Sabrina M. Heidemann

Wayne State University, Detroit, Michigan, United States

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Publications (50)165.22 Total impact

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    ABSTRACT: The objectives were to determine if tumor necrosis factor (TNF)-α, leukotriene (LT)B4 and 8-isoprostane (IP) were present in the exhaled breath condensate (EBC) and total lung lavage (TLL) of mechanically ventilated rats, 4 and 24 h after administration of Staphylococcal entertoxin (SEB) and to find out if these mediators in the EBC correlate with the concentration in the TLL. Rats were assigned to control (n = 8); 4 h (n = 8) or 24 h (n = 8) groups after SEB. The rats were mechanically ventilated and EBC and TLL were collected for TNF-α, LTB4 and 8-IP. TNF-α was higher in the EBC of rats at 24 h after SEB when compared to control [34.5 (16-62 versus 2 (14-30) pg ml-1, p < 0.05] and also in the TLL [113.5 (70-460) versus 59 (35-79) pg ml-1, p < 0.04]. LTB4 was higher in the EBC of 24 h SEB rats, when compared to control [42 (28-50) versus 36 (29-37) pg ml-1, p < 0.01] and also in the TLL [179 (116-232) versus 114 (80-187) pg ml-1, p < 0.05). 8-IP was similar among the groups. No correlation was observed between TNF-α, LTB4 or 8-IP in the EBC compared to the TLL. TNF-α and LTB4 may be indicators of inflammation and oxidative lung injury but the EBC does not correlate with TLL concentrations.
    Journal of Breath Research 03/2013; 7(2):026003. DOI:10.1088/1752-7155/7/2/026003 · 4.63 Impact Factor
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    ABSTRACT: Purpose Collection of exhaled breath condensate (EBC) is a non-invasive method to obtain inflammatory mediators in the lung. The objectives of the study were to 1) to determine if EBC could be collected in a rat model of pneumonia; 2) to show if the EBC contained TNFα and IL-6; 3) to see if the mediator concentration in the EBC correlated with the bronchoalveolar lavage (BAL); 4) to determine if an early inflammatory response in the lung was seen at different concentrations of enterotoxin. Methods 17 male rats were assigned to control group (n = 5) or to receive 250 (n = 4), 500 (n = 4), 1000 (n = 4) ng/kg of Staphylococcal enterotoxin b by endotracheal administration. The rats were allowed to recover and 4 hrs later, a tracheostomy was performed. The rats were ventilated using a small animal ventilator. This ventilator had a one way exhalation port which was connected to a long tube to collect the rats' exhaled breath. The tube was cooled with dry ice and the EBC was collected over 90 min. The rats were sacrificed after the EBC collection and BAL was performed on the excised lung. Both the EBC and the BAL were analyzed for TNF α and IL- 6 using ELISA kits. Results TNFα in the EBC correlated with the concentration in the BAL,(r= 0.49, p =0.021) (fig) The volume of EBC was 279 ± 54 ml for the control group and 288 ± 64 ml, 305 ± 67 ml, and 325 ± 70 ml for the rats receiving 250, 500 and 1000 ng Staphlococcal enterotoxin b respectively. To look for inflammation, the control group was compared to enterotoxin group regardless of dose received. BAL TNFα was different between control and enterotoxin groups (89 ± 44 vs. 223 ± 121 pg/ml, p <.04) but were similar in the EBC (3 ± 7 vs. 9 ± 9 pg/ml, p =0.2). IL-6 concentration was higher in the BAL of the enterotoxin groups compared to the control group (28 ± 4 vs. 190 ± 152 pg/ml ) but was similar in the EBC (1 ± 3 vs. 3 ± 7 pg/ml). Conclusions EBC can be collected in a rat model of pneumonia. Concentration of TNFα in the EBC correlated with the TNFα in the BAL. IL6 in the EBC did not correlate with the IL 6 in the BAL. More sensitive assays may detect lower concentrations of TNFα and IL-6 in the EBC. Different concentrations of the enterotoxin showed a similar inflammatory response in the first 4 hrs after the enterotoxin delivery.
    2011 American Academy of Pediatrics National Conference and Exhibition; 10/2011
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    ABSTRACT: Exhaled breath condensate (EBC) may contain mediators of acute lung injury. The objectives were to determine if EBC could be collected in a mechanically ventilated rat, to measure tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the EBC after staphylococcal enterotoxin B administration (SEB) and to find out if the concentrations of TNF-α and IL-6 correlated with those in lung lavage. Four hours after SEB instillation, rats were placed on mechanical ventilation and EBC was collected over 90 minutes. Lung lavage was collected and white cell count was determined. TNF-α and IL-6 were measured in the EBC and lavage. EBC was available in a sufficient quantity (250-400 μL) for the measurement of cytokines. The rats that received SEB had an inflammatory response when compared to control rats as shown by an increase in white cell count. TNF-α and IL-6 were detected in the EBC. Concentration of TNF-α correlated with that in the lavage (r = .497, P = .021), whereas IL-6 did not. EBC can be collected in rats in sufficient quantities to study acute lung injury. TNF-α and IL-6 can be measured in the EBC. Correlation between TNF-α in the EBC and lavage was demonstrated in this rat model of lung injury.
    Experimental Lung Research 10/2011; 37(9):563-7. DOI:10.3109/01902148.2011.611963 · 1.41 Impact Factor
  • Sabrina M Heidemann · Michael Fiore · Sandeep Sood · Steven Ham ·
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    ABSTRACT: To determine if eosinophils are activated to release the cationic proteins, eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) in shunt obstruction, and to find out if these proteins are associated with ventriculoperitoneal shunt failure. This was a prospective observational study carried out in a 20-bed tertiary pediatric intensive care unit. Patients studied were children aged 0-18 years with suspected ventriculoperitoneal shunt malfunction requiring shunt revision. No interventions were performed. Cerebrospinal fluid (CSF) was analyzed for cell count and EDN and ECP concentrations. Patients were prospectively followed for 6 months to evaluate shunt failure. In a 2-month period, 56 shunt revisions were performed on 56 children. Three children had culture-proven infection. Eosinophilia, defined as ≥ 5% eosinophils in the CSF, was present in 9 out of 53 children (17%). The 3 patients with infection did not have eosinophilia and were excluded from further analysis. Patients with CSF eosinophilia had higher concentrations of ECP (1.38 ± 0.66 vs. 0.41 ± 0.15 ng/ml; p = 0.013) and EDN (16.94 ± 5.83 vs. 4.69 ± 1.33 ng/ml; p = 0.011). Patients with CSF eosinophilia did not have more ventriculoperitoneal shunt revisions within 6 months (6 of 9) compared to those who did not have eosinophilia (21 of 44; p = 0.50). However, patients with higher levels of ECP in the CSF required more shunt revisions within 6 months of their surgeries (p < 0.05). In patients with malfunctioning ventriculoperitoneal shunts, CSF eosinophils are activated and release ECP and EDN. The presence of ECP is associated with a shorter shunt life.
    Pediatric Neurosurgery 12/2010; 46(4):255-8. DOI:10.1159/000320130 · 0.33 Impact Factor
  • Alexander R Santos · Sabrina M Heidemann · Henry L Walters · Ralph E Delius ·
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    ABSTRACT: To determine whether inhaled steroid administration after cardiopulmonary bypass will attenuate pulmonary inflammation and improve lung compliance and oxygenation. Randomized, prospective, double-blind, placebo-controlled clinical trial. Children's Hospital of Michigan, intensive care unit. Thirty-two children <2 yrs of age with congenital heart disease requiring cardiopulmonary bypass. Participants were randomly assigned to one of two groups. Group 1 (n = 16) received an inhaled steroid, Budesonide (0.25 mg/2 mL), and group 2 (n = 16) received an inhaled placebo (2 mL of inhaled 0.9% saline). The nebulizations were given at the end of cardiopulmonary bypass, 6 hrs after cardiopulmonary bypass, and 12 hrs after cardiopulmonary bypass. Two hours after each nebulization, bronchoalveolar lavage for interleukin-6 and interleukin-8 was collected. The concentrations of interleukin-6 and interleukin-8 in the bronchoalveolar lavage increased in both groups after cardiopulmonary bypass. Interleukin-6 peaked 2 hrs after cardiopulmonary bypass and was decreasing by 14 hrs after cardiopulmonary bypass. However, administration of corticosteroid did not affect the production of interleukin-6 when compared with the placebo group (378 +/- 728 vs. 287 +/- 583 pg/mL pre-cardiopulmonary bypass, 1662 +/- 1410 vs. 1584 +/- 1645 pg/mL at the end of cardiopulmonary bypass, 2601 +/- 3132 vs. 3677 +/- 4935 pg/mL 2 hrs after cardiopulmonary bypass, and 1792 +/- 3100 vs. 1283 +/- 1344 pg/mL 14 hrs after cardiopulmonary bypass; p > .05). Likewise, interleukin-8 in the lavage fluid was similar in both the placebo and steroid groups at all time points (570 +/- 764 vs. 990 +/- 1147 pg/mL pre-cardiopulmonary bypass, 1647 +/- 1232 vs. 1394 +/- 1079 pg/mL at the end of cardiopulmonary bypass, 1581 +/- 802 vs. 1523 +/- 852 pg/mL 2 hrs after cardiopulmonary bypass, and 1652 +/- 1069 pg/mL vs. 1808 +/- 281 pg/mL 14 hrs after cardiopulmonary bypass; p > .05). Lung compliance and oxygenation were similar in both groups. Cardiopulmonary bypass is associated with a pulmonary inflammatory response. Inhaled corticosteroid did not affect the pulmonary inflammatory response as measured by interleukin-6 and interleukin-8 concentrations in the lung lavage after cardiopulmonary bypass. Pulmonary mechanics and oxygenation were not improved by the use of inhaled corticosteroid.
    Pediatric Critical Care Medicine 09/2007; 8(5):465-9. DOI:10.1097/01.PCC.0000282169.11809.80 · 2.34 Impact Factor
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    Sabrina M Heidemann · Maria Glibetic ·
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    ABSTRACT: Neutrophil infiltration commonly occurs in acute lung injury and may be partly responsible for the inflammatory response. However, acute lung injury still occurs in the neutropenic host. The objectives of this study are to determine if inflammation and acute lung injury are worse in neutropenic versus the normal host after endotoxemia. Rats were divided into four groups: 1) control, 2) neutropenic, 3) endotoxemic and 4) endotoxemic and neutropenic. Tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP-2) were measured in the blood, lung lavage and for mRNA in the lung. Arterial blood gases were measured to determine the alveolar-arterial oxygen gradient which reflects on lung injury. In endotoxemia, the neutropenic rats had lower plasma TNF-alpha (116 +/- 73 vs. 202 +/- 31 pg/ml) and higher plasma MIP-2 (26.8 + 11.9 vs. 15.6 + 6.9 ng/ml) when compared to non-neutropenic rats. The endotoxemic, neutropenic rats had worse lung injury than the endotoxemic, non-neutropenic rats as shown by increase in the alveolar-arterial oxygen gradient (24 +/- 5 vs. 12 +/- 9 torr). However, lavage concentrations of TNF-alpha and MIP-2 were similar in both groups. Neutrophils may regulate TNF-alpha and MIP-2 production in endotoxemia. The elevation in plasma MIP-2 in the endotoxemic, neutropenic rat may be secondary to the lack of a neutrophil response to inhibit production or release of MIP-2. In endotoxemia, the severe lung injury observed in neutropenic rats does not depend on TNF-alpha or MIP-2 produced in the lung.
    Journal of Inflammation 03/2007; 4:7. DOI:10.1186/1476-9255-4-7 · 2.02 Impact Factor
  • Swati Garekar · Sabrina M Heidemann · Maria Glibetic ·
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    ABSTRACT: Pretreatment with heat confers cardiopulmonary protection in endotoxemic animals. This mechanism may be through suppression of pro-inflammatory mediator production. The objectives of this study were to determine the effect of heat stress on tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 (MIP-2) in a lipopolysaccharide-exposed macrophage cell line and to study the relationship between TNF-alpha and MIP-2 production. Heat pretreatment resulted in decreased TNF-alpha transcription and translation by lipopolysaccharide-exposed macrophages; and increased MIP-2 concentration without additional effect in transcription. Administration of TNF-alpha antibody prior to exposure to lipopolysaccharide resulted in increased MIP-2 concentration suggesting that TNF-alpha acts to down-regulate MIP-2 production. The mechanism by which heat stress causes an increase in MIP-2 concentration may be secondary to its suppressing effect on TNF-alpha production.
    Journal of Endotoxin Research 02/2006; 12(2):87-92. DOI:10.1179/096805106X89071 · 3.06 Impact Factor
  • Sabrina M Heidemann · Maria Glibetic ·
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    ABSTRACT: The objective of this study is to determine if heat stress prior to endotoxemia diminishes cardiopulmonary dysfunction by attenuating the cytokine inflammatory response. Rats were assigned to either: 1) neutropenia; 2) heat; 3) neutropenia, LPS; or 4) heat, neutropenia, LPS. Heart rate, blood gases, and blood, lung lavage, and lung mRNA for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and macrophage inflammatory protein (MIP)-2 were measured. Heat given before LPS resulted in a similar A-a O(2) gradient as the heat-alone and neutropenic groups (8 +/- 8 versus 8 +/- 7 versus 4 +/- 3 mm Hg) and a lower A-a O(2) gradient when compared to the neutropenic, LPS rats (8 +/- 8 versus 22 +/- 8 mm Hg, p < 0.003). Blood, lung lavage, and lung mRNA for TNF-alpha, IL-1beta, and MIP-2 were similar in the LPS rats regardless of heat. Heart rate was similar in both LPS groups but higher than non-LPS groups. Heat pretreatment attenuates lung injury in the neutropenic, endotoxemic rat but not by decreasing TNF-alpha, IL-1beta, or MIP-2 in the lung. Heat prior to LPS did not prevent cardiac dysfunction in neutropenic rats.
    Inflammation 03/2005; 29(1):47-53. DOI:10.1007/s10753-006-8969-4 · 2.21 Impact Factor
  • Jagadish Urs · Sabrina M Heidemann ·
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    ABSTRACT: An exaggerated pro-inflammatory response in endotoxemia may lead to multiple organ damage including acute lung injury. Heat stress prior to endotoxemia results in attenuation of inflammation possibly by decreasing cytokine production. Monocyte chemoattractant protein (MCP)-1, a pro-inflammatory cytokine, is responsible for monocyte recruitment into the lung in acute lung injury. The objective of this study is to determine if pretreatment with heat results in decreased MCP-1 production in the lungs of endotoxemic rats at a transcriptional or post-transcriptional level. Rats were assigned to one of four groups: control, heat alone, heat with or without endotoxin. Rats were made endotoxemic by injection of Escherichia coli lipopolysaccharide. MCP-1 was measured in lavage fluid and MCP-1 mRNA in the lung tissue. Endotoxemia resulted in production of MCP-1. Control and heat alone rats had 21+/-4 vs. 20+/-3 pg/ml, p=0.75. MCP-1 concentration was decreased in the lavage fluid of pre-heated when compared to non-heated endotoxemic rats (37+/-28 vs. 70+/-35 pg/ml, p <0.02 ). However, the MCP-1 mRNA was higher in the heated compared to non-heated endotoxemic rats (1.59+/-0.35 vs. 0.74+/-0.51, MCP-1/beta-actin mRNA, p <0.01). Control and heat alone rats had undetectable mRNA MCP-1 in the lungs. Heat stress prior to endotoxemia results in decreased production of MCP-1 by a post-transcriptional mechanism.
    Cytokine 06/2004; 26(6):243-6. DOI:10.1016/j.cyto.2004.02.008 · 2.66 Impact Factor
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    ABSTRACT: The optimum strategy for mechanical ventilation in a child with status asthmaticus is not established. Volume-controlled ventilation continues to be the traditional approach in such children. Pressure-controlled ventilation may be theoretically more advantageous in allowing for more uniform ventilation. We describe our experience with pressure-controlled ventilation in children with severe respiratory failure from status asthmaticus. Retrospective review. Pediatric intensive care unit in a university-affiliated children's hospital. All patients who received mechanical ventilation for status asthmaticus. Pressure-controlled ventilation was used as the initial ventilatory strategy. The optimum pressure control, rate, and inspiratory and expiratory time were determined based on blood gas values, flow waveform, and exhaled tidal volume. Forty patients were admitted for 51 episodes of severe status asthmaticus requiring mechanical ventilation. Before the institution of pressure-controlled ventilation, median pH and Pco(2) were 7.21 (range, 6.65-7.39) and 65 torr (29-264 torr), respectively. Four hours after pressure-controlled ventilation, median pH increased to 7.31 (6.98-7.45, p <.005), and Pco(2) decreased to 41 torr (21-118 torr, p <.005). For patients with respiratory acidosis (Pco(2) >45 torr) within 1 hr of starting pressure-controlled ventilation, the median length of time until Pco(2) decreased to <45 torr was 5 hrs (1-51 hrs). Oxygen saturation was maintained >95% in all patients. Two patients had pneumomediastinum before pressure-controlled ventilation. One patient each developed pneumothorax and subcutaneous emphysema after initiation of pressure-controlled ventilation. All patients survived without any neurologic morbidity. Median duration of mechanical ventilation was 29 hrs (4-107 hrs), intensive care stay was 56 hrs (17-183 hrs), and hospitalization was 5 days (2-20 days). Based on this retrospective study, we suggest that pressure-controlled ventilation is an effective ventilatory strategy in severe status asthmaticus in children. Pressure-controlled ventilation represents a therapeutic option in the management of such children.
    Pediatric Critical Care Medicine 03/2004; 5(2):133-8. DOI:10.1097/01.PCC.0000112374.68746.E8 · 2.34 Impact Factor
  • K M Daphtary · S M Heidemann · M Glibetic ·
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    ABSTRACT: The objective of our study was to determine the role of ibuprofen in protecting neutropenic rats from cardiopulmonary injury due to endotoxemia. We hypothesized that ibuprofen would offer pulmonary protection by altering cytokine production. Neutropenic rats received E. coli lipopolysaccharide (LPS) alone or ibuprofen and LPS. After 4 h, arterial blood gases, heart rate and blood pressure were measured. Blood and bronchoalveolar lavage fluid (BALF) were collected for TNF- alpha and MIP-2 concentrations. Lung tissue for iNOS mRNA and myeloperoxidase were obtained. The ibuprofen group had decreased heart rate and better oxygenation. Ibuprofen suppressed TNF- alpha and MIP-2 production in blood and MIP-2 concentrations in BALF. Lung mRNA for iNOS was higher in the ibuprofen group. Neutrophil infiltration in the lung was similar in both groups. Ibuprofen attenuated cardiopulmonary dysfunction by decreasing the early cytokine response. The balance of vasodilator to vasoconstrictor production in the lung may favor vasodilation as shown by increased iNOS mRNA and suppression of thromboxane.
    Prostaglandins Leukotrienes and Essential Fatty Acids 09/2001; 65(2):59-65. DOI:10.1054/plef.2001.0289 · 2.35 Impact Factor
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    ABSTRACT: The use of high-frequency oscillatory ventilation (HFOV) has increased dramatically in the management of respiratory failure in pediatric patients. We surveyed ten pediatric centers that frequently use high-frequency oscillation to describe current clinical practice and to examine factors related to improved outcomes. Retrospective, observational questionnaire study. Ten tertiary care pediatric intensive care units. Two hundred ninety patients managed with HFOV between January 1997 and June 1998. None. Patients were classified according to presence or absence of preexisting lung disease, symptomatic respiratory syncytial virus infection, or presence of cyanotic heart disease or residual right-to-left intracardiac shunt. In addition, patients for whom HFOV acutely failed were analyzed separately. Those patients with preexisting lung disease were significantly smaller, had a significantly higher incidence of pulmonary infection as the triggering etiology, and had a significantly greater duration of conventional ventilation before institution of HFOV compared with patients without preexisting lung disease. Stepwise logistic regression was used to predict mortality and the occurrence of chronic lung disease in survivors. In patients without preexisting lung disease, the model predicted a 70% probability of death when the oxygenation index (OI) after 24 hrs was 28 in the immunocompromised patients and 64 in the patients without immunocompromise. In the immunocompromised patients, the model predicted a 90% probability of death when the OI after 24 hrs was 58. In survivors without preexisting lung disease, the model predicted a 70% probability of developing chronic lung disease when the OI at 24 hrs was 31 in the patients with sepsis syndrome and 50 in the patients without sepsis syndrome. In the patients with sepsis syndrome, the model predicted a 90% probability of developing chronic lung disease when the OI at 24 hrs was 45. Given the number of centers involved and the size of the database, we feel that our results broadly reflect current practice in the use of HFOV in pediatric patients. These results may help in deciding which patients are most likely to benefit from aggressive intervention by using extracorporeal techniques and may help identify high-risk populations appropriate for prospective study of innovative modes of supporting gas exchange (e.g., partial liquid breathing or intratracheal pulmonary ventilation).
    Critical Care Medicine 01/2001; 28(12):3913-9. DOI:10.1097/00003246-200012000-00031 · 6.31 Impact Factor
  • Sabrina M. Heidemann · Lesley Lomo · John P. Ofenstein · Ashok P. Sarnaik ·
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    ABSTRACT: To determine whether heat stress protects the endotoxemic rat by up-regulation of the counterinflammatory cytokine interleukin (IL)-10, thereby attenuating the inflammatory response. A total of 16 rats were assigned to either the heat stress group (n = 8) or the control group (n = 8). The heat stress group was warmed to a temperature of >42 degrees C (107.6 degrees F) rectally for 10-15 mins; 20 hrs later, all rats were intubated, paralyzed, and ventilated. After jugular venous and arterial catheterization, endotoxin was given intravenously. Arterial blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necrosis factor (TNF)-alpha, nitric oxide metabolites (NO), IL-10, and macrophage inflammatory protein (MIP)-2. The alveolar macrophages were removed, counted, and then incubated for 24 hrs. The supernatant was analyzed for TNF-alpha, NO, IL-10, and MIP-2. University research laboratory. Male Sprague-Dawley rats (n = 16). Administration of heat before endotoxin infusion. Alveolar-arterial oxygen gradient was lower in the heat stress group at 4 and 5 hrs after endotoxemia. Plasma and alveolar macrophage supernatant concentrations of TNF-alpha, NO, and IL-10 were not affected by heat. Plasma and alveolar macrophage supernatant MIP-2 concentrations were higher in endotoxemic rats receiving heat pretreatment compared with controls. Our study demonstrates that heat leads to pulmonary protection of short duration in severe endotoxemia. This protection was not mediated by plasma TNF-alpha, IL-10, or NO. Contrary to our hypothesis, pretreatment with heat increased rather than decreased the plasma MIP-2 concentration and alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveolar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 production by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased MIP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.
    Critical Care Medicine 06/2000; 28(5):1465-8. DOI:10.1097/00003246-200005000-00035 · 6.31 Impact Factor
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    Girish G Deshpande · Sabrina M Heidemann · Ashok P Sarnaik ·
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    ABSTRACT: Elevated plasma lactate has been shown to correlate with mortality in patients with septic shock. Heat stress prior to sepsis has resulted in reduction in acute lung injury and mortality. We investigated whether heat stress resulted in decreased plasma lactate concentration and protected the lung by decreasing the inflammatory response to sepsis. Plasma lactate concentration was elevated in septic rats without prior heat stress. Lactic acid levels were significantly lower in heat-treated septic rats (P < 0.05) and were not significantly different when compared with control rats. Septic rats with or without heat pretreatment had significantly higher myeloperoxidase activity in the lung than did control groups. Heat pretreatment did not prevent neutrophil infiltration or inflammatory mediator production in the lung. Prior heat stress ameliorates lactic acidemia in rat sepsis. Heat stress did not attenuate the pulmonary inflammatory process. The mechanism of heat-induced protection from lactic acidemia in sepsis needs to be further explored.
    Critical Care 02/2000; 4(1):45-9. DOI:10.1186/cc649 · 4.48 Impact Factor
  • J P Ofenstein · SM Heidemann · A Juett-Wilstermann · AP Sarnaik ·
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    ABSTRACT: Pretreatment with heat decreases mortality and acute lung injury in the rat septic shock model, presumably by the production of heat shock proteins (HSP). However, endotoxin, a severe cell stresser, has not been shown to induce HSP 70. We investigated the effects of severe endotoxemia on the expression of specific protective stress proteins, including HSP 72 (inducible HSP 70), HSP 32 (heme oxygenase-1), and HSP 90. Fifteen rats received intravenously either 3 mg/kg of endotoxin (E. coli O127:B8 lipopolysaccharide, LPS) (n=9) or saline (n=6). Two hr later the spleen was removed and splenocytes were separated into three groups and analyzed for specific HSP by Western blot. In Group 1, both endotoxin-treated and saline-treated splenocytes were incubated for 3 hr at 37 degrees C. In Group 2, the splenocytes were washed twice, then heat shocked for 30 min at 42 degrees C and subsequently incubated for 2.5 hr at 37 degrees C. In Group 3, splenocytes were washed twice, then incubated for 3.0 hr at 37 degrees C. HSP 90 & HSP 70c (constitutive) were present in all groups. Consistent with observations by others, HSP 72 was not induced in Group 1. HSP 72 was induced in both the saline-treated and endotoxin-treated splenocytes after heating (Group 2). However, in the absence of heat stress, HSP 72 was present in endotoxin-treated but not in saline-treated splenocytes after incubation (Group 3). Conversely, HSP 32, while present in Group 1 splenocytes, was not detected in the endotoxin-treated splenocytes of Group 2 and Group 3, but was present in the saline-treated cells. In conclusion, endotoxemic shock results in induction of HSP 72 and depletion of HSP 32, but only after the cells have been washed and further incubated.
    Annals of clinical and laboratory science 02/2000; 30(1):92-8. · 0.91 Impact Factor
  • Ashok P. Sarnaik · Sabrina M. Heidemann ·

    Critical Care Medicine 10/1999; 27(9):2069-70. DOI:10.1097/00003246-199909000-00081 · 6.31 Impact Factor
  • S M Heidemann · J P Ofenstein · A.P. Sarnaik ·
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    ABSTRACT: Ibuprofen, a cyclooxygenase inhibitor, improves pulmonary and cardiovascular injury in endotoxemia. We studied the mechanism of the beneficial effects of ibuprofen in relation to production of inflammatory mediators which influence vascular tone in endotoxemia. Rats were randomly assigned to one of three groups: (1) control, (2) endotoxemia alone; and (3) ibuprofen pretreatment and endotoxemia. Plasma and lung lavage concentrations of tumor necrosis factor, thromboxane B2 (TXB2), leukotriene (LT) C4,D4,E4 and nitric oxide (NO) were determined over a 2 h period. Pretreatment with ibuprofen resulted in increased survival, and attenuation of pulmonary and cardiovascular dysfunction when compared to the rats receiving endotoxin alone. The marked elevation in plasma TXB2 concentration in endotoxemic rats was prevented by pretreatment with ibuprofen. Similarly, pretreatment with ibuprofen prevented the decrease in lung lavage NO levels in endotoxemic rats. The improved survival and cardiopulmonary protection in endotoxemic rats pretreated with ibuprofen appears to be related to decreased thromboxane production and preservation of endothelial production of nitric oxide.
    Prostaglandins Leukotrienes and Essential Fatty Acids 04/1999; 60(3):181-5. DOI:10.1054/plef.1999.0023 · 2.35 Impact Factor
  • Amit P Sarnaik · Sabrina M Heidemann · Ashok P Sarnaik ·

    Pediatric Research 04/1999; 45(4, Part 2 of 2). DOI:10.1203/00006450-199904020-00273 · 2.31 Impact Factor
  • Sabrina M. Heidemann · Swati Garekar · Ashok P. Sarnaik ·

    Pediatric Research 04/1999; 27(4). DOI:10.1097/00003246-199901001-00351 · 2.31 Impact Factor
  • Girish Deshpande · Sabrina M Heidemann · Ashok P Sarnaik ·

    Pediatric Research 04/1999; 45(4). DOI:10.1203/00006450-199904020-00231 · 2.31 Impact Factor