[Child with a vascularized throat mass]. / Kind mit gefäßreichem "Kloß" im Hals.

We report the case of an 11-year-old girl with difficultly speaking and a history of singular, self-limiting oral bleeding. Clinical and radiological examination in the emergency room showed a vascularized tumor of the base of the tongue, which almost completely occluded the oropharynx. After complex anesthesiologic preparation and endoluminal embolization, the tumor was safely removed by transoral laser microsurgery. Histology revealed a rare benign schwannoma of the oropharynx. Further clinical examinations and genetic screening were recommended.

Effects of perfluorohexan vapor on gas exchange, respiratory mechanics, and lung histology in pigs with lung injury after endotoxin infusion.

BACKGROUND: Inhaled perfluorohexan vapor has been shown to improve gas exchange and pulmonary mechanics in oleic acid- and ventilator-induced lung injury. However, in the clinical setting, lung injury frequently occurs in the context of systemic inflammation and consecutive lung injury, which may be induced experimentally by intravenous administration of endotoxin. The authors studied whether vaporized perfluorohexan is efficacious during endotoxin-induced lung injury in domestic pigs. METHODS: Twenty-two pigs (29 [23, 31] kg body weight [first, third interquartile]; tracheostomy) were anesthetized and mechanically ventilated. In the endotoxin (n = 8) and perfluorohexan groups (n = 7), we administered endotoxin of Escherichia coli 111:B4, 1 mg.kg . h for 1 h and 10 microg.kg.h for 5 h in consecutive order. In the perfluorohexan group, inhalation of the test drug was started 2 h 30 min after the start of the intravenous endotoxin and terminated after 30 min. In a control group (n=7), animals were instrumented and observed over time without further intervention. Oxygenation function was assessed from oxygen partial pressures (Po2, blood gases) and calculated shunt fraction. Respiratory compliance was calculated from airway pressure and tidal volume. Measurements were performed before and every hour during endotoxin infusion. RESULTS: After 6 h of endotoxin, gas exchange and pulmonary compliance were deteriorated in the endotoxin group (Pao2: 184 [114, 289] vs. 638 [615, 658] mmHg, pulmonary shunt fraction: 30 [23, 38] vs. 4 [3, 6]%, respiratory compliance: 12 [11, 14] vs. 22 [19, 23] ml/mbar; P < 0.05, endotoxin vs. control). Inhalation of vaporized perfluorohexan did not improve Pao 2 (107 [60, 221] mmHg), pulmonary shunt fraction (32 [26, 58]%), or respiratory compliance (14 [10, 17] ml/mbar) when compared with intravenous endotoxin (not significant, perfluorohexan vs. endotoxin). CONCLUSIONS: Inhalation of vaporized perfluorohexan does not improve pulmonary gas exchange or respiratory compliance in endotoxin-induced porcine lung injury.

Effect of prostaglandin I2 analogues on left ventricular diastolic function in vivo.

The prostaglandin I2 analogues epoprostenol and iloprost increase left ventricular contractility. Therefore, we hypothesize that the prostaglandin I2 analogues epoprostenol and iloprost improve also left ventricular diastolic function. To test this hypothesis, the effects of epoprostenol and iloprost on left ventricular diastolic function were assessed in vivo and compared to two vasodilators sodium nitroprusside and adenosine, not formerly associated with changes of left ventricular contractility. Eleven pigs (25.9+/-2.8 kg, balanced anaesthesia) were exposed to the short-acting intravenous vasodilators sodium nitroprusside, adenosine and epoprostenol in a randomized cross over design. The long-acting iloprost was administered at the end of the protocol. The drugs are titrated to achieve a 25% reduction of diastolic aortic pressure. Active isovolumic relaxation properties of the left ventricle were assessed by the maximum velocity of left ventricular pressure drop. Passive phase of relaxation and filling was assessed by the determination of end diastolic compliance during a preload reduction manoeuvre. The maximum velocity of left ventricular pressure drop worsened during the infusion of sodium nitroprusside (baseline: -1950; sodium nitroprusside: -1293 mm Hg/s, p<0.05, Wilcoxon signed rank test versus vs. baseline) and adenosine (baseline: -2015; adenosine: -1345 mm Hg/s, p<0.05), but remained stable during the infusion of the prostaglandins (baseline: -1943; epoprostenol: -1785 mm Hg/s; baseline: -2042; iloprost: -1923 mm Hg/s). End diastolic compliance was not altered significantly by any vasodilator. Interstitial myocardial cAMP increased during the infusion of epoprostenol (7.60 to 13.87 fmol/ml, p<0.05) and tended to increase during the infusion of iloprost (7.56 to 11.66 fmol/ml, p=0.21). The prostaglandin I(2) analogues epoprostenol and iloprost preserved the early phase of active isovolumic relaxation, presumably mediated by myocardial cAMP, whereas sodium nitroprusside and adenosine impaired early active isovolumic relaxation. Passive relaxation and filling properties remained stable during the infusion of each applied vasodilator in the intact left ventricle in vivo.

The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo.

OBJECTIVE: The principal effects of prostaglandin I(2) are vasodilation and inhibition of platelet aggregation induced by a rise in the intracellular second messenger cAMP. In the heart a rise in intracellular myocardial cAMP increases contractility. We examined whether prostaglandin I(2) increases left ventricular contractility in vivo. The effects of epoprostenol and iloprost on left ventricular contractility were assessed in vivo and compared to the effects of adenosine and sodium nitroprusside, which exerts vasodilatory properties independently of cAMP. DESIGN AND SETTING: Prospective, randomized, cross-over in a university laboratory. SUBJECTS: Eleven pigs (25.9+/-2.8 kg, balanced anesthesia). INTERVENTIONS: Each animal was exposed to intravenous sodium nitroprusside, adenosine, and epoprostenol in randomized order. Iloprost was administered at the end due to its longer half-life. The dose was titrated to achieve a 25% reduction in diastolic aortic pressure. MEASUREMENTS AND RESULTS: Left ventricular contractility was assessed before, during, and after each intervention by determination of the endsystolic elastance with the conductance method. While there was no change in endsystolic elastance upon the infusion of adenosine and sodium nitroprusside; endsystolic elastance increased in the case of epoprostenol (57%) and iloprost (71%). CONCLUSIONS: Left ventricular contractility is increased in vivo by epoprostenol and iloprost but not by adenosine or sodium nitroprusside at equipotent hypotensive dose. A contribution of sympathetic reflex activation of cardiac nerves on the increase in left ventricular contractility cannot be completely ruled out.