The association between gastroesophageal reflux (GER) and upper airway obstruction in children is recognized but not well understood. Our objective was to determine if the creation of a model of upper airway obstruction in dogs would cause GER and to determine if the GER is related to intrathoracic pressure changes. Five dogs underwent evaluation with esophageal manometry and pH probe at baseline and 1 week after creation of an upper airway obstruction. Airway obstruction was created by placement of a fenestrated cuffed tracheostomy tube, which was then capped and the cuff was inflated, requiring the animals to breathe via the fenestrations. The negative inspiratory pressure (Pes) (+/- SD) increased from 11.8 +/- 4.8 cm H(2)O at baseline to 17.6 +/- 4.9 cm H(2)O 1 week after creation of an airway obstruction (p = .029). None of the dogs had GER at baseline with a reflux index (RI) value of 0.0; however, 1 week after creation of airway obstruction, three out of five dogs had GER, with a mean RI value of 21.2 +/- 21.2. There was a significant (p = .023) correlation (r = .928) of the changes in Pes and RI values following airway obstruction. Upper airway obstruction (UAO) does cause GER in this canine model. Severity of GER is significantly correlated with Pes changes.

Aims: The purpose of this study was to determine that the administration of an angiotensin converting enzyme (ACE) inhibitor enalapril would confer protection against doxorubicin-induced experimental heart failure, and attenuate the development of left ventricular dysfunction. Methods: Seventeen dogs were chronically instrumented with an intracoronary catheter and received doxorubicin weekly for 4 weeks. Animals were assigned to two groups: group 1: untreated heart failure; and group 2: simultaneous enalapril administration (5 mg twice a week). Hemodynamic data were obtained at week 0 and 12. Echocardiography was performed weekly. Results: Survival improved with simultaneous enalapril administration (36% in group 1 vs. 100% in group 2, Ps0.04). The increase in the left ventricular end-diastolic pressure was significantly reduced at week 12 (17"1 mmHg in group 1 vs. 9"1 mmHg in group 2, Ps0.0042). The fall in left ventricular stroke work index was significantly prevented (52% in group 1 vs. 21% in group 2, Ps0.006). The increase in right ventricular end-diastolic diameter was significantly reduced by enalapril prophylaxis. Conclusion: Simultaneous treatment with enalapril was beneficial in the prevention of doxorubicin-induced cardiomyopathy.

Indications regarding surgical pulmonary embolectomy for treatment of submassive/massive acute pulmonary embolism remain controversial. An institutional experience with pulmonary embolectomy for acute pulmonary embolism (APE) was reviewed. A retrospective analysis of all patients undergoing pulmonary embolectomy for APE from September 2004 to January 2007 was conducted. Demographic data, clinical presentation and outcomes were analyzed. Fifteen patients underwent surgery for APE over a period of 27 months [average age 59.6 (range 35-89) years, (seven male, eight female)]. Six (40%) patients were admitted with known APE and nine patients exhibited post admission APE (seven - after surgical procedures, two - after cerebrovascular accident). Clinical presentation included dyspnea (86.67%), hemodynamic instability requiring continuous vasopressor support (40%), echocardiographic evidence of right ventricular dilatation (80%). Ten patients undergoing early/expedient embolectomy all survived while delayed surgery in the other five patients (>24 h) was associated with 60% mortality. Expanding indications for early surgical pulmonary embolectomy has stemmed from reliable echocardiographic identification of right ventricular compromise and recognition of these findings as harbingers of subsequent hemodynamic embarrassment. Our series underscores the benefit of early consideration and performance of pulmonary embolectomy in these critically ill patients.

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End-stage heart disease is a major health care issue and it represents one of the most costly diseases. Several experimental heart failure models have been developed; however, a single model is not widely accepted as representative of clinical heart failure. The doxorubicin-induced cardiomyopathy model was used in the current study to address two issues: 1) to define a standardized dose regimen of intracoronary doxorubicin infusion; and 2) to establish a method of determining the onset and time course of heart failure. Twenty dogs underwent placement of an intracoronary catheter. A total dose of 1 mg/kg of intracoronary doxorubicin was infused. Hemodynamics were obtained at weeks 0, 7, and 12. Echocardiography was performed weekly. Right and left ventricular biopsy specimens were examined at weeks 0 and 12. Survival after doxorubicin-induced cardiomyopathy was 60% at week 12. The development of heart failure was demonstrated by a significant decrease in left ventricular ejection fraction and cardiac index and a significant increase in left ventricular end-diastolic pressure and volume. The leukocyte count, hemoglobin, and hematocrit decreased significantly. Histologic changes of both the right and left ventricular myocardial biopsy specimens included myocellular hypertrophy, loss of myofibrillar material, and vacuolization. Intracoronary doxorubicin reliably produced an experimental model of accelerated heart failure that developed over the course of 12 weeks. Echocardiographic monitoring allowed a close surveillance of heart failure development. This model may be useful to evaluate the efficacy of cardiomyoplasty, mechanical assist devices, transplantation, and reduction ventriculoplasty.