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Biomedical subjects

T C Lloyd

Publications and source records attributed to T C Lloyd.

At least 37 records · Page 2Linked to original sources
PubMed1982

Effect of oleic acid injury on lung-heart interaction during ventricular filling.

Part of ventricular filling pressure is expended in deforming the lungs and oleic acid lung injury, which reduces lung compliance, might be expected to change the magnitude of this effect. Left ventricular pressure-volume curves from 13 treated and 13 uninjured dogs were compared. Curves were obtained by inflating a balloon in the flaccid left ventricle of the freshly dead dog. The extracardiac compliance component was determined by subtracting ventricular pressures observed when lungs were collapsed from those observed during inflation to levels duplicating both airway pressure and lung volume of uninjured dogs. We found that the respiratory system compliance opposing ventricular filling is much less than is predicted from the compliance opposing tidal ventilation. This suggests that cardiac filling imposes a local shape change rather than a general lung volume change. Injury only slightly decreased cardiac filling compliance although it markedly reduced lung inflating compliance. These results are consistent with citations showing that edema increases lung compliance by altering surface properties and airway closure with little change in tissue deformability. Thus, while edema may alter cardiac performance by changing pleural pressure, it has little influence on the pulmonary component of diastolic compliance.

Animals↗
PubMed1982

Respiratory system compliance as seen from the cardiac fossa.

Changes in cardiac size and shape should impose stresses on the surrounding lung and chest wall. To examine pressure-volume relationships of the cardiac fossa we measured pressures required to increase the pericardial volume of freshly killed dogs at different levels of lung inflation, first by expanding the pericardium uniformly and then by expanding only the left ventricle. In both cases we obtained linear pressure-volume relationships, the slopes of which expressed an apparent compliance. Compliance decreased as lung volumes were increased by raising end-expiratory pressure, and compliance with symmetrical pericardial filling exceeded that with asymmetrical (left ventricular) distension. These compliances were compared with the total respiratory system compliance measured during tidal ventilation, and we found that the compliance of the cardiac fossa was significantly less than would be predicted from lung and chest wall compliances as classically measured. We concluded that the respiratory system imposes a finite compliance load on cardiac filling that raises local epicardial pressure above ambient pleural pressure. This respiratory system load depends upon lung volume and the cardiac shape change.

Animals↗
PubMed1980

Failure of tracheal distension to inhibit breathing in anesthetized dogs.

Using anesthetized spontaneously breathing dogs, we compared the respiratory effects of tracheal distension with the effects of changes in lung volume before and after vagotomy. We used an endotracheal tube with a long cuff to distend the trachea to pressures of 10, 20, and 40 cmH2O. Lung volume increases were imposed by expiratory threshold loading, and volume was decreased by abdominal compression, both of which caused outward rib cage displacement. During expiratory loading, the tidal volume was unchanged but respiratory frequency and minute volume fell and an active expiratory effort appeared; whereas frequency and minute volume rose, but tidal volume fell during abdominal compression. Tracheal distension evoked no discernible change in breathing. Following vagotomy, tidal volume and minute volume fell, and frequency rose slightly, during expiratory loading but abdominal compression was without effect. After vagotomy, 40 cmH2O tracheal distension caused a slight frequency increase. We concluded that the potential role of tracheal deformation in the reflex control of breathing is insignificant in comparison with the other airways.

Animals↗
PubMed1980

Reflex effects of left heart and pulmonary vascular distension on airways of dogs.

Two types of experiments were performed in anesthetized dogs on cardiopulmonary bypass to see if pulmonary vascular congestion and left heart distension would induce reflex bronchoconstriction. First we distended the isolated left heart and lung vessels with blood while ventilating the lungs and measuring airflow, tidal volume, and transpulmonary pressures. Congestion reduced dynamic compliance and increased inspiratory resistance. Vagotomy increased compliance and decreased resistance but did not alter the effects of congestion. Then we measured changes in tracheal wall tension while we separately distended the pulmonary vessels and left heart. Left heart distension increased tracheal tension, whereas pulmonary congestion increased tension in some dogs but decreased it in others. All effects were eliminated by vagotomy. We concluded that although left heart distension and pulmonary vascular congestion may reflexly increase airway tone, pulmonary congestion may at some times reflexly reduce tone. None of these reflex changes, however, appear to be important in the modest (approximately 20%) changes in airflow dynamics observed during combined left heart and pulmonary vascular distension.

Airway Resistance↗
PubMed1979

Effects of extrapulmonary airway distension on breathing in anesthetized dogs.

Anesthetized dogs with open chests were perfused with a pump-oxygenator. We first observed the effects of intermittent periods of sustained inflation of both lungs, of only one lobe, and of an intra-airway balloon on the diaphragm electromyogram (EMG). Lung or lobe inflation with low pressures depressed respiratory frequency (fr) by prolonging expiratory time (TE) in proportion to inflating pressure, but balloon inflation was without effect. We next intermittently inflated one or two lobes after all others were ligated and thereafter inflated all the extrapulmonary airways following total lung excision. Lobe inflation, by varying TE, decreased fr at low pressures and often increased fr at higher pressures. Extrapulmonary airway distension slightly increased fr and the mean rate of rise of the integrated EMG, but decreased inspiratory time and peak EMG amplitude. TE was slightly prolonged by low pressures when using sustained airway pressurization but was shortened by higher pressures when distending cyclically. In comparison to lobe inflation, the effects from isolated airways were small, and the inhibitory effect of lung inflation could not be attributed to them.

Anesthesia↗
PubMed1978

Reflex effects of lung inflation and inhalation of halothane, ether, and ammonia.

Anesthetized dogs were perfused at constant pressure from an external oxygenator after removing their hearts. Systemic vascular resistance (SVR) and spontaneous breathing effors were monitored while the lungs were ventilated briefly at a low frequency with several tidal volumes and at a low volume with several frequencies. Inflation depressed respiratory activity and transiently lowered SVR to a minimum from which it spontaneously partially recovered. The transient and sustained SVR changes were directly related to peak inflating pressure, independent of the mode of ventilation. Pressurization of the sublaryngeal extrapulmonary airways and addition of ammonia to lung inspirate were without effect. Ventilation with 7% ether had no effect, but at 13% it occasionally increased respiratory activity. Ventilation with 7% halothane depressed SVR and stimulated respiration, whereas 13% caused vasodilation and apnea. The magnitudes of SVR responses to halothane and to inflation were uncorrelated. All effects of inflation and inhalants were eliminated by vagotomy. We condluded that the systemic vessels appear to respond to changes in respiratory minute volume; that this is brought about by intrapulmonary receptors, perhaps of more than one type; that two classical "irritants" have little effect in dogs; and that halothane has effects on breathing and SVR consistent with stimulation of J-receptors.

Ammonia↗
PubMed1978

Effects of pulmonary congestion and of left atrial distention on breathing in dogs.

Prior experiments showed that pulmonary congestion may initiate tachypnea from lung receptors and that left atrial distention has no significant effect on breathing, but in those experiments secondary reflexes could have determined the results. In this study we separately distended the entire pulmonary vascular bed, the arterial compartment, and the left atrium in dogs perfused and oxygenated by an external system while ventilating and while not ventilating the lungs. Distending pressures ranged from 20 to 70 Torr, and as output variables we measured the initial rate of inspiration, peak inspiratory magnitude, inspiratory duration, expiratory duration, and breathing frequency from the diaphragmatic electromyogram. Total vascular congestion caused prolongation of expiration and lowering of frequency without effect on inspiratory duration, its rate or magnitude. A smaller depression was induced from the arterial compartment. Left atrial distention, which failed to occur sufficiently often to be attributable to dogs in general, had much less effect. However, when a related change in breathing did occur, it was limited to a shortening of inspiratory duration.

Animals↗
PubMed1977

Cardiopulmonary baroreflexes: left ventricular effects.

Systemic vascular resistance of dogs perfused at constant arterial pressure by a pump oxygenator was used as a measure of left ventricular baroreflexes initiated by imposing pressure changes on the beating, as well as on the fibrillating, ventricle. In the unloaded beating heart mean left atrial and systolic ventricular pressures averaged 0.3 and 24 mmHg, respectively. Afterloads and preloads that increased systolic pressure to 63 mmHg while raising mean atrial pressures to 3.3 and 1.7 mmHg, respectively, had no effect on resistance. However, pressurization of the fibrillating ventricle caused vasodepressor responses proportional to the stimulus. The ventricular baroreflex had a significantly lower sensitivity and higher threshold than the vasodepressor reflex observed when simultaneously pressurizing the fibrillating ventricle, beating atrium, and lung vessels. On the basis of wall tension, the results are consistent with other reports that have shown ventricular baroreflexes to be initiated by systolic pressure in the range 100-150 mmHg, but not by diastolic pressure in the range 10-20 mmHg. A more sensitive reflex, able to respond to changes of ventricular filling pressure, arises from the left atrium and pulmonary veins.

Animals↗
PubMed1977

Effect of a left atrium-pulmonary vein baroreflex on peripheral vascular beds.

A step increase of left atrial and pulmonary venous pressure from 0 to 25 mmHg was used in anesthetized dogs with controlled arterial blood pressure to generate reflex systemic vasodilation. The resultant response of total peripheral resistance was an initial transient fall of about 40% which spontaneously regressed while the stimulus was maintained. Injections of differently tagged radioactive microspheres were used to measure selected organ blood flows prior to raising atrial pressure, at the response peak, during the steady state, and after recovery. Resistances of skin, skeletal muscle, kidney, and large intestine significantly fell upon atriovenous distention. The response in muscle, which greatly exceeded that of the other organs, was not sustained, whereas resistances of other responding beds remained depressed until the stimulus was removed. No significant responses occurred in small intestine, liver (hepatic artery), or adrenal gland.

Animals↗
PubMed1977

Cardiopulmonary baroreflexes: effects of pulmonary congestion and edema.

Systemic vasodepressor reflexes were initiated in pump-oxygenator perfused dogs by separately pressurizing the pulmonary vessels and the left cardiac chambers. Pulmonary vascular pressurization caused transient systemic vasodilation of a magnitude proportional to stimulus pressure over the range 0-65 cmH2O. The sensitivity of this reflex was sigificantly less than that of the left heart baroreflex. Mild pulmonary edema produced by a period of sustained congestion, and moderate edema, caused by sustained congestion in the presence of alloxan, had no discernible effect on systemic vasomotor tone or on subsequent pulmonary vascular baroreflexes. By comparison of these results with earlier studies in similar preparations I concluded that pulmonary arterial baroreflexes could alone produce the response obtained by pressurizing the entire pulmonary vascular bed. Although it was anticipated that type-J, irritant, and stretch receptors would be affected by congestion, no systemic vascular effects attributable to them were seen.

Animals↗
PubMed1975

Cardiopulmonary baroreflexes: effects of staircase, ramp, and square-wave stimulation.

Anesthetized dogs were pump perfused in a system that held systemic arterial pressure constant. Pulmonary arterial beds were pressurized, and the induced transient falls of systemic vascular resistance (SVR) were measured. An approximately linear relationship between percent fall of SVR and pulmonary artery pressure was obtained. Left atria and pulmonary venous beds were pressurized using square-pulse, staircase, and ramp wave forms, and changes in SVR were measured. The effect of varying the interval between stimuli was appraised. An approximately linear relationship was obtained for responses to square-wave left atrial forcing pressure (Pla). With staircase forcing, the change of SVR per unit change of Pla depended upon prestimulus Pla. With ramp forcing, responses increased approximately linearly with respect to the logarithm of the rate of pressure rise. Responses to square-wave stimulation varied directly with respect to the interstimulus interval. This study shows that left atrial-pulmonary vein baroreflexes are capable of producing substantial short-term falls of SVR, and that the response depends upon stimulus pressure, rate of pressure change, base-line pressure, and pressure history.

Animals↗