Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While in animal experiments neurogenically initiated pulmonary edema is a well known event and is supposed to be due to centrally initiated hemodynamic disturbances ("neurohemodynamics") in patients with severe cerebral lesions fulminant alveolar edema is reported to occur very rarely. The questions addressed by this study are: 1. whether and to what extent changes in extravascular lung water (EVTVL) can be demonstrated in patients with a severe isolated cerebral lesion; 2. whether a relationship between the severity of the cerebral lesion and accompanying EVTVL changes can be proven; and 3. whether or not EVTVL changes are associated with corresponding changes in intravascular hydrostatic and oncotic Starling parameters; i.e. cardiogenic or noncardiogenic pulmonary edema accompanying the cerebral lesion. This study included 44 patients presenting with a severe isolated cerebral lesion and decerebrate posturing on admission. EVTVL (by thermo-dye double-indicator technique), pulmonary gas exchange (AaDO2/pAO2), colloid oncotic pressure (COP) and mean systemic arterial (SAP), mean pulmonary arterial (PAP), and pulmonary capillary wedge pressures (PCWP) were measured from the day of admission to the 6th day after the acute cerebral lesion maximally; in addition the microvascular pressure in the pulmonary bed and intravascular filtration pressure were calculated from the above mentioned parameters. The neurological status on admission and throughout the observation period was scored using the Innsbruck Coma Scale (ICS) and the neurological outcome by the Glasgow Outcome Scale (GOS). Statistical analysis was performed using the distribution independent Kruskal Wallis test, the correlation coefficient r (Pearsan and Bravais), and the Spearman rank correlation (RSp); values are given as means +/- SEM; the significance has been set at P less than 0.05. Our results reveal an overall increase in EVTVL from 8.8 +/- 0.8 ml/kg on the day of admission up to 11.3 +/- 1.6 ml/kg on the 4th day. While survivors (n = 13) remained within the normal range of EVTVL (less than 9 ml/kg), non-survivors (n = 31) started at an already elevated level (10.05 +/- 1.04 ml/kg) and reached their maximum values (15.4 +/- 2.3 ml/kg) on day 3 to 4. In 3 non-survivors these increased initial EVTVL values were accompanied by pathologically increased intravascular pressures, indicating that hydrostatic mechanisms were involved in the EVTVL rises. While the hydrostatic pressures normalized spontaneously, EVTVL values stayed within the pathological range throughout the remaining observation period.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cardiovascular and pulmonary changes in patients with an isolated cerebral lesion. II. Extravascular lung water and pulmonary gas exchange ("neurogenic lung edema")]. 277 40

The effects of the serotonin receptor blocker, ketanserin, were studied in a porcine Pseudomonas adult respiratory distress syndrome model. Swine, weighing 14-30 kg, were anesthetized and ventilated with 0.5 FiO2 and 5 cm H2O positive end expiratory pressure. Three groups were studied: saline control (C, n = 9), continuous intravenous Pseudomonas aeruginosa, 5.0 X 10(8)CFU/kg/min (Ps, n = 8), and Pseudomonas and intravenous ketanserin, 0.2 mg/kg, given at 20 and 120 min after the onset of the Pseudomonas infusion (KET, n = 5). Pulmonary arterial (PAP) and systemic arterial (SAP) pressures, cardiac index (CI), thermal Cardio-Green extravascular lung water (EVLW), pulmonary albumin flux (slope index, SI), arterial blood gases, and whole blood serotonin levels were measured and pulmonary shunt and pulmonary (PVRI) and systemic (SVRI) vascular resistance indices were calculated. At 3 hr the Ps group demonstrated significant (P less than 0.05) increases in PAP (34 +/- 1 vs C 13 +/- 2 mm Hg), EVLW (14.4 +/- 2.2 vs C 4.3 +/- 1.2 ml/kg), SI (2.05 +/- 0.23 X 10(-3) vs C 0.38 +/- 0.09 X 10(-3) U/min), pulmonary shunt (67 +/- 15% vs C 9 +/- 3%), PVRI (1599 +/- 89 vs C 184 +/- 14 dyn X sec X cm-5/m2), and SVRI (4542 +/- 774 vs C 2087 +/- 129 dyn X sec X cm-5/m2) and decreases in CI (0.9 +/- 0.1 L/min/m2 vs C 2.8 +/- 0.2 L/min/m2), PaO2 (93 +/- 17 Torr vs C 203 +/- 15 Torr) and arterial blood serotonin concentration (23.5 +/- 13% decrease from basal). Treatment with ketanserin was associated with maintenance of PaO2 (KET 207 +/- 5 mm Hg vs C 203 +/- 15 mm Hg), pulmonary shunt (KET 8 +/- 3% vs C 9 +/- 3%), and CI (KET 2.3 +/- 0.1 L/min/m2 vs C 2.8 +/- 0.2 L/min/m2) at control levels and attenuated the Pseudomonas-induced increase in PVRI (873 +/- 37 vs Ps 1599 +/- 89 dyn X sec X cm-5/m2) and SVRI (2089 +/- 287 vs Ps 4542 +/- 774 dyn X sec X cm-5/m2), but did not alter the development of pulmonary edema. These data indicate that serotonin plays a role in the development of the V/Q mismatch and arterial hypoxemia observed in this model by a mechanism independent of changes in microvascular injury and permeability and was probably a result of reduced peripheral bronchiolar constriction.
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PMID:Serotonin receptor blockade improves cardiac output and hypoxia in porcine ARDS. 362 34