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Biomedical subjects

E D'Angelo

Publications and source records attributed to E D'Angelo.

At least 73 records · Page 4Linked to original sources

Mechanisms controlling inspiration studied by electrical vagal stimulations in rabbits.

UNLABELLED: Electrical stimulations of either constant (step) or linearly increasing (ramp) stimulus frequency (F) were applied with different timing during inspiration to the central ends of cut vagi of anaesthetized rabbits. Integrated diaphragmatic activity (Ad) time course during stimulation, after a period of common path (Tu) with control, increased at reduced rate for a substantial period before end-inspiration (Ti). With stimulations maintained into early expiration, the higher F, the shorter Tu and Ti and the smaller end-inspiratory Ad. Delaying the onset of stimulation or using ramp instead of step stimulations, shifted rightwards both F vs. Tu and F vs. Ti relationships which became steeper. With increasing delay, Ad at Ti or Tu became eventually independent of F. Short stimulations ineffective to shorten Ti, prolonged Ti beyond control, end-inspiratory Ad being smaller, the smaller Ti prolongation. IN CONCLUSION: (a) vagal input, beyond a time dependent threshold, exerts a graded inhibitory effect on central inspiratory output (CIO); (b) vagal input undergoes a certain degree of integration; (c) vagal inspiratory inhibitory effects are independent of CIO; (d) vagal input prevents some centrally generated activity inhibiting CIO.

Animals↗

Decay rate of inspiratory muscle pressure during expiration in man.

Decay rate of inspiratory muscle pressure (PmusI) was studied in 4 subjects during post-inspiratory period of zero flow (TEz) occurring under discontinuous inspiratory elastic load (DIL). End-inspiratory pressure (PmuseI) was increased by dead spaces or exercises. Decay rate was related to PmuseI by a power function with exponent greater than 1. It was not directly affected by concomitant changes of PCO2. It did not increase when an expiratory resistive load was added, i.e. when braking action of inspiratory muscles was no longer required. Time course of PmusI during TEz was more straight than exponential. Relative decay rate increased with PmuseI and with decrease of inspiratory or expiratory time. Experiments with resistive loads suggest that relative rate is mainly related to timing factors. During voluntary inspiratory efforts with closed airways, relative decay rate was not related to PmuseI, while decay rate increased linearly with PmuseI.

Adult↗

Acid-base balance of pleural liquid in dogs.

Acid-base balance and electrolyte concentrations were measured in dogs on small artificial hydrothoraces and in vitro on bicarbonate buffered Ringer solution on serosal and interstitial side of specimens of parietal pleura. Under steady conditions, pleural liquid PCO 2 was similar to and pH higher (delta = 0.022 +/- 0.006 SE) than that in mixed venous blood. Computed pleural liquid [HCO-3] was similar to that in venous plasma and hence less than that set by the Donnan effect, with which Na+ and Cl- approximately complied. In vitro, pH, [Na+], [Cl-], and computed [HCO-3] were significantly lower (delta = 0.030 +/- 0.004; -2.6 +/- 0.5; -1.2 +/- 0.5 and -1.7 +/- 0.2 meq/L, respectively) on the serosal than on interstitial side of pleural specimens, PCO2 being 42 mm Hg on both sides . HCO-3 and Na+ were not distributed according to transpleural potential (-0.4 +/- 0.1 mV on serosal side), suggesting an active transport of Na+ and HCO-3 from pleural liquid to blood. This, however, does not seem to add to the absorption pressure of plasma proteins in setting pleural liquid pressure.

Acid-Base Equilibrium↗

Breathing pattern in men during inspiratory elastic loads.

Breathing pattern was studied in men during inspiratory elastic load applied throughout breathing cycle (CL) or inspiration only (DL). VT decreased similarly under both loads: 40% during 1st loaded breath (1st), 25% after 1 min (min); so did Ti (15% at 1st, 25% at min); Te decreased by 35% under CL, 25% under DL, at both times. Under DL expiratory flow started after a lag of about 0.4 sec, required to raise alveolar pressure above atmospheric. In all subjects the inspiratory muscles activity increased at 1st and in 6 out of 8 the ventilatory response at min was essentially neurogenic. At 1st all subjects recruited expiratory muscles, decreasing FRC by 100--300 ml under DL' in most this phenomenon was negligible at min. Rate of decrease of inspiratory muscle pressure during period of zero flow under DL was proportional to end-inspiratory muscle pressure (Pmuse.i.) and to Pmuse.i./Ti. At beginning of expiration dPmus/dt was greater under DL: under this period difference of Pmus between CL and DL seems mainly due to muscle intrinsic properties.

Adult↗

Central and direct vagal dependent control of expiratory duration in anaesthetized rabbits.

In anaesthetized rabbits, total or partial (only inflation reflex nearly abolished) DC current vagal block was performed during inspiration (ITB and IPB), or expiration (ETB and EPB), or throughout the breathing cycle (CTB and CPB). During CTB inspiratory (Ti) and expiratory duration (Te) increased as after vagotomy. With ITB Ti equally Tivag; Te increased, but remained shorter than Tevag. During ETB, Ti was unchanged, Te increased, but remained shorter than Tevag. The sum of deltaTe during ITB and ETB equalled deltaTevag. During CPB and IPB, Ti and Te behaved as during ITB. With EPB, Ti was unchanged and Te shortened. Preferential stimulation of large myelinated fibers in the central vagal stumps during expiration lengthened Te. Inspiratory stimulation shortened both Ti and Te, restored breath timing of ETB, but not that of pre-vagotomy control. Hence, Te of eupneic breaths should depend on a central mechanism relating Te to preceding Ti and on expiratory vagal discharge, having both a small lengthening (from stretch receptors) and a variable shortening effect (from irritant receptors). Both central and peripheral mechanisms are affected by CO2 breathing.

Animals↗

Effects of single breath lung inflation on the pattern of subsequent breaths.

In rabbits, on release of lung inflations 0.4 to 3.3 times control VT and lasting 1 to 30 sec, VT, peak diaphragmatic activity (Ep) and inspiratory duration (Ti) increased, whereas expiratory duration (Te) decreased relative to pre-inflation values. Similar changes occurred between pre- and postinflation occluded breaths. These changes lasted from a few breaths up to 30 sec, and were positively correlated with magnitude and duration of inflations. Postinflation changes of pulmonary stretch receptor activity were relatively small and limited to 1-3 breaths. At chemical drive close to control: (a) postinflation VT vs Ti relationship moved to the right without changing its slope, Ti occluded eventually exceeding Ti after vagotomy; (b) the Te vs Ti relationship moved downwards, its slope being decreased and eventually abolished; (c) the average rate of rise of E was decreased. An increase of VT, Ep and Ti, and a decrease Te also occurred on release of stimulation of the central ends of the cut vagi producing apnea at FRC in mono- and bilateral vagotomized rabbits. Postinflation effects were mainly of central origin and tentatively explained as rebound phenomena within the respiratory center.

Animals↗

Hemoglobin-oxygen equilibrium at different hemoglobin and 2,3-diphosphoglycerate concentrations.

Hemoglobin-oxygen equilibrium curves at constant pH, ionic strength, and temperature were determined (a) on 2,3-DPG-free solutions at various hemoglobin (Hb) concentrations, (b) on solutions at various Hb concentrations but constant 2,3-DPG/Hb molar ratio, (c) on solutions at constant hemoglobin concentration but various 2,3-DPG/Hb molar ratios, and (d) on hemolysates at various Hb concentrations. Under all conditions the shape of the equilibrium curve was the same (n = 2.62 +/- 0.04, 33 experiments). Half-saturation pressure (P 1/2) did not change with increasing Hb concentration in case (a), whereas P 1/2 was linearly related to Hb concentration in case (b). In case (c) at 200 g/l Hb, P 1/2 increased sharply as 2,3-DPG/Hb molar ratio increased up to 0.4 but changed little as the ratio was further increased up to 1.5. This behavior is very different from that observed in diluted (5 g/l) solutions. P 1/2 of the hemolysates was also linearly related to Hb concentration but the slope was about twice that for case (b). These results cannot be explained by linked function theory or by a dimer-tetramer equilibrium. It is suggested that intermolecular interactions in the presence of organic phosphates may be responsible for the observed changes in Hb affinity for oxygen.

Dextrans↗

Effect of papain-induced emphysema on the distrubtion of pleural surface pressure.

Distribution of transpulmonary pressure (Ptp) at FRC, during spontaneous breathing, and during inflation of the relaxed respiratory system was studied in the supine, lateral and head-up postures after papain had been injected intratracheally into dogs. Functional and morphological changes of the lung resembling those of panlobular emphysema occurred in papain-treated dogs. In all postures the relationship between lung height and Ptp at FRC was steeper and shifted to the left of that obtaining for normal dogs. During artifical inflation changes of Ptp were larger in the dependent than in the upper lung and the vertical gradient of Ptp eventually disappeared, as observed in normal dogs. During spontaneous breathing changes of Ptp were uniform in the horizontal postures, but larger over the upper regions in the head-up posture; whereas they are uniform in all postures in normal dogs. From local Ptp values and lung P-V curve, distribution of specific lung volumes at FRC and ventilation during spontaneous breathing were assessed for both normal and papain-treated head-up dogs: the results agreed with those obtained using radioactive gases in normal and in elderly man or emphysematous subjects with no apparently localized lesions.

Animals↗

The effect of limb movements on the regulation of depth and rate of breathing.

In anesthetized dogs and rabbits passive or active limb movements (1) shifted to the left the relationship between tidal volume (Vt) and inspiratory time (Ti), (2) lowered the relationship between expiratory time (Te) and Ti and decreased its slope, and (3) increased the output to the inspiratory muscles (Vt/Ti). These effects increased with increasing the frequency of movements. Similar effects were obtained after vagotomy. When the stimulus was started during expiration. Te was shorted in spite of the previous unaffected Ti, Arterial PCO2 during exercise was similar (active movements) or below (passive movements) control value. Since other chemical and physical humoral factors do not seem involved, the whole increase of ventilation should be produced by neurogenic stimuli. The time course of Te, Ti and VT/Ti at the onset and at the offset of limb movements indicates an abrupt and a slow component in the neurogenic drive. A single contraction of the limb during expiration of inspiration affected the timing and the VT/Ti of 3-8 breaths.

Animals↗

Effect of rib cage or abdomen compression at iso-lung volume on breathing pattern.

In anesthetized rabbits a small compression of the rib cage (RC) caused a marked increase of breathing frequency (f), a marked reduction of expiratory duration (Te), a reduction of inspiratory duration (Ti) and tidal volume (VT), while an equal decrease of lung volume produced by abdominal compression(AC) caused a smaller increase of f and no change of Ti, and a slight increase of VT. Similar results occurred when normal end-expiratory volume was maintained during compression. The phenomena disappeared after bilateral vagotomy, whereas persisted after cordotomy in T1. Similar results occurred in dogs (with the exception that VT decreased during AC), whereas in cats only RC increased f by shortening Te. RC caused a marked increase of discharge in 11 out of 19 irritant receptor fibers, whereas AC caused an increase only in 2. In most of the pulmonary stretch receptor fibers the change of activity produced by compression paralleled the lung volume change. The effects of vagal cooling on Ti, Te and the VT-Ti relationship with and without compression suggest irritant receptors as responsible for the different ventilatory pattern during RC and AC.

Abdomen↗

Vertical gradients of pleural and transpulmonary pressure with liquid-filled lungs.

In supine dogs with saline-filled lungs the vertical gradient of pleural surface pressure (VGPpl) was not significantly different from -1 cm H2O/cm and that of transpulmonary pressure (VGPtp) was not significantly different from zero. Hence the hydrostatic gradient of the liquid was entirely taken up by the chest wall, the ribs being rigid in the direction of gravity and the diaphragm facing an equal hydrostatic gradient on both sides. In head-up dogs VGPpl was -0.8 cm H2O/cm when the level of the liquid in the filling system was 19.5 cm below the lung top and -0.5 cm H2O/cm when this level corresponded to the top. The hydrostatic gradient of the liquid was not entirely taken up by the rib cage because of its uneven regional compliance and VGPtp was reversed with respect to that of the air-filled lung. With fluorocarbon (specific gravity 1.75) filled lungs in the supine posture VGPpl was about -1.28 cm H2O/cm and VGPtp was reversed. In the head-up posture VGPpl was about -1.2 cm H2O/cm and VGPtp was reversed.

Airway Resistance↗