Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where John D. Lang is active.

Publication


Featured researches published by John D. Lang.


Anesthesiology | 1996

Magnetic resonance imaging of the upper airway. Effects of propofol anesthesia and nasal continuous positive airway pressure in humans.

Mali Mathru; Oliver Esch; John D. Lang; Michael E. Herbert; Gregory Chaljub; Brian Goodacre; Eric vanSonnenberg

Background Anesthetic agents inhibit the respiratory activity of upper airway muscles more than the diaphragm, creating a potential for narrowing or complete closure of the pharyngeal airway during anesthesia. Because the underlying mechanisms leading to airway obstruction in sleep apnea and during anesthesia are similar, it was hypothesized that anesthesia-induced pharyngeal narrowing could be counteracted by applying nasal continuous positive airway pressure (CPAP). Methods Anesthesia was induced in ten healthy volunteers (aged 25-34 yr) by intravenous administration of propofol in 50-mg increments every 30-s to a maximum of 300 mg. Magnetic resonance images of the upper airway (slice thickness of 5 mm or less) were obtained in the awake state, during propofol anesthesia, and during administration of propofol plus 10 cm nasal CPAP. Results Minimum anteroposterior diameter of the pharynx at the level of the soft palate decreased from 6.6+/-2.2 mm (SD) in the awake state to 2.7+/-1.5 mm (P < 0.05) during propofol anesthesia and increased to 8.43+/-2.5 mm (P < 0.05) after nasal CPAP application. Anteroposterior diameter of the pharynx at the level of the dorsum of the tongue increased from 7.9+/-3.5 mm during propofol anesthesia to 12.9+/-3.6 mm (P < 0.05) after nasal CPAP. Pharyngeal volume (from the tip of the epiglottis to the tip of the soft palate, assuming this space to be a truncated cone) significantly increased from 2,437+/-1,008 mm3 during propofol anesthesia to 5,847+/-2,827 mm3 (P < 0.05) after nasal CPAP application. Conclusions In contrast to the traditional view that relaxation of the tongue causes airway obstruction, this study suggests that airway closure occurs at the level of the soft palate. Application of nasal CPAP can counteract an anesthesia-induced pharyngeal narrowing by functioning as a pneumatic splint. This is supported by the observed reduction in anteroposterior diameter at the level of the soft palate during propofol anesthesia and the subsequent increase in this measurement during nasal CPAP application.


Journal of Trauma-injury Infection and Critical Care | 1997

Therapy of Patients with Head Injuries: Key Parameters for Management

Donald S. Prough; John D. Lang

BACKGROUNDnSecondary brain injury, presumed secondary to ischemia, increases the mortality and morbidity of traumatic brain injury. Although many mechanisms appear to be involved, many potential ischemic insults results from changes in readily observable physiologic variables.nnnMETHODSnA focused search of scientific articles published in English to determine what data are available to suggest parameters within which key physiologic variables should be maintained.nnnRESULTSnFew data demonstrate that maintenance of variables within specific ranges alters outcome; however, considerable evidence establishes association with poor outcome and hypotension, intracranial hypertension, and cerebral venous saturation. Key parameters vary somewhat based upon the phase of treatment after injury. Other variables, such as systemic oxygen delivery and brain saturation measured by near-infrared spectroscopy, are less well linked to outcome.nnnCONCLUSIONSnFurther research is necessary to establish that manipulation of physiologic variables to maintain them within preset ranges improves outcome.


Journal of Transplantation | 2012

The Hepatoprotective Effect of Sodium Nitrite on Cold Ischemia-Reperfusion Injury

Wei Li; Zihui Meng; Yuliang Liu; Rakesh P. Patel; John D. Lang

Liver ischemia-reperfusion injury is a major cause of primary graft non-function or initial function failure post-transplantation. In this study, we examined the effects of sodium nitrite supplementation on liver IRI in either Lactated Ringers (LR) solution or University of Wisconsin (UW) solution. The syngeneic recipients of liver grafts were also treated with or without nitrite by intra-peritoneal injection. Liver AST and LDH release were significantly reduced in both nitrite-supplemented LR and UW preservation solutions compared to their controls. The protective effect of nitrite was more efficacious with longer cold preservation times. Liver histological examination demonstrated better preserved morphology and architecture with nitrite treatment. Hepatocellular apoptosis was significantly reduced in the nitrite-treated livers compared their controls. Moreover, liver grafts with extended cold preservation time of 12 to 24 hours demonstrated improved liver tissue histology and function post-reperfusion with either the nitrite-supplemented preservation solution or in nitrite-treated recipients. Interestingly, combined treatment of both the liver graft and recipient did not confer protection. Thus, nitrite treatment affords significant protection from cold ischemic and reperfusion injury to donor livers and improves liver graft acute function post-transplantation. The results from this study further support the potential for nitrite therapy to mitigate ischemia-reperfusion injury in solid organ transplantation.


Clinical and Experimental Immunology | 2005

One-hit, two-hit . . . is there really any benefit?

John D. Lang; Judy M. Hickman-Davis

Lung injury resulting from the systemic inflammatory response syndrome (SIRS), be it infectious (sepsis) or not, remains a significant contributor to patient morbidity and mortality worldwide [1]. While the mortality from acute respiratory distress syndrome (ARDS) has decreased to between 30 and 40%, approximately 20% will die of refractory hypoxaemia and the rest from the multiple organ dysfunction syndrome (MODS) [2]. Thus, with the prevalence of lung injury remaining substantial and the acquisition of lung injury not being inconsequential, investigators continue to search for mechanisms, management strategies and therapeutic treatments that will benefit those patients in need.


Journal of Critical Care | 1999

A novel approach to monitor tissue perfusion: Bladder mucosal Pco2, Po2, and pHi during ischemia and reperfusion☆

John D. Lang; David J. Evans; Luiz Poli deFigueiredo; Steve Hays; Mali Mathru; George C. Kramer

PURPOSEnThe purpose of this study is to determine if monitoring urinary bladder PCO2, PO2, and calculated intramucosal pH would be a reliable index of tissue perfusion.nnnMATERIALS AND METHODSnThis nonrandomized controlled study was conducted in a laboratory at a university medical center. Eight immature female Yorkshire pigs were studied with T-9 aortic cross-clamping for 30 minutes followed by a 60-minute period of reperfusion. Cystotomy was performed for placement of a Foley catheter and Paratrend 7 O2/CO2 sensor.nnnRESULTSnBaseline hemodynamic and metabolic measurements were obtained along with measurements of bladder mucosal PO2 and PCO2 (mean+/-SEM). Blood flow measured with microspheres confirmed absence of blood flow during occlusion and hyperemia during reperfusion. Bladder mucosal PO2 decreased from 42+/-14.0 mm Hg (5.6 kPa) to 1.3+/-1.3 mm Hg (1.4 kPa) during the 30-minute interval of ischemia. This was followed by an increase of bladder PO2 to greater than baseline values at the end of the reperfusion period. Bladder mucosal Pco2 increased from 57+/-4.7 mm Hg (7.6 kPa) to 117+/-7.1 mm Hg (15.6 kPa) (P < .05) during ischemia. During reperfusion the Pco2 returned to baseline levels (55+/-4.0 mm Hg [7.3 kPa]). Calculated bladder mucosal pHi declined from 7.31+/-0.04 to 7.08+/-0.05 (P < .05) during the ischemic period and after reperfusion pHi was 7.17+/-0.03.nnnCONCLUSIONSnMonitoring urinary bladder PO2, PCO2, or calculating pHi may provide a simple and reliable means of monitoring tissue perfusion.


Archive | 1997

Update on Neurologic Intensive Care Medicine

John D. Lang; Donald S. Prough

Neurologic intensive care has advanced substantially over the past several decades. Improvements in monitoring of cerebral vascular function and neurologic function have permitted early recognition of important physiologic abnormalities. Improved understanding of the pathophysiology of various acute neurologic insults has prompted more precise pharmacologic and physiologic interventions. The present review will discuss current medical management of increased intracranial pressure (ICP), management of patients with subarachnoid hemorrhage (SAH), and management of acute stroke. The first two categories of insults often are associated with surgical procedures. Although acute stroke rarely is managed surgically, insights into current management of stroke may provide insights into management of patients at risk for cerebral ischemia.


Blood | 2006

Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation

Jack H. Crawford; T. Scott Isbell; Zhi Huang; Sruti Shiva; Balu K. Chacko; Alan N. Schechter; Victor M. Darley-Usmar; Jeffrey D. Kerby; John D. Lang; David W. Kraus; Chien Ho; Mark T. Gladwin; Rakesh P. Patel


Chest | 2002

Oxidant-Antioxidant Balance in Acute Lung Injury

John D. Lang; Philip McArdle; Philip O'Reilly; Sadis Matalon


American Journal of Respiratory and Critical Care Medicine | 2005

Hypercapnia via Reduced Rate and Tidal Volume Contributes to Lipopolysaccharide-induced Lung Injury

John D. Lang; Mario Figueroa; K.David Sanders; Mutay Aslan; Yuliang Liu; Phillip Chumley; Bruce A. Freeman


American Journal of Physiology-lung Cellular and Molecular Physiology | 2000

Hypercapnia induces injury to alveolar epithelial cells via a nitric oxide-dependent pathway

John D. Lang; Phillip Chumley; Jason P. Eiserich; Alvaro G. Estévez; Thad Bamberg; Ahmad Adhami; John P. Crow; Bruce A. Freeman

Collaboration


Dive into the John D. Lang's collaboration.

Top Co-Authors

Avatar

Rakesh P. Patel

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

Donald S. Prough

University of Texas Medical Branch

View shared research outputs
Top Co-Authors

Avatar

Jack H. Crawford

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

Yuliang Liu

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

Balu K. Chacko

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

Phillip Chumley

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

T. Scott Isbell

University of Alabama at Birmingham

View shared research outputs
Top Co-Authors

Avatar

Alan N. Schechter

National Institutes of Health

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

David W. Kraus

University of Alabama at Birmingham

View shared research outputs
Researchain Logo
Decentralizing Knowledge