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Biomedical subjects

J Butler

Publications and source records attributed to J Butler.

At least 271 records · Page 15Linked to original sources
PubMed1982

Mechanism by which positive end-expiratory pressure increases cerebrospinal fluid pressure in dogs.

We investigated possible mechanisms by which positive end-expiratory pressure (PEEP) increased cerebrospinal fluid pressure (PCSF) in anesthetized mechanically ventilated dogs. In part I of the study, PEEP was applied in 5 cmH2O increments each lasting 1-2 min, before and after a snare separated the spinal from the cerebral subarachnoid space in each animal. Next, with the spinal cord still ligated, the dogs were ventilated without PEEP while superior vena cava pressure (PSVC) was raised in 5 cmH2O increments by means of a fluid reservoir connected with the superior vena cava. Cerebrospinal fluid pressure in the cisterna magna increased immediately and in parallel with PEEP before and after the spinal subarachnoid space was occluded and also increased when PSVC was raised independently; in all circumstances the increase in PCSF correlated closely with PSVC (r = 0.926). In part II of the study, arterial blood gases were drawn before and after PEEP was applied in the same increments and for the same duration as in part I. Cerebrospinal fluid pressure measured with a hollow skull screw again rose in parallel with PEEP, whereas arterial carbon dioxide tension rose only slightly at 60 s. In part III of the study, mean arterial pressure (Pa) was allowed to decrease with PEEP or was held constant by distal aortic obstruction and volume infusion. Cerebrospinal fluid pressure increased regardless of Pa, but the increase was greater when Pa was held constant than when it fell with PEEP. We conclude that PEEP increases PCSF primarily by increasing PSVC and decreasing cerebral venous outflow. This effect is augmented if cerebral arterial inflow is increased as well.

Animals↗
PubMed1982

Estimation of transmural cardiac pressures during ventilation with PEEP.

Assessment of ventricular performance during positive end-expiratory pressure (PEEP) requires accurate measurement of transmural cardiac pressures. We investigated the influence of PEEP on the atrial and juxtacardiac pressures estimated by different methods in eight dogs. Left atrial pressure was measured by hydraulic and transducer-tipped catheter systems. Juxtacardiac pressure was estimated by an esophageal balloon and by air- and fluid-filled mediastinal wafer sensors. The supine canine heart was observed radiographically to lift and tilt during PEEP subjecting the left atrial catheters and the fluid-filled mediastinal wafer to a hydrostatic pressure increase. The esophageal balloon seriously underestimated the pressure increment occurring during the application of PEEP in the supine (but not prone) position, perhaps because mediastinal weight was lifted from the esophagus during lung distension. Similar phenomena were also observed in three human subjects. We conclude that lung distension lifts and tilts the heart in a supine preparation causing a hydrostatic increase of intracavitary pressure and attenuation of the esophageal pressure increment. These effects help to account for the apparent alterations of ventricular compliance and performance previously attributed to PEEP.

Animals↗
PubMed1982

A Starling resistor regulates cerebral venous outflow in dogs.

This investigation was undertaken to determine whether a Starling resistor or venous waterfall effect exists between the sagittal sinus and the cerebral veins such that increases in sagittal sinus pressure (Pss) do not abolish cerebral venous outflow and to examine two possible contributions of extracranial venous valves in regulating outflow. Anesthetized dogs were subjected to positive end-expiratory pressure (PEEP) before and after intracranial pressure (Pic) was elevated by inflation of an epidural balloon. PEEP raised Pss equally in all animals, but Pic and cerebral venous pressure (Pcv) increased less in the presence of intracranial hypertension. When Pss was low, passage of a catheter in the cerebral vein in and out of the sagittal sinus demonstrated an abrupt drop in pressure as the sinus was entered. When Pss was raised and lowered independently of superior vena caval pressure (Psvc) the changes in Pic and Pcv were less when Pss was decreased than when it was increased. Sustained increases and decreases in Psvc caused increases and decreases in Pcv, Pic, Pss, and external jugular venous pressure (Pejv) regardless of whether external jugular venous valves were present or absent. We conclude that a Starling resistor between the sagittal sinus and the cerebral veins regulates cerebral venous outflow when Pss is increased by PEEP and other maneuvers that raise Psvc. The waterfall maintains Pcv and Pic at normal levels when Psvc and Pss are reduced. Extracranial venous valves are not essential to this mechanism.

Animals↗
PubMed1982

Federal health program reforms: implications for child health care.

The "Omnibus Budget Reconciliation Act of 1981" included a number of provisions designed to reduce federal spending for health care and to increase state authority over health programs. Evidence concerning the financial condition and health care needs of children served by federally-financed health programs, and recent trends in coverage and eligibility, make it possible to assess the likely impact of the new legislation. One conclusion seems clear: extensive federal funding reductions cannot be accommodated by eliminating excesses. While reforms of the Medicaid program may be advisable for a number of reasons, a simple reduction to funding will have serious, adverse consequences for poor children.

Aid to Families with Dependent Children↗
PubMed1981

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.

Chemical Phenomena↗
PubMed1981

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.

Animals↗
PubMed1981

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.

Adolescent↗
PubMed1981

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.

Animals↗
PubMed1981

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.

Animals↗
PubMed1981

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.

Animals↗
PubMed1981

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.

Animals↗