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Jack J Haitsma

Publications and source records attributed to Jack J Haitsma.

At least 19 recordsLinked to original sources
PubMed2006

Year in review 2005: Critical Care--respirology: mechanical ventilation, infection, monitoring, and education.

We summarize all original research in the field of respiratory intensive care medicine published in 2005 in Critical Care. Twenty-seven articles were grouped into the following categories and subcategories to facilitate rapid overview: mechanical ventilation (physiology, spontaneous breathing during mechanical ventilation, high frequency oscillatory ventilation, side effects of mechanical ventilation, sedation, and prone positioning); infection (pneumonia and sepsis); monitoring (ventilatory monitoring, pulmonary artery catheter and pulse oxymeter); and education (training and health outcome).

Critical Care↗
PubMed2006

The effect of open lung ventilation on right ventricular and left ventricular function in lung-lavaged pigs.

INTRODUCTION: Ventilation according to the open lung concept (OLC) consists of recruitment maneuvers, followed by low tidal volume and high positive end-expiratory pressure, aiming at minimizing atelectasis. The minimization of atelectasis reduces the right ventricular (RV) afterload, but the increased intrathoracic pressures used by OLC ventilation could increase the RV afterload. We hypothesize that when atelectasis is minimized by OLC ventilation, cardiac function is not affected despite the higher mean airway pressure. METHODS: After repeated lung lavage, each pig (n = 10) was conventionally ventilated and was ventilated according to OLC in a randomized cross-over setting. Conventional mechanical ventilation (CMV) consisted of volume-controlled ventilation with 5 cmH2O positive end-expiratory pressure and a tidal volume of 8-10 ml/kg. No recruitment maneuvers were performed. During OLC ventilation, recruitment maneuvers were applied until PaO2/FiO2 > 60 kPa. The peak inspiratory pressure was set to obtain a tidal volume of 6-8 ml/kg. The cardiac output (CO), the RV preload, the contractility and the afterload were measured with a volumetric pulmonary artery catheter. A high-resolution computed tomography scan measured the whole lung density and left ventricular (LV) volumes. RESULTS: The RV end-systolic pressure-volume relationship, representing RV afterload, during steady-state OLC ventilation (2.7 +/- 1.2 mmHg/ml) was not significantly different compared with CMV (3.6 +/- 2.5 mmHg/ml). Pulmonary vascular resistance (OLC, 137 +/- 49 dynes/s/cm5 versus CMV, 130 +/- 34 dynes/s/cm5) was comparable between groups. OLC led to a significantly lower amount of atelectasis (13 +/- 2% of the lung area) compared with CMV (52 +/- 3% of the lung area). Atelectasis was not correlated with pulmonary vascular resistance or end-systolic pressure-volume relationship. The LV contractility and afterload during OLC was not significantly different compared with CMV. Compared with baseline, the LV end-diastolic volume (66 +/- 4 ml) decreased significantly during OLC (56 +/- 5 ml) ventilation and not during CMV (61 +/- 3 ml). Also, CO was significantly lower during OLC ventilation (OLC, 4.1 +/- 0.3 l/minute versus CMV, 4.9 +/- 0.3 l/minute). CONCLUSION: In this experimental study, OLC resulted in significantly improved lung aeration. Despite the use of elevated airway pressures, no evidence was found for a negative effect of OLC on RV afterload or LV afterload, which might be associated with a loss of hypoxic pulmonary vasoconstriction due to alveolar recruitment. The reductions in the CO and in the mean pulmonary artery pressure were consequences of a reduced preload.

Animals↗
PubMed2006

Pathophysiology of unilateral pulmonary aspergillosis in an experimental rat model.

Because little is known about the pathophysiology of invasive pulmonary aspergillosis (IPA), we examined changes in pulmonary and general physiology during this disease in an animal model. In a model of fatal left-sided IPA, 19 persistently neutropenic rats were monitored for clinical signs including body temperature, body weight and respiratory distress. A separate group of nine rats with IPA was used for measurements of arterial blood pressure, arterial O2 and CO2 pressure, lung compliance and surfactant function. Body temperature and body weight decreased, whereas respiratory distress increased during progression of the disease. Compared to uninfected controls, in rats with IPA arterial blood pressure and lung compliance were significantly lower, and left lung minimal surface tension was significantly higher. Right lung surfactant function was not affected. Arterial O2 and CO2 pressures were not different between rats with IPA and uninfected controls. Infection with Aspergillus fumigatus in neutropenic rats resulted in hypothermia, body weight loss and respiratory distress. Loss of left lung function was probably compensated by the uninfected right lung, even in a late stage of the disease. Circulatory failure was a major feature in the terminal phase of the infection.

Animals↗
PubMed2006

Open lung ventilation preserves the response to delayed surfactant treatment in surfactant-deficient newborn piglets.

OBJECTIVE: Delayed surfactant treatment (>2 hrs after birth) is less effective than early treatment in conventionally ventilated preterm infants with respiratory distress syndrome. The objective of this study was to evaluate if this time-dependent efficacy of surfactant treatment is also present during open lung ventilation. DESIGN: Prospective, randomized controlled animal study. SETTING: University-affiliated research laboratory. SUBJECTS: Thirty-eight newborn piglets. INTERVENTIONS: Following repeated whole-lung lavage, animals were randomly allocated to conventional positive pressure ventilation (PPVCON) using a positive end-expiratory pressure (PEEP) of 5 cm H2O and a tidal volume of 7 mL/kg or open lung positive pressure ventilation (PPVOLV). During PPVOLV, collapsed alveoli were actively recruited and thereafter stabilized with sufficient PEEP. Within each ventilation group, animals received surfactant (25 mg/kg) either after 2 hrs (PPVCON-2 and PPVOLV-2) or after 4 hrs (PPVCON-4 and PPVOLV-4) of ventilation. A control group received surfactant immediately after lung lavage. Following surfactant administration, all animals were conventionally ventilated for an additional 2 hrs. MEASUREMENTS AND MAIN RESULTS: Two hours after surfactant treatment, both oxygenation and lung mechanics showed a clear deterioration in the PPVCON-4 group compared with PPVCON-2 and the control group. However, this deterioration of the surfactant response over time was not observed during PPVOLV. Analysis of the bronchoalveolar lavage fluid obtained at the end of the experiment showed that the protein concentration and the conversion of large to small aggregate surfactant was significantly higher in the PPVCON-4 group compared with the PPVCON-2 group while comparable in both PPVOLV groups. In addition, interleukin-8 and myeloperoxidase levels tended to be higher in the PPVCON-4 group compared with the PPVOLV-4 group. CONCLUSIONS: In contrast to conventional ventilation, open lung ventilation preserves the response to delayed surfactant treatment in surfactant-deficient newborn piglets. This sustained response is accompanied by an attenuation of secondary lung injury.

Animals↗
PubMed2006

Surfactant therapy in adults with acute lung injury/acute respiratory distress syndrome.

PURPOSE OF REVIEW: Several phase II and phase III studies have been performed to investigate safety, efficacy and the improvement of survival due to exogenous surfactant instillation in patients with acute lung injury or acute respiratory distress syndrome. In this review we will discuss the most recent of these studies, paying particular attention to differences in the composition of the exogenous surfactant used, the diverse modes of delivery and dose of therapy and the influence of mechanical ventilation. RECENT FINDINGS: Several phase II studies performed on patients with acute lung injury or acute respiratory distress syndrome and a phase III study performed on a pediatric population have shown beneficial effects of surfactant on oxygenation and survival. No effect of exogenous surfactant has been shown on survival in phase III studies in adult patients. SUMMARY: The changes in the surfactant system of patients with acute lung injury and acute respiratory distress syndrome form the rationale for the instillation of exogenous surfactant. There is enough evidence to use surfactant instillation for pediatric patients with acute lung injury. Due to the results of the randomized controlled trials performed so far, however, exogenous surfactant is not recommended for routine use in patients with acute lung injury or acute respiratory distress syndrome. In the future, other surfactants with different compositions may show beneficial effects.

Clinical Trials, Phase II as Topic↗
PubMed2006

Contrast media inhibit exogenous surfactant therapy in rats with acute respiratory distress syndrome.

AIM: To test the effects of various contrast media on the pulmonary surfactant system. MATERIAL AND METHODS: In a rat model of acute respiratory distress syndrome (ARDS) induced by lung lavage, the effects of surfactant suspended in saline were compared with surfactant suspended in the contrast media Visipaque, Gastrografin, Omnipaque, Telebrix M, Telebrix and Hexabrix, to establish their influence on oxygenation and lung mechanics. RESULTS: After the induction of ARDS, surfactant instillation improved oxygenation, total lung capacity (TLC(35)), volume at 5 cm H(2)O end-expiration (V(5)) and Gruenwald index. The effects of Visipaque and Gastrografin were comparable with those of surfactant alone from 90 min onwards and at 120 min, respectively. Surfactant suspended in the other contrast media resulted in significantly lower values in the above-mentioned parameters. Surface tension was lowest in surfactant suspended in saline alone. Surfactant suspended in Visipaque and Gastrografin had lower surface tension compared with surfactant suspended in the other contrast media. CONCLUSION: The ionic and non-ionic contrast media used in this study, cause an impairment of the physico-chemical behaviour of exogenous surfactant. Therefore, these contrast media cannot be regarded as safe in case of accidental exposure.

Animals↗
PubMed2006

Pulmonary coagulopathy as a new target in therapeutic studies of acute lung injury or pneumonia--a review.

OBJECTIVES: To review the involvement of coagulation and fibrinolysis in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), pulmonary infection, and ventilator-induced lung injury (VILI). DATA SOURCE: Published articles on experimental and clinical studies of coagulation and fibrinolysis in ALI/ARDS, pneumonia, and mechanical ventilation. CONCLUSIONS: Alveolar fibrin deposition is an important feature of ALI/ARDS and pulmonary infection. The mechanisms that contribute to disturbed alveolar fibrin turnover are localized tissue factor-mediated thrombin generation and depression of bronchoalveolar urokinase plasminogen activator-mediated fibrinolysis, caused by the increase of plasminogen activator inhibitors. These effects on pulmonary coagulation and fibrinolysis are regulated by various proinflammatory cytokines and are similar to those found in the intravascular spaces during severe systemic inflammation. Some studies also suggest that pulmonary coagulopathy is a feature of VILI. Recent studies have demonstrated the beneficial effect of anticoagulant therapy in sepsis. Theoretical considerations suggest that this anticoagulant therapy will benefit patients with primary lung pathology including VILI, but clinical studies are needed to examine this hypothesis before such therapy is to be advocated as a standard of care in critically ill patients.

Blood Coagulation Disorders↗
PubMed2005

Alveolar fibrinolytic capacity suppressed by injurious mechanical ventilation.

OBJECTIVE: To investigate the effect of mechanical ventilation on alveolar fibrinolytic capacity. DESIGN AND SETTING: Randomized controlled animal study in 66 Sprague-Dawley rats. SUBJECTS AND INTERVENTIONS: Test animals received intratracheal fibrinogen and thrombin instillations; six were killed immediately (fibrin controls), and the others were allocated to three ventilation groups (ventilation period: 225 min) differing in positive inspiratory pressure and positive end-expiratory pressure, respectively: group 1, 16 cmH2O and 5 cmH2O (n=17); group 2, 26 cmH2O and 5 cmH2O (n=16); group 3, 35 cmH2O and of 5 cmH2O (n=17). Ten animals that had not been ventilated served as healthy controls. MEASUREMENTS AND RESULTS: After animals were killed, we measured D-dimers, plasminogen activator inhibitor (PAI) 1, and tumor necrosis factor alpha in the bronchoalveolar lavage fluid and calculated lung weight and pressure/volume (P/V) plots. The median D-dimer concentration (mg/l) decreased with increasing pressure amplitude (192 in group 1, IQR 119; 66 in group 2, IQR 107; 29 in group 3, IQR 30) while median PAI-1 (U/ml) increased (undetectable in group 1; 0.55 in group 2, IQR 4.55; 3.05 in group 3, IQR 4.85). PAI-1 level was correlated with increased lung weight per bodyweight (Spearman's rank correlation 0.708). Tumor necrosis factor alpha concentration was not correlated with PAI-1 level. CONCLUSIONS: Alveolar fibrinolytic capacity is suppressed during mechanical ventilation with high pressure amplitudes due to local production of PAI-1.

Analysis of Variance↗
PubMed2005

Surfactant pretreatment ameliorates ischemia-reperfusion injury of the lung.

OBJECTIVE: To investigate whether surfactant pretreatment provides lung protection in an animal model of lung ischemia-reperfusion injury (LIRI). METHODS: Male Sprague-Dawley rats (n=100) were randomised to receive intratracheally administered surfactant or no pretreatment. One hour thereafter, animals underwent 120min of warm ischemia of the left lung, or were sham-operated. A third group served as healthy untreated controls. Animals were killed on day 1, 3 or 7. Blood gas values were measured and lung compliance was recorded. Broncho-alveolar lavage fluid (BALf) was obtained to assess the amount of alveolar protein, the ratio of small to large aggregate surfactant phospholipids (SA/LA ratio), and leukocyte infiltration (granulocytes, macrophages and lymphocytes, measured by Flow Cytometry). RESULTS: LIRI resulted in a mortality rate of 17% and significantly decreased lung compliance and PaO(2) (day 1 and 3 P<0.001, day 7 P<0.05) as compared to sham-operated and healthy controls. On day 1 more protein was present in the alveoli of ischemic lungs (P<0.001) than in sham-operated and healthy controls. Furthermore, LIRI resulted in an increased SA/LA ratio in the left lung on day 1 (P<0.05) and caused infiltration of granulocytes (day 1, 3 and 7 (P<0.01)), macrophages (day 3 (P<0.05) and 7 (P<0.01) and lymphocytes (day 3 and 7 (P<0.01)) in the BALf as compared to sham-operated and healthy controls. Surfactant pretreatment improved survival, lung compliance (day 3 P<0.001) and PaO(2) (day 1, 3 (P<0.01 and 7 (P<0.05)). It also reduced protein leakage (P<0.05) and prevented an increase in the SA/LA ratio (P<0.01). Although the number of macrophages and granulocytes in the BALF was increased on day 1 and 3 (P<0.01) after surfactant pretreatment as compared to all other groups, the number of lymphocytes was reduced on day 3 (P<0.05). CONCLUSIONS: The present study shows that surfactant pretreatment enhances recovery of lung function and lung mechanics after LIRI, resulting in normal parameters from day 3 onwards. Surfactant pretreatment in this LIRI model may provide useful information to improve donor lung function after lung transplantation.

Animals↗
PubMed2005

Effects of hyperbaric treatment in cerebral air embolism on intracranial pressure, brain oxygenation, and brain glucose metabolism in the pig.

OBJECTIVE: To evaluate the effects of hyperbaric oxygen treatment after cerebral air embolism on intracranial pressure, brain oxygenation, brain glucose/lactate metabolism, and electroencephalograph. DESIGN: Prospective animal study. SETTING: Hyperbaric chamber. SUBJECTS: Eleven Landrace/Yorkshire pigs. INTERVENTIONS: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods. After injection of air into the internal carotid artery, animals were treated immediately (at 3 mins; t = 3) or at 60 mins (t = 60) with U.S. Navy Treatment Table 6 for 4.48 hrs. RESULTS: At the end of hyperbaric oxygen treatment, intracranial pressure in the t = 60 group (39 +/- 8 mm Hg) was significantly higher than in the t = 3 group (27 +/- 6 mm Hg), brain oxygenation values for group t = 3 and t = 60 were 66 +/- 14 and 52 +/- 15 mm Hg, respectively (no significant difference from baseline), and there were no pathologic scores in the visually assessed electroencephalograph. However, there was a significant decrease in brain glucose and a significant increase in brain lactate in both groups at the end of the 5-hr study period. CONCLUSIONS: Hyperbaric oxygen treatment initiated at both 3 and 60 mins after embolization decreased the deleterious effects of cerebral air embolism on intracranial pressure and brain metabolism. Therefore, this model appears suitable to test the application of hyperbaric oxygen treatment with a delay >60 mins after embolization, as is often the case in the clinical situation.

Animals↗
PubMed2004

Reducing atelectasis attenuates bacterial growth and translocation in experimental pneumonia.

Besides being one of the mechanisms responsible for ventilator-induced lung injury, atelectasis also seems to aggravate the course of experimental pneumonia. In this study, we examined the effect of reducing the degree of atelectasis by natural modified surfactant and/or open lung ventilation on bacterial growth and translocation in a piglet model of Group B streptococcal pneumonia. After creating surfactant deficiency by whole lung lavage, intratracheal instillation of bacteria induced severe pneumonia with bacterial translocation into the blood stream, resulting in a mortality rate of almost 80%. Treatment with 300 mg/kg of exogenous surfactant before instillation of streptococci attenuated both bacterial growth and translocation and prevented clinical deterioration. This goal was also achieved by reversing atelectasis in lavaged animals via open lung ventilation. Combining both exogenous surfactant and open lung ventilation prevented bacterial translocation completely, comparable to Group B streptococci instillation into healthy animals. We conclude that exogenous surfactant and open lung ventilation attenuate bacterial growth and translocation in experimental pneumonia and that this attenuation is at least in part mediated by a reduction in atelectasis. These findings suggest that minimizing alveolar collapse by exogenous surfactant and open lung ventilation may reduce the risk of pneumonia and subsequent sepsis in ventilated patients.

Animals↗
PubMed2004

Hyperventilation impairs brain function in acute cerebral air embolism in pigs.

OBJECTIVE: To evaluate, in a model of cerebral air embolism (CAE), the effects of ventilation-induced hypocapnia and hyperoxemia on intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain oxygen (PbrO(2)), brain carbon dioxide (PbrCO(2)), brain pH (brpH) and levels of brain glucose and lactate. DESIGN AND SETTING: Prospective animal study in a university medical center. SUBJECTS: Fifteen Landrace/Yorkshire pigs. INTERVENTIONS: In 15 anesthetized pigs ICP, PbrO(2), PbrCO(2) and brpH were measured with multi-parameter sensors, and brain glucose and lactate by microdialysis. All these parameters were recorded for 2 h after injection of air into the internal carotid artery. Nine animals were hyperventilated (PaCO(2 )+/-25 mmHg) and hyperoxygenated (FiO(2) 1.0) and six animals were normoventilated (PaCO(2)()+/-40 mmHg with an FiO(2) 0.4) and served as controls. RESULTS. In the treatment group the ICP rose from 8+/-1 to 52+/-6 mmHg, which was similar to that in the control group (12+/-1 to 57+/-8 mmHg). At the end of the 2-h study period, there were no significant differences in PbrO(2), PbrCO(2) and brpH between the two groups. The decreased brain glucose and increased brain lactate reached severe pathological values in both groups by the end of the 2-h study period. CONCLUSIONS: Hypocapnia and hyperoxemia in acute CAE did not improve pathological functional brain parameters compared with normoventilated controls. Similarly, the pathological changes in brain glucose/lactate could also not be improved by hypocapnia and hyperoxemia.

Animals↗
PubMed2004

Surfactant therapy for acute lung injury/acute respiratory distress syndrome.

PURPOSE OF REVIEW: Currently, three phase III surfactant replacement trials for acute lung injury (ALI)/acute respiratory distress syndromes (ARDS) patients are underway. Although the efficacy of surfactant replacement therapy will first have to be proved in these phase III trials, recent reports indicate some enticing possibilities for the future of surfactant therapy. RECENT FINDINGS: Patients requiring mechanical ventilation show alterations in their endogenous surfactant composition. Depending on the type of lung injury or the elapsed time, modifications to surfactant preparations could enhance the efficacy of these preparations. Surfactants that closely resemble natural surfactant, especially those containing surfactant proteins (SP-B/C) and nonphospholipids (cholesterol), are able to restore normal surfactant physiology. Furthermore, lipids that are able to withstand degradation by lipases could further enhance surfactant therapy. SUMMARY: If surfactant therapy fulfills the promises expected from the ongoing phase III trials, future surfactant preparations may even enhance therapy efficacy and restore the altered endogenous surfactant pool as soon as possible.

Animals↗
PubMed2004

Open lung ventilation improves gas exchange and attenuates secondary lung injury in a piglet model of meconium aspiration.

OBJECTIVE: Previous studies failed to show clear benefits of high-frequency ventilation compared with conventional positive pressure ventilation (PPV(CON)) in experimental meconium aspiration syndrome. However, none of these studies applied an open lung ventilation strategy (OLC), which aims to reduce intrapulmonary shunt due to alveolar collapse. We hypothesized that, if combined with an open lung strategy, both high-frequency oscillatory ventilation (HFOV(OLC)) and positive pressure ventilation (PPV(OLC)) would improve gas exchange and attenuate ventilator-induced lung injury in experimental meconium aspiration syndrome. DESIGN: Prospective, randomized animal study. SETTING: Research laboratory of a large university. SUBJECTS: Forty-two newborn piglets. INTERVENTIONS: Thirty minutes after intratracheal meconium instillation, 36 newborn piglets were assigned to one of three ventilation groups-PPV(OLC), HFOV(OLC), or PPV(CON)-and ventilated for 5 hrs. In both OLC groups, collapsed alveoli were actively recruited and thereafter stabilized using the lowest possible airway pressures. During PPV(CON), ventilator settings were adjusted to prevent critical hypoxia (Pao2 <60 torr [8 kPa]). Six animals served as saline controls. MEASUREMENTS AND MAIN RESULTS: Compared with the PPV(CON) group, arterial oxygenation and lung mechanics were superior in both OLC groups and the saline controls. Analysis of the bronchoalveolar lavage fluid obtained after 5 hrs of ventilation showed increased myeloperoxidase activity in the PPV(CON) group compared with both OLC groups and saline controls. Alveolar protein influx was not different between the groups. Histologic analysis revealed a higher lung injury score in the PPV(CON) group compared with the PPV(OLC) and the HFOV(OLC) groups. CONCLUSIONS: Application of the OLC during PPV and HFOV is feasible in experimental meconium aspiration syndrome and results in superior oxygenation and less ventilator-induced lung injury compared with PPV(CON).

Animals↗
PubMed2004

Response to exogenous surfactant is different during open lung and conventional ventilation.

OBJECTIVE: Previous studies have shown that the efficacy of exogenous surfactant is dose-dependent during conventional positive pressure ventilation (PPVCON). The present study aimed to determine whether this dose-dependent relationship is also present during open lung (OLC) ventilation. We also explored the effect of exogenous surfactant on the ventilation pressures applied during ventilation. DESIGN: Animal study. SETTING: University-affiliated research laboratory. SUBJECTS: Seventy-two newborn piglets. INTERVENTIONS: After repeated whole lung lavage, animals were randomly allocated to two surfactant groups receiving either 100 mg/kg surfactant (S100) or 25 mg/kg surfactant (S25) or to a control group receiving a bolus of air. Within each group, animals were randomly assigned to either PPVCON, open lung PPV (PPVOLC), or open lung high-frequency oscillatory ventilation (HFOVOLC) and ventilated for 5 hrs. MEASUREMENTS AND MAIN RESULTS: The ventilation pressures decreased in a dose-dependent way, showing the largest reduction in the S100 group. In both OLC groups, oxygenation, lung mechanics, and polymorphonuclear neutrophils analyzed in bronchoalveolar lavage were independent of the surfactant dose. In the PPVCON group, however, there was a clear dose-dependency, resulting in a deterioration of oxygenation and lung mechanics and an increase in polymorphonuclear neutrophils as the surfactant dose decreased. Although comparable between the three ventilation groups, bronchoalveolar lavage interleukin-8 concentrations significantly increased in all ventilation groups as the surfactant dose increased. Alveolar protein influx and conversion of large to small aggregate surfactant were higher during PPVCON compared with both OLC groups. There were no differences in the surfactant treatment response between PPVOLC and HFOVOLC. CONCLUSION: Exogenous surfactant enables a reduction in ventilation pressures. Compared with PPVCON, the efficacy of surfactant treatment is less dose-dependent during open lung ventilation. Surfactant conversion during open lung ventilation is reduced compared with PPVCON. Exogenous surfactant seems to up-regulate bronchoalveolar lavage interleukin-8 concentrations, independent of the ventilation strategy.

Analysis of Variance↗
PubMed2003

Surfactant in newborn compared with adolescent pigs: adaptation to neonatal respiration.

Surfactant composition and function differ between vertebrates, depending on pulmonary anatomy and respiratory physiology. Because pulmonary development in pigs is similar to that in humans, we investigated surface tension function, composition of phospholipid molecular species, and concentrations of surfactant protein (SP)-A to -D in term newborn pigs (NP) compared with adolescent pigs (AP), using the pulsating bubble surfactometer, mass spectrometry, high-performance liquid chromatography, and immunoblot techniques (IT). NP was more potent than AP surfactant in reaching minimal surface tension values near zero mN/m. Whereas SP-A and SP-D were comparable, SP-B and SP-C were increased 3- to 4-fold in NP surfactant. Moreover, fluidizing phospholipids such as palmitoylmyristoyl-PC (PC16:0/14:0) and palmitoylpalmitoleoyl-PC (PC16:0/16:1) were increased at the expense of PC16:0/16:0 (32.4 +/- 0.6 versus 44.5 +/- 3.2%, respectively). Whereas concentrations of total anionic phospholipids were similar in NP and AP surfactant (9.9 +/- 0.3 and 12.0 +/- 0.3%, respectively), phosphatidylinositol was the predominant anionic phospholipid in NP surfactant. We conclude that, compared with AP, NP surfactant displays better surface tension function under dynamic conditions, which is associated with increased concentrations of SP-B and SP-C, as well as fluidizing phospholipids at the expense of PC16:0/16:0.

Age Factors↗
PubMed2003

Ventilator-induced heat shock protein 70 and cytokine mRNA expression in a model of lipopolysaccharide-induced lung inflammation.

OBJECTIVE: To investigate the effect of mechanical ventilation with no PEEP (ZEEP) and 4 cmH(2)O PEEP on heat shock protein 70 (HSP70) and pulmonary inflammatory cytokine expression in a model of lipopolysaccharide (LPS) induced lung inflammation. DESIGN AND SETTING: Prospective, randomized, experimental animal study. SUBJECTS AND INTERVENTIONS: We challenged 42 male Sprague-Dawley rats intratracheally with LPS. After 24 h the rats were randomly assigned to one of the ventilation strategies. Rats received either 4 h of mechanical ventilation with ZEEP or mechanical ventilation with 4 cmH(2)O PEEP. A nonventilated control group received LPS only. Lung pathology after LPS challenge was evaluated by histology to assess baseline lung injury. HSP70 and cytokine mRNA levels were measured in total lung homogenates. RESULTS: PaO(2) levels and lung histology revealed no deterioration after PEEP ventilation and severe deterioration after ZEEP ventilation. There was a significant higher expression of HSP70 and IL-1beta mRNA in the lungs of the ZEEP group than in the PEEP group and nonventilated controls. In the ZEEP group high HSP70 levels were correlated inversely with low IL-1beta mRNA and low IL-6 mRNA. CONCLUSIONS: We propose that HSP70 expression protects the lung against ventilator-induced lung injury by decreasing cytokine transcription in the lung.

Animals↗