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Biomedical subjects

Peter Rosenberger

Publications and source records attributed to Peter Rosenberger.

18 recordsLinked to original sources
PubMed2006

Endothelial catabolism of extracellular adenosine during hypoxia: the role of surface adenosine deaminase and CD26.

Extracellular levels of adenosine increase during hypoxia. While acute increases in adenosine are important to counterbalance excessive inflammation or vascular leakage, chronically elevated adenosine levels may be toxic. Thus, we reasoned that clearance mechanisms might exist to offset deleterious influences of chronically elevated adenosine. Guided by microarray results revealing induction of endothelial adenosine deaminase (ADA) mRNA in hypoxia, we used in vitro and in vivo models of adenosine signaling, confirming induction of ADA protein and activity. Further studies in human endothelia revealed that ADA-complexing protein CD26 is coordinately induced by hypoxia, effectively localizing ADA activity at the endothelial cell surface. Moreover, ADA surface binding was effectively blocked with glycoprotein 120 (gp120) treatment, a protein known to specifically compete for ADA-CD26 binding. Functional studies of murine hypoxia revealed inhibition of ADA with deoxycoformycin (dCF) enhances protective responses mediated by adenosine (vascular leak and neutrophil accumulation). Analysis of plasma ADA activity in pediatric patients with chronic hypoxia undergoing cardiac surgery demonstrated a 4.1 +/- 0.6-fold increase in plasma ADA activity compared with controls. Taken together, these results reveal induction of ADA as innate metabolic adaptation to chronically elevated adenosine levels during hypoxia. In contrast, during acute hypoxia associated with vascular leakage and excessive inflammation, ADA inhibition may serve as therapeutic strategy.

Adenosine Deaminase↗
PubMed2006

Effect of hydroxyethyl starch on vascular leak syndrome and neutrophil accumulation during hypoxia.

OBJECTIVE: Several studies have suggested that intravenous hydroxyethyl starch treatment may dampen acute inflammatory responses. It is well documented that limited oxygen delivery to tissues (hypoxia) is common in acute inflammation, and numerous parallels exist between acute responses to hypoxia and to inflammation, including the observation that both are associated with increased vascular leakage and neutrophil infiltration of tissues. Therefore, we compared functional influences of hydroxyethyl starch on normoxic or posthypoxic endothelia. DESIGN: Laboratory study. SETTING: University hospital. SUBJECTS: Cultured human microvascular endothelial cells and mice (C57BL/6/129 svj). INTERVENTIONS: We measured functional influences of hydroxyethyl starch on normoxic or posthypoxic endothelia. MEASUREMENTS AND MAIN RESULTS: Studies to assess endothelial barrier function in vitro indicated that the addition of hydroxyethyl starch promotes endothelial barrier in a dose-dependent fashion and hydroxyethyl starch-barrier effects are increased following endothelial hypoxia exposure (human microvascular endothelial cells, 48 hrs, 2% oxygen). Treatment of human microvascular endothelial cells with hydroxyethyl starch resulted in a dose-dependent increase in 157-phosphorylated vasodilator-stimulated phosphoprotein, a protein responsible for controlling the geometry of actin-filaments. Neutrophil adhesion was decreased in the presence of physiologically relevant concentrations of hydroxyethyl starch in vitro, particularly after endothelial hypoxia exposure. Using a murine model of normobaric hypoxia, increases in vascular leakage and pulmonary edema associated with hypoxia exposure (4 hrs at 8% oxygen) were decreased in animals treated with intravenous hydroxyethyl starch. Increases of tissue neutrophil accumulation following hypoxia exposure were dampened in hydroxyethyl starch-treated mice. CONCLUSIONS: Taken together, these results indicate that hypoxia-induced increases in vascular leakage and acute inflammation are attenuated by hydroxyethyl starch treatment.

Acute Disease↗
PubMed2006

Acute hemodynamic collapse after induction of general anesthesia for emergent pulmonary embolectomy.

Patients undergoing pulmonary embolectomy often experience hemodynamic deterioration during induction of general anesthesia (GA). Therefore, we studied the incidence and possible risk factors for hemodynamic deterioration during GA induction. Fifty-two consecutive patients undergoing emergent pulmonary embolectomy at our institution were included. Hemodynamic collapse after GA induction was defined as hypotension refractory to vasopressor, inotrope, or fluid administration, requiring cardiopulmonary resuscitation followed by urgent institution of cardiopulmonary bypass (CPB). Demographic variables, comorbidities, specific location of thromboemboli, preoperative inotropic support, and anesthetic drugs used for GA induction were evaluated as possible risk factors. After GA induction, hemodynamic collapse occurred in 19% of patients (n = 10). However, the occurrence of hemodynamic instability was not predicted by any of the evaluated risk factors. In addition, the incidence of in-hospital mortality did not differ between hemodynamically stable or unstable patients (10%; 4 of 42 versus 10%; 1 of 10 patients, respectively). In conclusion, hemodynamic deterioration after GA induction develops frequently during emergent pulmonary embolectomy. On the basis of our experience from this study and the unpredictable nature of hemodynamic deterioration, we suggest that patients undergoing pulmonary embolectomy should be prepared and draped before GA induction, and a cardiac surgical team should immediately be available for emergent institution of cardiopulmonary bypass.

Acute Disease↗
PubMed2006

The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery.

According to guidelines established by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists, life-threatening hemodynamic disturbances are classified as a category I indication for the intraoperative use of transesophageal echocardiography (TEE). However, the usefulness of TEE during intraoperative cardiac arrest and its impact on patient management have not been rigorously investigated. Using our departmental TEE database, we identified a population of 22 patients who underwent noncardiac surgical procedures and experienced unexpected intraoperative hemodynamic collapse requiring the initiation of Advanced Cardiac Life Support procedures between the time of induction of general anesthesia and the termination of the surgical procedure. Results of TEE examinations, patient records, detailed operative records, and outcome of patients were reviewed for the utility of TEE to diagnose the etiology of the hemodynamic collapse. Furthermore, the impact on subsequent patient management was evaluated. A primary suspected diagnosis of the underlying pathological process was established in 19 of 22 patients with TEE, including 9 with thromboembolic events, 6 with acute myocardial ischemia, 2 with hypovolemia, and 2 patients with pericardial tamponade. A definitive diagnosis could not be made in 3 patients with TEE. In 18 patients, TEE guided specific management beyond implementation of Advanced Cardiac Life Support protocols, including the addition of surgical procedures in 12 patients. Fourteen patients survived to leave the operating room, and 7 of these patients were eventually discharged from the hospital. Thus, TEE may provide additional diagnostic information in patients with intraoperative cardiac arrest and may directly guide specific, potentially life-saving therapy.

Adult↗
PubMed2005

Role of transesophageal echocardiography in patients with suspected aortic dissection.

Patients with acute aortic dissection of the ascending aorta benefit from rapid surgical intervention. We report a patient with suspected acute aortic dissection based on history and transthoracic echocardiography findings. This patient was taken to the operating room without further workup, where transesophageal echocardiography (TEE) revealed acute myocardial infarction and mitral regurgitation due to papillary muscle rupture. The patient underwent coronary bypass grafting and mitral valve replacement. This case demonstrates that intraoperative TEE can be used as a primary diagnostic modality to rule out aortic dissection, and can provide a definitive etiology for cardiogenic shock before a planned surgical intervention.

Aged↗
PubMed2005

Chest tube suction-associated unilateral negative pressure pulmonary edema in a lung transplant patient.

We describe a 29-yr-old male, status post-bilateral lung transplant, who developed unilateral negative pressure pulmonary edema induced by chest tube suction in association with bilateral bronchial anastomotic strictures. We conclude that negative pressure pulmonary edema may occur secondary to high levels of negative pressure applied to the intrapleural space via chest tubes in the presence of partial large airway obstruction. Post-lung transplant patients may be especially at risk because of compromised lymphatic drainage.

Adult↗
PubMed2004

Transesophageal echocardiography for detecting extrapulmonary thrombi during pulmonary embolectomy.

BACKGROUND: Pulmonary embolectomy is an evolving surgical procedure for the treatment of severe pulmonary embolism. In addition to removing pulmonary thromboemboli, the achievement of optimal results also requires identification and extraction of intrathoracic, extrapulmonary thromboemboli from the right atrium, right ventricle, and the superior or inferior vena cava. Otherwise, these thromboemboli may become the source of recurrent pulmonary embolism. Intraoperative transesophageal echocardiography is frequently used during pulmonary embolectomy as a guide for the surgeon and a monitor of cardiac performance. However, its utility for detecting concurrent intrathoracic, extrapulmonary thromboemboli has not been thoroughly investigated. METHODS: The study population included 50 consecutive patients undergoing emergent pulmonary embolectomy. Results from preoperative diagnostic studies including transthoracic echocardiography; ventilation/perfusion scan, pulmonary angiography, and computed tomography were reviewed, along with the intraoperative echocardiographic reports for the presence of intrathoracic extrapulmonary thromboemboli. In addition, the surgical operative notes were consulted to determine the impact of intraoperative transesophageal echocardiography on surgical decision making. RESULTS: Extrapulmonary intrathoracic thromboemboli were identified preoperatively in 8 patients (16%). Intraoperatively, thromboemboli were identified in 5 additional patients by transesophageal echocardiography, adding to a total of 13 patients with extrapulmonary thrombi (26%). Intraoperative transesophageal echocardiography provided the sole source of evidence that directed surgical management in 10% (5 of 50) of all patients undergoing pulmonary emboletcomy. CONCLUSIONS: Intraoperative transesophageal echocardiography identified intrathoracic, extrapulmonary thomboemboli in 26% of patients undergoing pulmonary embolectomy, resulting in an alteration of surgical management in 10% of patients. These findings support the critical role of intraoperative echocardiography during pulmonary embolectomy.

Adult↗
PubMed2004

Utility of intraoperative transesophageal echocardiography for diagnosis of pulmonary embolism.

Pulmonary embolism (PE) is associated with significant perioperative morbidity and mortality. Transesophageal echocardiography (TEE) may permit direct visualization of PE or secondary signs of pulmonary artery (PA) obstruction. However, its utility in diagnosing PE in the intraoperative setting has yet to be defined. Therefore, we performed intraoperative TEE examinations in 46 patients immediately before pulmonary embolectomy. TEE examinations were reviewed for signs of thromboemboli within the right, left, and main PA, and secondary signs of acute PA obstruction (right ventricular dysfunction, moderate-to-severe tricuspid regurgitation, leftward bowing of the interatrial septum). The definitive location of thromboemboli was determined from the surgical record. Echocardiographic evidence for the presence of PE was correctly demonstrated in 46% of all patients (n = 21 of 46). However, the sensitivity for direct visualization of thromboemboli at any specific location was only 26%. TEE was least sensitive for thromboemboli in the left PA (17%). TEE evidence of right ventricular dysfunction was observed in 96%, tricuspid regurgitation in 50%, and leftward interatrial septal bowing in 98% of examinations. Therefore, the use of intraoperative TEE to diagnose acute PE via direct visualization is limited. Indirect TEE evidence of PA obstruction may be helpful in supporting a diagnosis of PE.

Adult↗
PubMed2003

Decreased proopiomelanocortin mRNA in lymphocytes of chronic alcoholics after intravenous human corticotropin releasing factor injection.

BACKGROUND: Alcohol abuse may involve an altered neuroendocrine response that mediates lymphocyte-derived proopiomelanocortin (POMC) production and inflammation. We investigated POMC messenger RNA (mRNA) expression in human lymphocytes ex vivo and their relation to plasma ACTH and immunoreactive beta-endorphin (IR-beta-EP) after intravenous injection of human corticotropin releasing factor (hCRF) in chronic alcoholics (n = 12) and nonalcoholics (n = 12) before surgery. Lipopolysaccharide-stimulated interleukin (IL)-1 receptor antagonist (IL-1 Ra) as a marker for chronic inflammation was determined. METHODS: Chronic alcohol abuse was diagnosed according to DSM-IV criteria and alcohol consumption >60 g/day. A reverse transcription-polymerase chain reaction method with total RNA and subsequent solid phase minisequencing was used to quantify lymphocytic POMC mRNA after intravenous hCRF injection. Plasma ACTH, cortisol, and lipopolysaccharide-stimulated IL-1 Ra of monocytes were measured by enzyme-linked immunosorbent assay, and plasma IR-beta-EP was measured by using radioimmunoassay. RESULTS: Baseline values of POMC mRNA content in lymphocytes and IL-1 Ra of chronic alcoholics were significantly increased compared with nonalcoholics (p < 0.01). Thirty minutes after intravenous hCRF injection, a significant increase of lymphocytic POMC mRNA was measured (p < 0.05) in nonalcoholics, whereas in chronic alcoholics a significant decrease was observed (p < 0.05). CONCLUSIONS: Chronic alcoholic patients had an altered neuroendocrine immune axis before intravenous hCRF administration and were not able to adjust to intravenous CRF injection by increasing lymphocytic POMC mRNA expression.

Adult↗
PubMedDate not supplied

Critical role of inferior vena caval filter placement after pulmonary embolectomy.

Surgical pulmonary embolectomy is a definitive treatment for patients with severe pulmonary embolism (PE). Postoperative placement of an inferior vena caval filter (IVCF) may prevent recurrent PE. We present a patient who underwent pulmonary embolectomy in whom postoperative placement of an IVCF was postponed due to hemodynamic instability and severe hemorrhage. Recurrent PE was recognized 12 hours after the initial surgery, and required reoperative pulmonary embolectomy. This report documents that recurrent PE can occur early after pulmonary embolectomy even in the presence of coagulopathy. Therefore, concurrent IVCF placement should be considered during or immediately after pulmonary embolectomy to prevent recurrent pulmonary embolism.

Embolectomy↗