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S N Mink

Publications and source records attributed to S N Mink.

35 records · Page 2Linked to original sources
PubMed1987

Density dependence of maximal flow is lung volume dependent during bronchoconstriction.

We examined the changes in maximum expiratory flow (Vmax) and the density dependence of maximum expiratory flow (delta Vmax) during histamine-induced bronchoconstriction in dogs. Histamine acid phosphate solution was nebulized into the airways of six dogs to produce predominantly peripheral airway obstruction. Vmax air, Vmax with the dogs breathing 80% He-20% O2 (delta Vmax), and airway sites of flow limitation (choke points) were examined at four lung volumes (VL), which ranged from 51 to 23% of the control vital capacity (VC). The findings were interpreted in terms of the wave-speed theory of flow limitation. At all VL, Vmax air decreased during bronchoconstriction by approximately 30% compared with the control value. Resistances peripheral to a 0.3-cm-diam airway were increased about threefold with histamine, whereas resistances between 0.6-cm-diam bronchi and main-stem bronchi increased just slightly. Airway diameters were measured in the air-dried lung at 20 cmH2O transpulmonary pressure. Our results showed that only at 44% VC did delta Vmax decrease in all experiments after histamine to indicate peripheral obstruction (mean: 68.5 to 45%). At 23% VC, delta Vmax increased slightly, from 22 to 28%. At 23 and 36% VC, substantial differences in the wave-speed variables between air and HeO2 were present before bronchoconstriction, so that delta Vmax was low in some dogs, although peripheral airway obstruction was not evident. When bronchoconstriction was produced, delta Vmax at 23% VC could not be decreased further and even increased in four of six dogs. Thus changes in delta Vmax at given lung volume may not reflect the predominant site of airflow obstruction during bronchoconstriction.

Airway Obstruction↗
PubMed1986

Mechanism of reduced maximum expiratory flow in dogs with compensatory lung growth.

We examined the mechanism of the reduced maximum expiratory flow rates (Vmax) in a dog model of postpneumonectomy compensatory lung growth. During forced expiration, a Pitot-static tube was used to locate the airway site of flow limitation, or choke point, and to measure dynamic intrabronchial pressures. The factors determining Vmax were calculated and the results analyzed in terms of the wave-speed theory of flow limitation. Measurements were made at multiple lung volumes and during ventilation both with air and with HeO2. Five of the puppies had undergone a left pneumonectomy at 10 wk of age, and 5 littermate controls had undergone a sham operation. All dogs were studied at 26 wk of age, at which time compensatory lung growth had occurred in the postpneumonectomy group. Vmax was markedly decreased in the postpneumonectomy group compared with control, averaging 42% of the control flow rates from 58 to 35% of the vital capacity (VC). At 23% of the VC, Vmax was 15% less than control. Choke points were more peripheral in the postpneumonectomy dogs compared with controls at all volumes. The total airway pressure was the same at the choke-point airway in the postpneumonectomy dogs as that in the same airway in the control dogs, suggesting that the airways of the postpneumonectomy dogs displayed different bronchial area-pressure behavior from the control dogs. Despite the decreased Vmax on both air and HeO2, the density dependence of flow was high in the postpneumonectomy dogs and the same as controls at all lung volumes examined.

Airway Resistance↗
PubMed1985

Forced expiration and HeO2 response in canine peripheral airway obstruction.

We examined the effect of peripheral airway obstruction on parameters of maximum expiratory flow (Vmax) in a canine model of bronchiolitis obliterans (B). B was produced by the repeated intrabronchial instillations of a 1% nitric acid solution in seven dogs (group B). In seven control dogs (group C), a normal saline solution was used. During forced vital capacity deflation, Vmax on air, the relative increase in Vmax on 80% He-20% O2 (delta Vmax), and airway sites of flow limitation "choke points" (CP) were determined at multiple lung volumes (VL). The findings were interpreted in terms of the wave-speed theory of flow limitation. Wave-speed parameters were identified with a pressure-measuring device positioned in the airway. Compared with the findings for group C, Vmax decreased substantially at the lower VL (less than 50% vital capacity) in group B, whereas there were no changes in delta Vmax at any VL. CP were identified in central airways in both groups but were slightly more upstream in group B. Our analysis indicated that the reduction in Vmax in group B was due to an increase in upstream frictional pressure losses (Pfr) that caused a relative reduction in the pressure head, so that choking occurred in slightly upstream airways. delta Vmax did not change in group B because with CP identified in central airways, Pfr were density dependent, and significant differences in head loss on the two gas mixtures did not occur. Choking therefore occurred with similar wave-speed variables on the two gas mixtures, and delta Vmax was maintained.

Airway Obstruction↗
PubMed1985

Increased gravitational stress does not alter maximum expiratory flow.

We measured maximum expiratory flow-volume (MEFV) curves in six seated subjects during normal (+1 Gz) and increased (+2 and +3 Gz) gravitational stress. Full MEFV curves, initiated at total lung capacity, were recorded, as were partial MEFV curves, initiated at approximately 60% of the vital capacity. Data were acquired in all subjects breathing air at +1 and +2 Gz; results were available for three subjects breathing 80% He-20% O2 at +1 and +2 Gz, and in two subjects, results were obtained at +3 Gz. Changes in gravitational stress were not associated with changes of either full or partial MEFV curves. The known increase in differences of regional lung volume and recoil caused by increased gravitational stress did not influence maximum expiratory flow. Though increased gravitational stress probably changed regional emptying sequences little during full MEFV maneuvers, substantial changes of emptying sequence were expected during partial maneuvers. It is possible that such changes in emptying sequence occurred but were not associated with changes in maximum flow because the latter was determined by choking in central airways common to all regions.

Adult↗
PubMed1985

Vascular and interstitial mechanics in canine pulmonary emphysema.

We examined the changes in vascular and interstitial mechanics in pulmonary emphysema (PE) using a canine lobar model. PE was produced in the left lower lobe (LLL) of five dogs (group E) by six weekly intrabronchial instillations of the enzyme papain. In five control dogs (group C), a normal saline solution was used. In our in vivo preparation, vascular flow (Q) to the LLL was measured. Inflow (Ppa) and outlow (Pv) pressures to the LLL could be varied independently. The relationship of Ppa to Q was examined in zones 2 and 3 of West. The slope of the Ppa-Q relationship was used to determine vascular conductance, whereas the extrapolation to zero flow in zone 2 conditions represented the mean pressure required for vascular recruitment (Pi). Lobar weight gain was measured continuously. Following step increases in Ppa, the rapid increase in wet weight measured when Q to the LLL was zero was used to obtain vascular compliance (C). Subsequent slow increases in wet weight were used to determine the rate of fluid exchange with the interstitium (Qf). The slope of the Qf-Ppa relationship represented fluid conductance (Kf). The extrapolation to zero Qf gave the minimal pressure required for continuous edema formation (Pm). Compared with group C, vascular conductance (G) decreased and Pi increased in group E, whereas fluid conductance (Kf) and Pm increased. The decrease in G most likely resulted from the loss of vascular cross-sectional area in emphysematous lungs, whereas the increase in Pi was possibly due to mechanical changes in the lung interstitium which increased vessel closure. We propose that the increase in Kf in group E reflected an increase in interstitial conductance, such that due to structural changes in the interstitium in emphysematous lungs, tissue resistance to fluid flux decreased.

Airway Resistance↗
PubMed1984

Dynamic lung function in dogs with compensatory lung growth.

Nine puppies underwent left pneumonectomy at 10 wk of age while nine sex-matched littermates had a sham operation, and all animals were studied at 25 wk of age. Postpneumonectomy dogs demonstrated compensatory growth in that lung weight and total lung capacity (TLC) were the same as those of control animals when normalized for body weight. In postpneumonectomy dogs all lobes of the remaining right lung increased in weight, but this was most notable in the cardiac lobe which grew across the mediastinum. Subdivisions of lung volume were normal in postpneumonectomy animals except for residual volume (RV): RV/TLC was increased when compared with control animals. In intact dogs static pressure-volume curves of the lung and respiratory system did not differ between groups, and the static pressure-volume curves of excised lungs were closely similar. Maximum expiratory flow was sharply reduced in postpneumonectomy dogs, averaging 40% of flow in control dogs over the lower 50% of the vital capacity. In both groups the fractional increase in maximal expiratory flow during HeO2 breathing was substantial and similar. Regional compliances, resistances, and perfusion distribution were examined using 133Xe. Regional compliance and perfusion were reduced in the left hemithorax of postpneumonectomy dogs while regional resistances were increased.

Animals↗
PubMed1984

Pulmonary function tests in the detection of small airway obstruction in a canine model of bronchiolitis obliterans.

We compared parameters of maximal expiratory flow with other tests used in the detection of small airways obstruction (SAD) in a canine model of bronchiolitis obliterans. Bronchiolitis was produced by instilling a 1% solution of nitric acid into the airways of 8 dogs (Group N). In 5 control dogs, a normal saline solution was instilled (Group C). Plethysmographic lung volumes, oscillatory airway resistance (RL), and tests for SAD were examined after bronchiolitis was produced. To evaluate peripheral airway function, the single-breath nitrogen washout curve was used to obtain the slope of phase III and to estimate the lung volume at which a terminal increase in N2 concentration was observed (closing capacity). Maximal expiratory flow-volume curves while the dogs breathed air and 80:20 helium:oxygen (HeO2) were performed to obtain the air flow rate at 50% vital capacity (V50), the corresponding HeO2 flow rate (delta Vmax), and the lung volume at which air and HeO2 flow rates were equal (Viso). After injury, the histologic aspects of the lung in Group N showed acute and chronic inflammation of the small airways. The RL did not change in Group N, despite a relative increase in peripheral airway resistance, which when measured increased about 4 times. Compared with Group C, significant increases in closing capacity and Viso and significant decreases in V50 were observed in Group N. Although predicted to decrease in SAD, delta Vmax did not change. We conclude that delta Vmax is relatively insensitive to SAD. Possible mechanisms resulting in reduced V50 but maintained delta Vmax in this model were further examined in terms of the concepts outlined by the wave-speed theory of flow limitation.

Airway Obstruction↗
PubMed1984

Expiratory flow limitation and the response to breathing a helium-oxygen gas mixture in a canine model of pulmonary emphysema.

The pathophysiology of reduced maximum expiratory flow in a canine model of pulmonary emphysema was studied, and the results interpreted in terms of the wave-speed theory of flow limitation. According to this theory, maximum expiratory flow is related both to the cross-sectional area and compliance at an airway site where a critical gas velocity is first reached ("choke-point") and to gas density. Pulmonary emphysema was produced by the repeated instillations of the enzyme papain into the airways of six dogs. In five control dogs, a saline solution was instilled. During forced vital capacity deflation, in an open-chest preparation, maximum expiratory flow, choke-point locations, and the response to breathing an 80:20 helium/oxygen gas mixture were determined at multiple lung volumes. To locate choke-points, a pressure measuring device was positioned in the airway to measure lateral and end-on intrabronchial pressures, from which the relevant wave-speed parameters were obtained. In general, the reduced maximum expiratory flow in emphysema can be explained by diminished lung elastic recoil pressure and by altered bronchial pressure-area behavior, which results in a more peripheral location of choke-points that have smaller cross-sectional areas than controls. With respect to the density dependence of maximum expiratory flow, this response did not differ from control values in four dogs with emphysema in which frictional pressure losses upstream from choke-points did not differ on the two gas mixtures. In two dogs with emphysema, however, upstream frictional pressure losses were greater on helium/oxygen than on air, which resulted in a smaller cross-sectional area on helium/oxygen; hence density dependence decreased.

Animals↗
PubMed1983

Mechanism of reduced maximum expiratory flow in methacholine-induced bronchoconstriction in dogs.

Airway sites of flow limitation ["choke points" (CP)] were identified during forced deflation in open-chest dogs before (C) and after (B) bronchoconstriction was produced by nebulizing a solution of methacholine chloride into their airways. CP were identified in two respective groups. In group I (n = 8) a retrograde catheter was used to locate CP and in the other a Pitot static tube (group II, n = 5), CP were identified at multiple lung volumes (VL) over the lower one-half of total lung capacity. Both groups showed similar findings at each condition. At B, corresponding values of maximum expiratory flow (Vmax) at each VL decreased to about 10% of those at C. Movement of CP relative to their original location varied at each VL and, especially at the lower VL, showed little peripheral movement. In group I, equal pressure points were also measured and were found to move peripherally at all the measured VL. In group II, cross-sectional area (A*) and airway compliance (K) at CP were estimated. During bronchoconstriction, A* decreased at the respective VL, and airways became less compliant. The reduction in Vmax could be explained in terms of changes in A* and K as described by wave-speed theory, and Vmax decreased because A* decreased. The decrease in A* was related in part to an increase in viscous pressure losses that reduced total pressure at CP and also in part to a change in the pressure-area behavior of bronchi at CP. Their relative effects on reducing A* and Vmax were examined.

Airway Obstruction↗
PubMed1983

The physiology of recovery in experimental pneumococcal pneumonia.

Lobar distribution of pulmonary perfusion, arterial PO2 (PaO2), intrapulmonary shunt (Qs/Qt) and post mortem lobe wts were measured in 12 dogs with experimental lobar pneumococcal pneumonia. Six dogs (group I) had both perfusion and gas exchange measurements performed 48 h after an inoculum of Streptococcus pneumoniae was placed in a left lower lobe bronchus. Six other dogs (group II) had perfusion determinations before the induction of pneumonia and again 96 h after inoculation, at which time gas exchange measurements were performed. To ensure that group II dogs were recovering from the acute pneumonia, penicillin treatment was instituted at 48 h and continued until the time of study at 96 h. An improvement in gas exchange between the acute and convalescent states was demonstrated and was associated with a 50% reduction in excess wet wt and a 25% reduction in perfusion of the infected lower lobe. We conclude that improvement in gas exchange during recovery from acute lobar pneumonia is due, in part, to air space clearing with improved ventilation and, in part, to reduced perfusion of poorly ventilated lung. The results suggest that arterial hypoxemia in acute pneumonia is aggravated by vasodilatation or blockade of local hypoxic vasoconstriction by some aspect of the acute inflammatory response, and that the hypoxic vasoconstrictor response is restored during convalescence.

Acute Disease↗
PubMed1982

Plasma volume expansion in canine pneumococcal pneumonia: its effects on respiratory gas exchange and pneumonia size.

Patients with pneumococcal pneumonia are often given fluids intravenously for hydration and maintenance of circulating blood volume. We studied the effects of plasma volume expansion on respiratory gas exchange and pneumonia size in a canine model of lobar pneumonia. Seven ventilated anesthetized dogs (Group T) with left lower lobe pneumococcal pneumonia were infused with dextran 75 in 0.9% saline solution to increase the pulmonary capillary wedge pressure to 10 mmHg for 3 h. These were compared with 7 control dogs (Group C) with left lower lobe pneumonia. Measurements of cardiac output, intrapulmonary shunt (QS/QT), and lobar distribution of perfusion were taken at baseline (B), immediately after volume infusion (V), and 3 h later (F); similar intervals were used in control animals. In Group T, QS/QT increased significantly from 24% at B to 34% at F. Part of this increase in QS/QT occurred immediately after volume infusion (29% at V) and was associated with the concomitant increase in cardiac output (4.7 L/min at B to 10.6 L/min at F). In Group C, there were no changes in cardiac output or QS/QT. At autopsy, mean wet weight for both lower lobes in Group T were greater than in Group C. Accordingly, small elevations in pulmonary capillary wedge pressure associated with fluid administration caused large increases in lobar wet weights. At least in part, these increases represented transudation of plasma and crystalloid into alveolar spaces and suggested large increases in extravascular lung liquid flux from inflamed vessels in infected lung.

Animals↗
PubMed1981

The effect of unilateral PEEP on gas exchange and pulmonary perfusion in canine lobar pneumonia.

Positive end-expiratory pressure (PEEP) has little beneficial effect in improving gas exchange in canine left lower lobe (LLL) pneumonia. This is true because while PEEP improves lobar gas exchange, it also increases relative perfusion (QL) to the diseased lobe. The authors hypothesized that PEEP administered to only the diseased lung would avoid the increased QLLL. Six dogs with LLL pneumonia in which PEEP was applied only to the left lung were observed. The dogs were studied supine and each lung was ventilated separately with 100 per cent O2. Measurements of arterial oxygen tension (PaO2), shunt (Qs/Qt) and lobar distribution of pulmonary perfusion were made before, during, and after 12 cm H2O PEEP. Changes in QLLL expressed as per cent of cardiac output were determined using radiolabeled microspheres. PEEP improved PaO2 from 310 +/- 86 to 532 +/- 58 torr and Qs/Qt from 29 +/- 5 per cent to 12 +/- 5 per cent, returning after PEEP to 337 +/- 84 torr and 26 +/- 5 per cent, respectively. QLLL per cent did not increase during PEEP. These results suggest that unilateral PEEP improves regional gas exchange within the pneumonia lobe, probably by ventilating units which were previously perfused but not ventilated. Further, this improvement in regional gas exchange occurred without the diversion of blood flow towards consolidated lung that occurs with whole-lung PEEP, and so resulted in a substantial net improvement in overall gas exchange.

Animals↗
PubMed1981

Effect of pneumococcal lobar pneumonia on canine lung mechanics.

We produced left lower lobe (LLL) pneumococcal pneumonia in seven dogs and measured lung volumes and pulmonary mechanics before (day 1) and 48 h after (day 3) development of the infection. Compared with seven control dogs, total lung capacity (TLC) and functional residual capacity (FRC) decreased 550 and 140 ml, respectively, representing a 15% reduction from the initial value in both cases. Compliance measured during tidal breathing decreased by 30%, and even when corrected for the smaller FRC on day 3, specific compliance (CLsp) was reduced. At autopsy, the infected LLL had an excess weight of 89 g, and its 50% reduction in gas volume accounted for the decrease in TLC from day 1 to day 3. Compared with control dogs, there were no changes in the deflation pressure-volume curves of the noninfected lung of the pneumonia dogs. These results indicate that the reduction in TLC in bacterial lobar pneumonia was small and resulted from the reduced gas volume of the infected lobe. Assuming that the increased weight gain in the LLL represented 89 ml of exudate that filled alveoli, we propose that bacterial pneumonia reduced gas volume at FRC by filling alveoli with inflammatory exudate and further decreased TLC by preventing these alveoli from inflating. The reduced CLsp suggested nonventilation of air spaces in addition to those that were liquid filled and was consistent with nonventilation of the entire LLL.

Animals↗
PubMed1981

Effect of PEEP on gas exchange and pulmonary perfusion in canine lobar pneumonia.

We investigated the effects of positive end-expiratory pressure (PEEP) on respiratory gas exchange and pulmonary perfusion in 10 dogs with left lower lobe (LLL) pneumonia. In 6 dogs, measurements were made with the chest closed and 12 cmH2O were applied; in 4 other open-chest dogs (group O), 6 cmH2O were used. Both groups showed similar changes, and the individual results for all dogs were averaged. With the animals breathing 100% oxygen, total pulmonary shunt (Qs/Qt), arterial oxygen tension (PaO2), and the relative distribution of pulmonary blood flow were measured before, during, and after PEEP. During the control periods, QLLL when expressed as a percent cardiac output averaged 24 +/- 7%. With PEEP, QLLL increased by more than 50% to a mean value of 37 +/- 5%. Despite this increase, the respective values of Qs/Qt and PaO2 improved slightly from 28% and 288 Torr to 25% and 370 Torr. This result suggested that PEEP also improved regional gas exchange, and this finding was subsequently confirmed in Group O where the shunt fractions of the lower lobes were additionally measured. Accordingly, our results show that PEEP altered regional perfusion and shunt so that, on the mean, there was little change in total pulmonary shunt. Whether PEEP worsened or improved gas exchange in any individual experiment was dependent on the relative magnitude of the changes in each of these regional parameters.

Animals↗
PubMed1981

Pathophysiology of gas exchange and pulmonary perfusion in pneumococcal lobar pneumonia in dogs.

We placed an inoculum of Streptococcus pneumoniae type III into a left lower lobe bronchus of six dogs (group P), and in six other dogs (Group C) a sterile control inoculum was used. Measurements of shunt (Qs/Qt) and venous admixture (Qva/Qt) were made immediately before (day 1) and 48 h after (day 3) inoculation. All dogs in group P had extensive lobar pneumonia confirmed radiologically and at autopsy, whereas Group C had only small sterile lesions at the site of inoculation. In group P, mean Qs/Qt and Qva/Qt increased significantly to 0.15 and 0.21, respectively. Mean lobar Qs/Qt, calculated using blood samples from lobar veins at thoracotomy on day 3, was markedly increased in the pneumonia lobe (0.69) compared with the contralateral lower lobe (0.08), and alveolar ventilation of that lobe approached zero. Perfusion of the infected lobe determined by radioactive microspheres showed a variable and statistically nonsignificant decrease between control and infected states that was not affected by oxygen breathing. In group C there was no change between days 1 and 3 in gas exchange or in distribution of pulmonary perfusion. We conclude that hypoxemia in pneumonia was due to both increased shunt and venous admixture in the infected regions, and that local hypoxic vasoconstriction was in most instances ineffective in directing blood flow away from the consolidated lobe.

Animals↗
PubMed1980

How does HeO2 increase maximum expiratory flow in human lungs?

We used the retrograde catheter technique to investigate the effect of HeO2 on resistance to maximum expiratory flow (Vmax) in airways subsegments between alveoli and the equal pressure point (EPP), and between EPP and the flow-limiting segment (FLS). FLS were found at the same airway site in sublobar bronchi (i.d., 0.54 +/- 0.13 cm) on both air and HeO2 in the six human excised lungs studied. Static elastic recoil pressure (5 +/- 1 cm H2O) and the lateral pressure at FLS (critical transmural airway pressure -6 +/- 3 cm H2O) were not different on the two gases. delta Vmax averaged 37 +/- 8.9% and was similar to the value found in healthy subjects of similar age (66 +/- 10 yr). EPP were located on HeO2 in peripheral airways (i.d., 0.33 +/- 0.03 cm), and EPP on air were located more downstream. Resistance between EPP and FLS was highly density dependent. Resistance between alveoli and EPP behaved as if it were density independent, due in part to Poiseuille flow in the peripheral airways and in part to the consequent narrowing of peripheral airways on HeO2. This density-independent behavior in peripheral airways reduced delta Vmax on HeO2 from its predicted maximal amount of 62%. Assuming that FLS is the "choke point" these findings are consistent with wave-speed theory of flow limitation modified to include functionally density-independent pressure losses in peripheral airways. These results and conclusions are similar to those found in living dogs. They question previous interpretation of delta Vmax as an index of peripheral airway obstruction, and demonstrate the utility of the wave-speed theory in explaining complicated mechanisms of expiratory flow limitation.

Aged↗