equilibrium low-spin state of deoxyhaemoglobin is formed which has the characteristic haemochrome spectrum. This haemochrome state is ascribed to a weakly 6-coordinated structure of the haem, which is stabilised by the protonated distal histidine. Oxygen binding is not inhibited by the presence of the weak interaction in the haemochrome state. From the pH dependence of the biphasic behaviour of the oxygen binding a pK of about 8.8 is obtained which is ascribed to the deprotonation of the distal histidine which is in the proximity of a negative ion. A model is proposed to explain the complex spin-equilibria observed in methaemoglobin. The enthalpy of activation of the decay of the haemochrome state is about 53 kJ x mol(-1) and increases to 90 kJ x mol(-1) in the presence of 1 M methanol, indicating a strong interaction between methanol and haemoglobin. Around pH 8.4 the rate constant of the binding of oxygen to the haemochrome state is so high that it may well be diffusion controlled.
Enzymic markers to identify muscle-nerve formation during embryogenesis: modified myosin ATPase and silver-cholinesterase histochemical reactions.
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Kinetic data for redox reactions of cytochrome c with Fe(CN)5X complexes and the question of association prior to electron transfer.
Use of rigorous equilibration kinetics to evaluate rate constants for the Fe(CN)6 4- reduction of horse-heart cytochrome c in the oxidized form, cyt c (III), has shown that limiting kinetics do not apply with concentrations of Fe(CN)6 4- (the reactant in excess) in the range 2-10 x 10(-4) M, I = 0.10 M (NaCl). The reaction conforms to a first-order rate law in each reactant, and at 25 degrees C, pH 7.2 (Tris), it is concluded that K for association prior to electron transfer is less than 200 M-1. From previous studies at 25 degrees C, ph 7.0 (10(-1) M phosphate), I = 0.242 M (NaCl), a value K = 2.4 x 10(3) M-1 has been reported. Had such a value applied, some or all of the redox inactive complexes Mo(CN)8 4-, Co(CN)6 3-, Cr(CN)6 3-, Zr(C2O4)4 4- present in amounts 5-20 x 10(-4) M would have been expected to associate at the same site and partially block the redox process. No effect on rats was observed. With the reductants Fe(CN)5(4-NH2-py)3- and Fe(CN)5(imid)3-, reactions proceeded to greater than 90% completion and rate laws were again first order in each reactant. Rate constants (M-1 sec-1) at 25 degrees C, pH 7.2 (Tris), I = 0.10 M (NaCl), are Fe(CN)6 4- (3.5 x 10(4)), Fe(CN)5(4-NH2py)3- (6.7 x 10(5), and Fe(CN)5(imid)3- (4.2 x 10(5). Related reactions in which cyt c(II) is oxidized are also first order in each reactant, Fe(CN)6 3- (9.1 x 10(6)), Fe(CN)5(NCS)3- (1.3 x 10(6)), Fe(CN)5(4-NH2py)2- (3.8 x 10(6) at pH 9.4), and Fe(CN)5(NH3)2- (2.75 x 10(6) at ph 8). Redox inactive Co(CN)6 3- (1.0 x 10(-3) M) has no effect on the reaction of Fe(CN)6 3- which suggests that a recent interpretation for the Fe(CN)6 3- oxidation of cyt c(II), I = 0.07 M, may also require reappraisal.
Anxiolytic effects of low dosage nitrous oxide-oxygen mixtures administered continuously in apprehensive subjects.
We observed the effect of low doses of nitrous oxide on the cardiovascular and respiratory systems, the cortisol output in blood and saliva, and the degree of sedation and analgesia of 20 volunteers. A psychologic screening inventory was also performed. We found nitrous oxide, at low dosage, to be primarily an anxiolytic and not an analgesic or amnesic agent. The nasally inhaled concentrations necessary to induce an anxiolytic effect varied from subject to subject, ranging from 30% to 65% and averaging 35% to 40%. This finding justifies the use of the gas to relieve anxiety instead of nonvolatile parenterally administered psychosedatives and narcotics. Nitrous oxide is preferable because its action is established within several minutes, it is rapidly eliminated at the conclusion of a procedure, and the sensorium is clear after five or six minutes. The gas is simply and safely administered with fail-safe apparatus designed specifically for this purpose. The technic is admirably suited for use in ambulatory care units where minor surgical or dental procedures are performed.
Lung volume and pleural pressure effects on ventricular function.
To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.
Functional aspects of canine bronchial-pulmonary vascular communications.
Experiments in anesthetized open-chest dogs indicated that blood from the canine bronchial circulation may drain into both the arterial and venous sides of the alveolar drain into both the arterial and venous sides of the alveolar vessel bed. Evan's blue dye injected into the systemic circulation appeared in the effluent from a left lower lobe pulmonary arterial segment in which inflow was stopped with a snare and outflow through the alveolar vessel bed was stopped by maintaining zone 1 conditions. To determine the influence of mean systemic arterial pressure on lobar bronchial flow, flows from arterial and venous cannulas were measured at different mean systemic arterial pressures (lung volume history constant). Influence of lung volume and transpulmonary pressure (Ptp) change were each examined utilizing the hysteresis characteristics of the lung pressure-volume curve. Mean total flows ranged from 2.26 to 5.26 ml/min with 43.61% draining through the arterial side. Flow decreased with lower systemic arterial pressure, high Ptp, and higher lung volume. Distribution of flow was influenced only by lung volume changes. Results indicate that the communication sites contributing to the arterial drainage are located within the alveolar vessel bed. Since bronchial flow drains to both sides of the alveolar vessel bed, it must be considered when interpreting results from "isolated" pulmonary circulation preparations.
Effect of positive end-expiratory pressure on canine ventricular function curves.
Recent observations have been interpreted to suggest altered ventricular function during ventilation with positive end-expiratory pressure (PEEP), apart from the effect of reduced preload. We constructed ventricular function curves in 14 anesthetized dogs as PEEP was varied under closed- and open-chest conditions. The systemic venous flow of the animal was diverted through an external circuit so that blood return to the right atrium could be varied stepwise from 1--4.5 l/min before and after 15 cmH2O PEEP was applied to the airway. Pressures adjacent to the heart were measured with thin fluid-filled water sensors to enable estimation of transmural pressure. Alterations in ventricular function were assessed by comparing tangential slopes as well as the atrial pressure differences separating the curves at high and low stroke volumes. Sensitivity of this method to cardiac depression was demonstrated by similar comparisons made before and after propranolol. Curves using transmural pressure on and off PEEP were statistically indistinguishable. We conclude that hemodynamic changes resulting from PEEP are attributable to the combined effects of reduced preload and raised juxtacardiac pressure, without ventricular dysfunction.
Mechanical effect of lung distention with positive pressure on cardiac function.
To investigate the contribution of local mechanical factors to the alteration in ventricular function that occurs during ventilation with positive end-expiratory pressure (PEEP), the hemodynamic effects of increasing end-expiratory pressure with both lungs ventilated, and with the upper lobes, lower lobes, right and left lungs selectively ventilated, were examined in 20 anesthetized open-chest dogs. The rise in pressure between the lungs and heart exceeded that of the ipsilateral atrium. Increasing PEEP with both lungs ventilated caused atrial and mediastinal (juxtacardiac) pressures to increase and stroke volume to decrease more than with ventilation of smaller lung volumes. Patterns causing distention of lung tissue adjacent to the right heart were associated with the greatest decrease of stroke volume. Decreasing stroke volume related more closely to increasing right atrial than to left atrial pressure. We concluded that juxtacardiac pressure increases markedly as the lungs distend, even in an open-chest preparation, and that preload reduction on this basis, not ventricular impairment, best explains diminished cardiac output during ventilation with PEEP.
Constancy of functional residual capacity in the supine position during hypoxia and hyperoxic hypercapnia.
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The pulmonary function test: cautious overinterpretation.
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Avoidance of masking difficulties using electrocochleography. Case report.
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Effects of positive end-expiratory pressure on intracranial pressure in dogs with intracranial hypertension.
Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in the absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.
Partial characterization of a lymphoid cell line (Reh) product with leukocyte inhibitory factor (LIF) activity.
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