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Biomedical subjects

G F Nieman

Publications and source records attributed to G F Nieman.

36 records · Page 2Linked to original sources
PubMed1994

Unilateral smoke inhalation increases pulmonary blood flow to the injured lung.

Smoke inhalation (SI) affects the homogeneity of lung perfusion possibly by increasing alveolar surface tension. Anesthetized dogs (n = 8) were ventilated with a tracheal divider and a dual ventilator. One lung (left or right) was exposed to 5 minutes of SI while the other remained on room air. Total pulmonary blood flow (cardiac output) was measured by thermal dilution and left lung blood flow was measured with an ultrasonic flow probe. Since SI is associated with elevation of alveolar surface tension (AST), we studied a second group of dogs (n = 6) in which AST was increased in one lung with aerosolized dioctyl sodium sulfosuccinate (OT). The OT elevates AST without otherwise damaging the lung. Unilateral SI resulted in systemic hypoxemia (Pao2 fell from 91 +/- 6 to 55 +/- 4 mm Hg) and increased venous admixture (9 +/- 2% to 29 +/- 4%) both of which remained different from baseline values (p < 0.05) for 2 hours. Blood flow to the smoke exposed lung increased gradually and became significantly larger than that to the contralateral normal lung 2 hours following inhalation (smoke lung = 64% +/- 6% and normal lung = 36% +/- 6% of total blood flow). Following smoke exposure, pulmonary vascular resistance (PVR) increased with time in the unexposed normal lung (baseline = 8.7 +/- 1.4; 2 hours post smoke = 22.6 +/- 7.9 mm Hg/L/min, p < 0.05); PVR did not change in the smoke injured lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Exosurf treatment following wood smoke inhalation.

Pulmonary surfactant deactivation is an important factor in the pathophysiology caused by wood smoke inhalation. Surfactant replacement is beneficial in treatment of surfactant-deficient neonates and possibly the adult respiratory distress syndrome (ARDS). In this study, the effect of exogenous Exosurf treatment for acute wood smoke injury was examined in four groups of rabbits. All groups were anaesthetized, placed on a ventilator, and surgically prepared for haemodynamic, peak airway pressure (P(aw)), and blood gas measurements. Rabbits were monitored for 2 h following smoke or sham smoke inhalation. At the conclusion of the experiment pulmonary oedema and surfactant function were measured. A Control group (n = 5) was followed without intervention. A Smoke group (n = 4) was ventilated with wood smoke for 3 min. A third group (Smoke+Exo, n = 4) was subjected to smoke followed by pulmonary instillation of Exosurf (5 ml/kg). Saline (5 ml/kg) was instilled into the lungs of the fourth group (n = 3) as a control for Exosurf instillation. Saline, Smoke and Smoke+Exo all significantly lowered PO2 and elevated P(aw) compared to baseline and the Control group. Exosurf treatment did not reduce the pulmonary oedema or restore surfactant function caused by smoke exposure. This study indicates that wood smoke inhalation acutely damages the lung and that administration of Exosurf by instillation is not an effective treatment.

Airway Resistance↗
PubMed1991

Methylprednisolone does not protect the lung from inhalation injury.

Most clinical studies suggest that corticosteroids are contraindicated in the treatment of acute smoke inhalation. However, they are still used in critical situations with the hope that they might reverse the acute pathophysiological responses to smoke inhalation and thus reduce the severity of the illness or make survival possible. These experiments were done to study the effect of methylprednisolone on the response to smoke inhalation in anaesthetized mongrel dogs. Three experimental protocols were followed: (I) haemodynamics, gas exchange, lung compliance, and lung water were evaluated; (II) pulmonary vascular permeability was assessed by cannulating the afferent tracheobronchial lymphatic and calculating the osmotic reflection coefficient (sigma d) at high lung lymph flows; (III) pulmonary surfactant function was studied using a Wilhelmy balance. Methylprednisolone alone did not alter any measured values compared with those seen in control animals. Treatment with methylprednisolone (30 mg/kg) prior to smoke exposure did not attenuate any of the adverse responses typically seen after smoke inhalation. These data indicate that methylprednisolone does not protect the lung from the acute physiological consequences of inhalation injury.

Animals↗
PubMed1990

Surfactant displacement by plasma lavage results in pulmonary edema.

The effects of plasma lavage on pulmonary surfactant and edema were studied in anesthetized open-chest dogs. After instrumentation and baseline measurements, citrated autologous plasma (1.5 ml/kg) was lavaged into each lung (n = 6). A control group was administered the same dose of buffered saline solution (n = 4). Hemodynamic parameters, blood gases, and lung compliance were monitored for 2 hours after lavage. Surfactant function, assessed with a Wilhelmy balance, and extravascular lung water measured gravimetrically were determined at the end of the experiment. Immediately after plasma lavage, a nonsegmental atelectasis was observed on the lung surface. Little change was seen in vascular pressures or cardiac output in either group, whereas partial pressure of oxygen in arterial blood and static compliance fell significantly after plasma lavage. Two hours after lavage, a large amount of white foam was observed in both large and small airways in the plasma group. Plasma but not saline lavage elevated surface tension minimum in pulmonary tissue. Airway foam contained functional surfactant; addition of plasma to normal surfactant on the Wilhelmy balance did not inhibit surfactant function. Extravascular lung water was increased in the plasma compared with the saline lavage group. These data suggest that plasma usurps surfactant from the alveolar hypophase rather than inhibiting its ability to lower surface tension. Because little change was measured in vascular pressures and it is unlikely that autologous plasma increases vascular permeability, we conclude that the edema was the result of high alveolar surface tension.

Animals↗
PubMed1990

Positive end-expiratory pressure accelerates lung water accumulation in high surface tension edema.

The effect of positive end expiratory pressure (PEEP) on the rate of lung water accumulation with high surface tension pulmonary edema was examined. Alveolar surface tension was elevated by inhalation of 15 mg/kg of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Hemodynamic measurements, blood gases, and colloid oncotic pressures were recorded in anesthesized dogs for 2 hours after surfactant displacement and elevation of PEEP to 10 cm H2O pressure (group II; n = 10). These data were compared with those of an identical protocol that used only 5 cm H2O PEEP (group I; n = 10). Pulmonary extravascular water volume (PEWV) was measured gravimetrically at the end of the experiment. OT inhalation resulted in an immediate fall in Pao2 and rise in venous admixture (QVa/QT), with little change in colloid oncotic pressure or left atrial pressure. In group I, Pao2 and QVa/QT did not improve significantly over 2 hours, whereas both returned to near baseline in group II. PEWV was elevated in group I compared with normal PEWV (historic controls; n = 11) (6.1 +/- 0.07 - 3.6 +/- 0.01 ml/gm dry lung; p less than 0.01); however, PEWV in group II (9.1 +/- 1.0 ml/gm dry lung; p less than 0.01) was greater than in both group I and historic controls. These data indicate that high alveolar surface tension induces pulmonary edema and PEEP accelerates this edema formation.

Animals↗
PubMed1989

Wood smoke inhalation increases pulmonary microvascular permeability.

The effect of wood smoke inhalation (SI) on pulmonary vascular permeability was studied in open-chested, anesthetized dogs. Animals were divided into two groups. A prenodal lymphatic vessel was cannulated in group I (n = 7), and baseline (BL) lung lymph flow (QL) and lymph (CL) and plasma (CP) protein concentrations were measured. The animals' lungs were then ventilated with wood smoke for 5 minutes. Left atrial pressure (Pla) was increased above baseline (mean 16.7 +/- 2.2 mm Hg), and the ratio of CL to CP was used to assess endothelial permeability at high lymph flows. There was little change in either QL (BL: 27 +/- 9; SI: 27 +/- 5 microliters/min) or CL/CP (BL: 0.76 +/- 0.03; SI: 0.74 +/- 0.02) after SI at normal Pla. Elevation of Pla caused a significant increase in QL (136 +/- 15 microliters/min), but CL/CP (0.67 +/- 0.02) failed to decrease significantly at high lymph flows. In group II (n = 15) total protein concentration of airway fluid was compared with that of plasma after smoke inhalation, intravenous alloxan, and increased Pla. The ratio of protein concentration in airway fluid to plasma after SI (0.70 +/- 0.07) was greater than that obtained with increased Pla (0.64 +/- 0.07) but less than that after alloxan (0.85 +/- 0.04). These data indicate that SI in the dog results in a moderate increase in pulmonary vascular permeability that is less severe than that induced by alloxan.

Animals↗
PubMed1988

Smoke inhalation.

An attempt has been made to review the characteristics of fire and smoke and the epidemiology of smoke inhalation to identify some of the many variables which interact to control the severity of the injury. An experimental model appropriate to study the pulmonary injury of smoke victims who survive to enter the health care system is described. Experiments which define how smoke damages the lung are reviewed in an effort to explain why the smoke-damaged lung is vulnerable to additional stress and why those with an injured lung and a burn have such a high mortality rate.

Adult↗
PubMed1988

Effects of crystalloid on lung fluid balance after smoke inhalation.

Inhalation injury occurs in 21% of flame burn victims who require large fluid volumes for resuscitation and have a mortality rate greater than 30%. This study was done to determine how vulnerable the smoke-injured lung is to fluid accumulation when crystalloids are infused rapidly. Mongrel dogs were exposed to smoke and 10% body-weight Ringer's lactate in three groups: (I) fluid only, (II) smoke only, and (III) smoke and fluid. The increase in wet-dry lung weight ratio was 2% in Group I, 28% in Group II, and 42% in Group III, consistent with pulmonary edema present only in Group III. The decrease in colloid oncotic pressure was similar in both of the groups that were given fluid, and the rise in the surface tension minimum of lung extracts was similar in both of the groups that were exposed to smoke. The smoke-injured lung loses the ability to protect itself when challenged with fluid. Reduced oncotic pressure is not responsible. Changes in microvascular pressure, endothelial and epithelial damage, and surfactant inactivation interact to cause this increase in extravascular lung water.

Animals↗
PubMed1988

Effect of increased alveolar surface tension on segmental pulmonary vascular resistance.

The site of change in pulmonary vascular resistance (PVR) after surfactant displacement with the detergent diocytl sodium sulfosuccinate (OT) was studied in the isolated canine left lower lobe preparation. Changes in PVR were assessed using the arterial and venous occlusion technique and the vascular pressure-flow relationship. Changes in alveolar surface tension were confirmed from measurements of pulmonary compliance as well as from measurements of surface tension of extracts from lung homogenates. After surfactant depletion (the perfusion rate constant) the total pressure gradient (delta PT) across the lobe increased from 13.4 +/- 1 to 17.1 +/- 0.8 mmHg. This increase in delta PT was associated with a significant increase in the arterial and venous gradients (3.7 +/- 0.3 to 4.9 +/- 0.4 and 5.7 +/- 0.5 to 9.4 +/- 0.6 mmHg, respectively) and a decrease in middle pressure gradient (4.1 +/- 0.8 to 2.9 +/- 0.6 mmHg). The vascular pressure-flow relationship supported these findings and showed that the mean slope increased by 52% (P less than 0.05), whereas the pressure intercept decreased slightly but not significantly (3.7 +/- 0.7 to 3.2 +/- 0.8 mmHg). These results suggest that the resistance of arteries and veins increases, whereas the resistance of the middle segment decreases after surfactant depletion. These effects were apparently due to surface tension that acts directly on the capillary wall. Direct visualization of subpleural capillaries supported the notion that capillaries become distended and recruited as alveolar surface tension increases. In the normal lung (perfused at constant-flow rate) changes in alveolar pressure (Palv) were transmitted fully to the capillaries as suggested by equal changes in pulmonary arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of positive end-expiratory pressure on alveolar capillary perfusion.

Positive end-expiratory pressure (PEEP) increases arterial carbon dioxide tension and alveolar dead space by reducing alveolar capillary perfusion. The two likely mechanisms by which PEEP reduces alveolar capillary perfusion are reduction of cardiac output or compression of pulmonary capillaries within interalveolar septa, or both mechanisms. This study attempts to quantitate the impact of each of these mechanisms on alveolar capillary perfusion in anesthetized dogs by restoring cardiac output to baseline values with dextran 70 infusion after application of 15 cm H2O PEEP. Alveolar capillary perfusion was assessed directly through the visceral pleura by in vivo photomicroscopy. PEEP resulted in a fall in cardiac output and alveolar capillary perfusion with a concomitant rise in alveolar dead space-tidal volume ratio and arterial carbon dioxide tension. Infusion of dextran 70 returned the cardiac output to baseline levels but only slightly increased alveolar capillary perfusion. Both dead space/tidal volume ratio and arterial carbon dioxide tension remained significantly elevated with PEEP even with normal cardiac output. Microscopically, alveolar capillaries appeared compressed and flattened by PEEP, which indicated a mechanical interruption of blood flow. Extra-alveolar vessels remained perfused with PEEP. PEEP increased dead space/tidal volume ratio 36%; restoration of cardiac output reduced dead space/tidal volume ratio only 7% and did not return alveolar capillary perfusion to baseline levels. These data indicate that most of the reduced alveolar perfusion with PEEP results from direct compression of alveolar capillaries and not from reduced cardiac output.

Animals↗
PubMed1987

Surfactant displacement by meconium free fatty acids: an alternative explanation for atelectasis in meconium aspiration syndrome.

Meconium, an ether extract of meconium, and the major free fatty acids of meconium (palmitic, stearic, and oleic acids) were all found to increase the surface tension minimum of dog lung extract in a Wilhelmy balance. Each of these fractions was instilled into the lungs of dogs (15 experimental, eight saline solution controls), and cardiac output, venous and arterial blood gases, pulmonary, atrial, and systemic pressures, airway pressure, and static lung compliance were serially monitored for 2 hours. Mean airway pressure increased and static lung compliance decreased significantly in all of the experimental groups. Although arterial pH and PaCO2 and the various hemodynamic measurements did not change during the experiment, PaO2 decreased significantly and did not return to baseline in all experimental groups. Extracts from atelectatic portions of experimental dog lung had a surface tension minimum of greater than 20 dynes/cm, whereas airway foam had a surface tension minimum of less than 10 dynes/cm, suggesting that the free fatty acids of meconium are able to strip surfactant from the alveoli.

Animals↗
PubMed1987

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance.

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5-3.8 mmHg greater during deflation than during inflation.

Animals↗
PubMed1986

Microvascular membrane permeability in high surface tension pulmonary edema.

Pulmonary edema was induced in dogs by an aerosol of detergent dioctyl sodium sulfosuccinate. The permeability of the pulmonary microvascular membrane was assessed by cannulating an afferent tracheobronchial lymphatic and comparing the lymph-to-plasma total protein concentration (CL/CP) during high lymph flows induced by increasing left atrial (LA) pressure after detergent aerosol. Base-line CL/CP of 0.69 +/- 0.02 fell to 0.55 +/- 0.03 with increased LA pressure alone. CL/CP fell to 0.47 +/- 0.02 when LA pressure was increased following detergent, 0.51 +/- 0.04 following an aerosol of the vehicle in which the detergent was dissolved, and 0.73 +/- 0.10 following intravenous alloxan. In additional animals protein concentration of the airway edema fluid was compared with that of plasma. The ration of protein concentration of airway fluid to plasma was 0.63 +/- 0.08 following detergent aerosol, 0.64 +/- 0.10 following increased LA pressure, and 0.94 +/- 0.09 following administration of alloxan. These data indicate no major increase in pulmonary microvascular permeability following detergent aerosol and support the concept that pulmonary edema is the consequence of reduced interstitial perimicrovascular hydrostatic pressure caused by increased alveolar surface tension.

Animals↗
PubMed1985

High surface tension pulmonary edema induced by detergent aerosol.

The effect of the detergent dioctyl sodium sulfosuccinate on pulmonary extravascular water volume (PEWV) was studied in adult anesthetized mongrel dogs. The detergent was dissolved as a 1% solution in a vehicle of equal volumes of 95% ethanol and normal saline and administered by ultrasonic nebulizer attached to the inspiratory tubing of a piston ventilator. Two hours following detergent aerosol PEWV measured gravimetrically was increased compared with either animals receiving no aerosol or those receiving an aerosol of vehicle alone. Loss of surfactant activity and increased alveolar surface tension were demonstrated by Wilhelmy balance studies of minced lung extracts, by a fall in static compliance, and by evidence of atelectasis and instability noted by gross observation and by in vivo microscopy. No significant changes in colloid oncotic pressure or pulmonary microvascular hydrostatic pressure were observed. These data suggest that pulmonary edema can be induced by increased alveolar surface tension and support the concept that one of the major roles of pulmonary surfactant is to prevent pulmonary edema.

Aerosols↗
PubMed1983

High surface tension pulmonary edema.

Dogs were anesthetized with pentobarbital and placed on a piston ventilator with room air. Ten animals received an endobronchial lavage of normal saline (3 mg/kg). Ten other animals received an endobronchial lavage of the same volume of a nonionic detergent, Tween 20, 5% in saline. Detergent lavage was shown by Wilhelmy balance to increase surface tension of lung extracts. Saline lavage did not alter the surface tension of lung extracts. No significant differences between the groups were noted in cardiac output, left ventricular and diastolic pressure, mean pulmonary artery pressure, or colloid oncotic pressure. Static compliance and arterial PO2 were decreased following detergent lavage. Animals were sacrificed 2 hr after lavage and pulmonary extravascular water volume (PEWV) was measured gravimetrically. Saline-lavaged lungs with normal surface tension had a PEWV of 4.3 ml/g dry lung. Tween-lavaged lungs with increased surface tension had a PEWV of 5.3 ml/g dry lung (P less than 0.005). When the estimated volume of residual lavage solution remaining in the lung parenchyma was subtracted from the total wet lung wt, the corrected PEWV was 3.62 +/- 0.12 ml/g dry lung for saline-lavaged lung and 4.76 +/- 0.19 ml/g dry lung for Tween-lavaged lung. PEWV for 11 control animals ventilated 2 hr without lavage was 3.61 +/- 0.13 ml/g dry lung. It is concluded that, experimentally, high alveolar surface tension can induce pulmonary edema even when pulmonary microvascular hydrostatic and colloid oncotic pressures are normal.

Animals↗
PubMed1981

Alveolar function following surfactant deactivation.

In vivo cinemicroscopic studies of subpleural alveoli were conducted in dogs for 4 h after pulmonary lavage with 5% Tween 20 and after lavage with normal saline. Saline-lavaged alveoli showed little change in alveolar size during tidal ventilation, whereas Tween lavage resulted both in alveolar recruitment and marked variation in alveolar size from end expiration to peak inspiration, with total collapse frequently occurring by end expiration. Following Tween, alveolar stability decreased, but alveolar capillary perfusion increased. Marked recovery of stability by 4 h was noted in most alveoli. Wilhelmy balance studies on lung extracts showed a decrease in surfactant function 30 min after Tween and a partial recovery of surfactant activity after 4 h. This study provides in vivo evidence that normal surfactant function is critical to alveolar stability and that alveolar stability is markedly restored 4 h after acute deactivation or displacement by Tween. Surfactant deactivation and loss of alveolar stability are associated with increased alveolar capillary perfusion creating significant ventilation-perfusion ratio abnormalities.

Animals↗
PubMed1980

The effect of smoke inhalation on pulmonary surfactant.

This paper details efforts to define the primary pathophysiology of acute smoke inhalation without the variables of infection, burns, or fluid resuscitation. A standard dose of smoke (wood and kerosene) was delivered at 37 C to mongrel dogs. The parameters studied included blood gases, carboxyhemoglobin, pulmonary and systemic hemodynamics, respiratory mechanics, surface tension area curves as an indication of surfactant activity, and in vivo photomicroscopy. The FiO2 of the smoke was 17 volumes per cent; the carbon monoxide 17,000 ppm. Immediately following smoke exposure, dense, nonsegmental atelectasis developed. Hemodynamic changes were insignificant, but the PaO2 fell to 49 mmHg; the right to left shunt rose from 5 to 41%. Surfactant reduction was significant: enough to cause an increase in the minimum surface tension from 7 to 22 dynes/cm. This surfactant loss may explain the atelectasis seen and the marked instability of subpleural alveolar walls. The data collected are consistent and support the acute inactivation of surfactant as one of the primary pathophysiologic events in smoke inhalation. The clinical correlation is good; surfactant loss may explain why victims of smoke inhalation are so vulnerable to fluid administration if they have thermal burns as well effectiveness of medical devices.

Animals↗