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Biomedical subjects

W Mitzner

Publications and source records attributed to W Mitzner.

At least 55 records · Page 3Linked to original sources
PubMed1986

Pulmonary blood flow affects recovery from constriction in dog lung periphery.

The influence of blood flow through the pulmonary circulation on the time course of recovery of the lung periphery from challenge with three bronchoconstrictive agents was studied in dogs. The rate of perfusion of the left lower lobe was varied between 0 and 300 ml/min. A fiber-optic bronchoscope (OD = 5.5 mm) was wedged in a small airway in the same lobe, and resistance to airflow through the collateral system was continuously monitored. The lung was challenged with histamine aerosol for 1 min, or with intravenous boluses of histamine, acetylcholine, or methacholine. The time constant (tau) of recovery from each of the challenges was measured under the various pulmonary blood flow conditions. The mean tau of the recoveries from histamine was inversely related to the rate of blood flow. However, pulmonary blood flow had no effect on recovery from challenge with acetylcholine or methacholine, two agents metabolized by cholinesterase in lung tissue. From this study we conclude that recovery of the lung periphery from histamine is perfusion dependent, whereas recovery from acetylcholine or methacholine is perfusion independent. This suggests that the rate of blood flow through the pulmonary circulation could play an important role in recovery of the peripheral airways from certain mediators of bronchoconstriction.

Acetylcholine↗
PubMed1986

Bronchial blood flow affects recovery from constriction in dog lung periphery.

We investigated the effect of eliminating the bronchial circulation on recovery time from intravenous histamine challenge in canine lung periphery. Results from animals with intact bronchial circulations were compared with a second group in which the left lower lobe was isolated in situ. The pulmonary artery to this lobe was perfused and a bronchoscope was wedged in a small airway, which provided an index of resistance to airflow through the collateral system. The lobe was challenged with intravenous histamine, and the time constant of recovery (tau) from bronchoconstriction was measured. With or without pulmonary blood flow, elimination of the bronchial circulation increased tau 44.4 and 48.5%, respectively. This increase was similar to that found by stopping pulmonary blood flow alone (56.5%). Histamine challenges were also performed in sympathectomized or vagotomized animals with intact bronchial circulations. Neither of these conditions increased tau. We conclude that blood flow through the bronchial circulation affects the recovery time from intravenous histamine challenge in the lung periphery to a degree similar to that of the pulmonary circulation.

Animals↗
PubMed1986

Lymph flow and lung weight in isolated sheep lungs.

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.

Animals↗
PubMed1985

Amniotic fluid prolactin and fetal lung maturation.

Concentrations of prolactin in amniotic fluid, fetal plasma, and maternal plasma were determined in 34 rhesus monkeys delivered by hysterotomy under general anesthesia at gestational ages of 110 to 160 days (term, 165 days). Included were 15 cases (gestational ages 110 to 143 days) in which the mothers received 2 mg of betamethasone intramuscularly daily for 3 days prior to delivery. Fetal lung maximum volumes were determined in addition to the following indices of fetal lung surfactant: lung alveolar stability, lung phosphatidylcholine concentrations, lung extract surface tensions, and amniotic fluid lecithin to sphingomyelin ratios. Amniotic fluid prolactin was found to correlate significantly with lung alveolar stability (r = 0.51; p less than 0.01), lung phosphatidylcholine (r = 0.51; p less than 0.01), lung extract surface tension (r = -0.39, p less than 0.05) and amniotic fluid lecithin/sphingomyelin ratio (r = 0.50; p less than 0.01). These correlations remained statistically significant even when the effects of gestational age were taken into account. These findings suggest that amniotic fluid may modulate fetal production of surfactant via its prolactin content.

Amniotic Fluid↗
PubMed1985

Effect of high-frequency ventilation on histamine-induced lung injury in dogs.

We compared the effects of high-frequency oscillation (HFO) and conventional mechanical ventilation (CMV) on dynamic lung compliance (Cdyn), venous admixture (Qsp/Qt), cardiac output, and total lung resistance (RL) in seven mongrel dogs with histamine-induced lung injury. Baseline measurements during CMV were followed by iv infusion of histamine at 100 micrograms/min. Cdyn, Qsp/Qt, cardiac output, and RL were measured in triplicate during CMV and then during HFO. Subsequently, at least one complete set of measurements was recorded again on CMV. During HFO, animals were ventilated at 15 Hz with a tidal volume of 70 to 80 ml. CMV was delivered at 15 to 18 breath/min with a tidal volume of 15 ml/kg. Histamine infusion produced a marked fall in Cdyn, a variable rise in RL, an inconsistent but usually progressive rise in Qsp/Qt, and hypotension. A period of ventilation with HFO made no difference in the Cdyn, Qsp/Qt, or cardiac output changes produced by histamine infusion.

Animals↗
PubMed1985

Model of gas transport during high-frequency ventilation.

We analyze gas exchange during high-frequency ventilation (HFV) by a stochastic model that divides the dead space into N compartments in series where each compartment has a volume equal to tidal volume (V). We then divide each of these compartments into alpha subcompartments in series, where each subcompartment receives a well-mixed concentration from one compartment and passes a well-mixed concentration to another in the direction of flow. The number of subcompartments is chosen on the basis that 1/alpha = (sigma t/-t)2, where -t is mean transit time across a compartment of volume, and sigma t is standard deviation of transit times. If (sigma t/-t)D applies to the transit times of the entire dead space, the magnitude of gas exchange is proportional to (sigma t/-t)D, frequency, and V raised to some power greater than unity in the range where V is close to VD. When V is very small in relation to VD, gas exchange is proportional to (sigma t/-t)2D, frequency, and V raised to a power equal to either one or two depending on whether the flow is turbulent or streamline, respectively. (sigma t/-t)D can be determined by the relation between the concentration of alveolar gas at the air outlet and volume expired as in a Fowler measurement of the volume of the dead space.

Humans↗
PubMed1985

Use of aerosols to measure in vivo volume-dependent changes in lung air space dimensions.

Using measurements of aerosol recovery following a 5-s breath hold [NRC(5)] as indices of lung air space dimensions, we evaluated the in vivo changes in these dimensions associated with changes in lung volume (VL). In anesthetized dogs, single breaths of a 1.2-micron monodisperse aerosol were introduced into the respirator's cycle at a number of isovolume points on the inflation and deflation limb of the pressure-volume curve for the dog's lungs. At isovolume, NRC(5) measured off the inflation limb was slightly larger than NRC(5) measured off the deflation limb, implying a larger mean air space dimension for the air space configuration on the inflation vs. the deflation limb. Since a constant aerosol tidal volume (VT) was used for all VL in all dogs, the proportion of the lung filled with aerosol, VT/VL = Pn (where Pn is defined as an index of aerosol penetration into the lung periphery), varied along with VL. In all dogs, we found that, for NRC(5) measurements with Pn less than 0.33, NRC(5) steadily increased with increasing VL, which implies an increasing mean air space dimension as VL increases. However, when we account for the effect that changes in Pn with increasing VL have on NRC(5), we conclude that the observed increase in NRC(5) with VL is primarily due to decreases in Pn and not increases in the mean air space dimension as VL increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1985

Effects of 10% formalin fixation on fixed lung volume and lung tissue shrinkage. A comparison of eleven laboratory species.

This species comparative study examined tissue shrinkage from a known physiologic lung volume through to the processed histologic section. Eleven mammalian species with body weights that spanned 3 orders of magnitude were studied. Air pressure-volume curves were determined to obtain total lung capacity (TLC) at 30 cmH2O. The lungs were then fixed by airway filling at 25 cmH2O pressure, and a displacement fixed lung volume was determined. Linear dimensions were systematically measured on fixed tissue blocks, embedded tissue blocks, and stained sections. Results indicated that the ratio of fixed lung volume to TLC ranged between 0.6 and 2.0. The corresponding ratios for linear dimensions ranged between 0.8 and 1.3 for all species. Histologic processing caused further shrinkage; the ratios of linear dimensions measured after and to those measured before processing ranged between 0.6 and 0.7. Thus, the degree of fixed lung volume achieved relative to TLC varies considerably more among species than does the histologic shrinkage caused by processing. We conclude that measurement of these changes in lung dimensions caused by fixation and histologic processing in the different species is essential, particularly in quantitative interspecies physiologic studies.

Animals↗
PubMed1984

Gas transport during high-frequency ventilation: theoretical model and experimental validation.

We present a theoretical model of gas transport through the dead space during high-frequency ventilation (HFV) with volumes less than dead space volume. The analysis is based on the axial distribution of transit times of gas moving through the dead space. The model predicts that for tidal volumes (V) much less than dead space (VD), gas exchange will be proportional to the product of frequency (f) and V2. If gas transport is analyzed in terms of Fick's law, then the effective diffusion coefficient (Deff) can be shown to be equal to fV2 times a constant, whose value equals the square of the coefficient of dispersion of axial transit times through the dead space (sigma t/t)2. Experimental results in straight tubes fit the predictions of this model quite well. A (sigma t/t) through the entire dead space of about 30% is more than sufficient to account for gas exchange during HFV in physical models or in intact animals. An axial dispersion of this magnitude can be measured directly from a typical Fowler dead space determination in healthy subjects.

Animals↗
PubMed1984

Lung compliance changes on high-frequency ventilation in normal dogs.

To test the hypothesis that high-frequency ventilation (HFV) promotes lung stability we compared the temporal course of dynamic lung compliance changes after two inflations on HFV with those occurring on conventional mechanical ventilation (CMV) at two different lung volumes, specifically with and without 5 cmH2O positive end-expiratory pressure (PEEP). In our first set of experiments we ventilated six anesthetized paralyzed dogs first with CMV, then with HFV, then again with CMV using tidal volumes of 15 ml/kg at rates of 16-18 times/min for CMV and less than 90 ml and a rate of 15 Hz for HFV. In our second set of experiments we ventilated six dogs for 4 h, the 1st h with CMV at 0 cmH2O end-expiratory pressure, the 2nd h with CMV with 5 cmH2O PEEP, the 3rd h with HFV at the same mean pleural pressure, and the 4th h again with CMV with 5 cmH2O PEEP. We found the decreases in dynamic compliance with time following hyperinflations were similar on HFV and CMV (P greater than 0.5) at both lung volumes. With the lower lung volume the initial dynamic compliance following hyperinflation also tended to fall progressively from one hour to the next despite the inflations. However, with PEEP the initial dynamic compliance over successive hours tended to rise from one hour to the next. We found that changes in dynamic compliance were not necessarily reflected in the venous admixture or alveolar to arterial O2 partial pressure gradients. We thus conclude that lung stability in normal dogs is not improved during HFV, and blood gases cannot be used to predict compliance changes.

Animals↗
PubMed1984

Physiological dead space during high-frequency ventilation in dogs.

Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. We found that VD was relatively constant at tidal volumes associated with normal ventilation (7-15 ml/kg) but fell sharply as VT was reduced further to tidal volumes associated with HFV (less than 7 ml/kg). The frequency required to maintain constant alveolar ventilation increased slowly as tidal volume was decreased from 15 to 7 ml/kg but rose sharply with attendant rapid increases in minute ventilation as tidal volumes were decreased to less than 7 ml/kg. At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.

Animals↗
PubMed1984

Mean airway pressure and alveolar pressure during high-frequency ventilation.

Studies and applications of high-frequency ventilation (HFV) are often performed under conditions of controlled mean airway pressure (Paw). In the present study we tested the assumption that controlling Paw adequately controls lung volume during HFV by investigating the relationship between a reliably measured Paw and the mean alveolar pressure (Palv) of the lungs during HFV of healthy dogs. We minimized the errors of Paw measurement due to the Bernoulli effect and various technical factors by appropriate choice of transducers, amplifiers, and measurement site. Palv was estimated by clamping the ventilator tube during oscillation and measuring the equilibration pressure of the lung and airways. Paw and Palv were determined as functions of frequency (8-25 Hz), tidal volume (60-90 ml), Paw (-5 to 12 cmH2O), and position of the animal (supine vs. lateral). We found that Paw could significantly underestimate Palv and that the degree of underestimation increased at higher frequencies, larger tidal volumes, and lower Paw. Shifting the animal from the supine to the lateral position greatly accentuated this effect. The elevation of Palv above Paw was seen to be a function of mean flow and largely independent of the frequency-tidal volume combination which produced the flow. A possible explanation of this pressure difference is that it results from differences in inspiratory and expiratory airway impedances, which in turn depend on airway geometry, compliance, lung volume, and expiratory flow limitation.

Airway Resistance↗
PubMed1983

A re-evaluation of the hemodynamic consequences of intermittent positive pressure ventilation.

The hemodynamic effects of intermittent positive pressure ventilation (IPPV) have generally been considered straightforward, being dominated by the inspiratory reduction in systemic venous return. Paradoxically, there is considerable debate regarding the effects of PEEP. We have studied both right ventricular (RV) and left ventricular (LV) performance during a single IPPV respiratory cycle in dogs with intact circulatory systems or the right heart bypassed in open and closed chest conditions. We have found that the "reverse pulsus paradoxus" during inspiration reflects both transmission of the increased intrathoracic pressure to the thoracic aorta and an increase in LV stroke volume (SV). This inspiratory increase in LVSV has been found to be influenced by, but not dependent on: (a) respiratory variations in RVSV; (b) variations in functional residual capacity or tidal volume altering pulmonary venous return and the degree of physical compression of the heart by the lungs; (c) an inspiratory decrease in RV volume, increasing LV diastolic compliance and, thus, probably improving pulmonary venous return; (d) a decreased transmural aortic diastole pressure reflecting an effective decrease in LV afterload produced by both the general increase in intrathoracic pressure and the direct compression of the heart; and (e) variations in the pulmonary vascular volume as indicated by changes in the transmural LV end-diastolic pressure. An understanding of IPPV during a single respiratory cycle facilitates an appreciation of the steady state hemodynamic effects of IPPV with or without PEEP. Our results imply that measurements made only at end-expiration, ignoring inspiratory events, may have serious limitations. Furthermore, they suggest that IPPV with PEEP should be evaluated as a form of LV assist in LV failure.

Animals↗
PubMed1983

Hypoxic constriction of alveolar and extra-alveolar vessels in isolated pig lungs.

To examine whether hypoxia causes constriction of alveolar or extra-alveolar vessels, we determined the relationships among transpulmonary pressure, pulmonary arterial pressure (Ppa), blood flow (Q), and transvascular fluid filtration rate (W) during normoxia (PO2 = 200 Torr) and hypoxia (PO2 = 50 Torr) in isolated pig lungs perfused with autologous blood. Left atrial pressures were always subatmospheric. The effects of lung inflation and hypoxic vasoconstriction on the Ppa-Q relationship were similar; when transpulmonary pressure was greater than 5 Torr, both shifted the curve to higher pressures in a parallel fashion. When transpulmonary pressure was 0-5 Torr, however, inflation had no effect on the Ppa-Q relationship during either normoxia or hypoxia. During normoxia at a transpulmonary pressure of 3.5 Torr, the relationship between fluid filtration rate and flow was characterized by a W of zero at Q less than 1.5 l/min and a rapid increase in W with Q above this value. Both hypoxia and inflation shifted this relationship to higher filtration rates in a parallel fashion. Furthermore, the combined effects of hypoxia and inflation on filtration rate were additive. These results suggest that hypoxia caused constriction of both alveolar and extra-alveolar vessels, resulting in increased intraluminal pressure and filtration of fluid in vessels upstream from the sites of constriction.

Animals↗
PubMed1983

Elastic characteristics of the lung perivascular interstitial space.

An analysis of the elastic behavior of the lung perivascular interstitial space during interstitial fluid accumulation is presented. Fluid accumulation must deform the lung parenchyma and vascular walls that form the interstitial space boundaries. The deformations of these boundaries are predicted from previously published data on the elastic properties of the boundary materials. The analysis gives the relationships among the elastic properties of the boundaries, the compliance of the interstitium, the lung volume, and the lung elastic recoil pressure. Values of the interstitial compliance are predicted to decrease with increasing lung recoil pressure and are dependent on the lung pressure-volume history. At low recoil pressures over 70% of the interstitial compliance results from deformation of the parenchyma. As the recoil pressure increases, either with increasing lung volume or due to the lung pressure-volume history, the contributions of the parenchymal and vascular wall deformations become similar. The predictions are generally consistent with published data on interstitial compliance obtained from measurements of isolated lung weight gain during vascular fluid transudation. This correlation suggests that the elastic behavior of the interstitial space can be accounted for by the known elastic properties of the boundary materials.

Animals↗
PubMed1983

Pulmonary hemodynamics and gas exchange properties during progressive edema.

In this investigation we have studied the effect of increments of pulmonary edema on pulmonary hemodynamics, and physiological and hemodynamic shunt in an isolated lung preparation. Hemodynamic shunt was defined by the slope of the relationship between pulmonary arterial and airway pressures; when the slope decreases, there is a greater degree of shunt. Cardiovascular changes were analyzed using a Starling resistor model of the pulmonary circulation where the effective downstream pressure to flow as seen from the pulmonary artery exceeds the pulmonary venous outflow pressure. This effective downstream pressure is referred to as the critical pressure (Pc), and at low lung inflation the locus of this critical pressure is in extra-alveolar vessels. With 3-4 h of progressive edema to an average of 185% initial lobe weight we found a progressive rise in pulmonary arterial pressure (Ppa) from 12.1 to 21.5 cmH2O. About one-third of this increase in Ppa resulted from an increased Pc and the remainder resulted from an increased resistance upstream from the locus of Pc. These results are consistent with the hypothesis that the interstitial accumulation of fluid creates enough of an increase in interstitial pressure to compress extra-alveolar vessels. There was no significant correlation between the amount of edema and the measured physiologic shunt, but the hemodynamic shunt showed a highly significant correlation. The hemodynamic shunt theoretically measures the extent of obstructed airways and may be a useful index of the degree of pulmonary edema.

Animals↗
PubMed1983

Role of alveolar recruitment in lung inflation: influence on pressure-volume hysteresis.

The behavior of terminal lung units (alveoli) with changes in lung volume is controversial. For example, different investigators using similar techniques have suggested that alveoli expand homogeneously or, conversely, get smaller with increases in lung volume. We studied this problem by filling excised dog lobes with monodisperse aerosol and observing deposition at zero airflow. Under these conditions, the deposition of particles is inversely proportional to a mean alveolar linear dimension (ALD). With this technique, changes in ALD were assessed as the lung ventilated along its pressure-volume (PV) curve. PV curves were generated using a rapid cycling technique that minimized trapping and allowed reversible regulation of inflation-deflation hysteresis. Irreversible changes in PV hysteresis were assessed by rinsing the lung with Tween. With significant PV hysteresis, the ALD progressively decreased with inflation to total lung capacity (TLC). With deflation from TLC, the ALD was unchanged until low volumes were reached, when it decreased markedly. When PV hysteresis was minimized (reversibly or irreversibly), inflation and deflation ALD were superimposed. These data are consistent with progressive alveolar recruitment with inflation to TLC and derecruitment with deflation. The correlation between alveolar dimensions and PV hysteresis suggests that shifts in the PV curve can be accounted for by changes in the population of units. The number open at any given point is determined by the dynamic history of inflation.

Aerosols↗