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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhalation injury was induced in chronically instrumented sheep (n = 9) by insufflating them with smoke from burning cotton cloth. Sham animals (n = 9) were insufflated with air. There were no temporal changes in any measured parameter of the sham animals. Smoke induced a depression in PaO2. There was a threefold elevation in protein-rich pulmonary lymph which was sustained for over 48 hours. The lymph-to-plasma oncotic pressure ratio was increased. The cardiac index, left atrial pressure, and pulmonary arterial pressure remained unchanged in both groups. After smoke inhalation, the interstitial levels of neutrophils increased while interstitial antiprotease activity was depressed. The lung lymph concentration of 6-keto prostaglandin F1a, the major metabolite of prostacyclin, was increased. These data suggest that the pulmonary injury following smoke inhalation is the result of an increase in lung microvascular permeability to protein with resultant pulmonary edema. The mechanisms responsible for these changes appear to be related to direct injury to the tracheobronchial tree by cytotoxic agents in the smoke; polymorphonuclear leukocytes; and, possibly, eicosanoids.
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PMID:The pulmonary lesion of smoke inhalation in an ovine model. 242 39

The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
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PMID:Iron toxicity in sheep. 253 32

We studied the effect of intratracheally infused bile acids on the respiratory and circulatory systems in anesthetized dogs. The bile acids used were cholic acid, deoxycholic acid, taurocholic acid, glycocholic acid and taurodeoxycholic acid. They were diluted to 1% or 10% with normal saline solution and 1 ml.kg-1 was infused into the trachea through an endotracheal tube under a controlled ventilation with air. Injection of 10% diluted bile acid, except for glycocholic acid, decreased PaO2 to less than 50 torr after 15 minutes and increased PaCO2 to above 60 torr after 2 hours. A butterfly shadow appeared in chest radiographs after 1 hour. Microscopic examinations revealed severe pulmonary edema and hemorrhage but circulatory depression was negligible. Hypoxia and hypercapnea were also observed in the 1% dilution group but to a smaller degree. Intrapulmonary water volume increased following injection of bile acid. Our results demonstrated that bile acids induce pulmonary damage.
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PMID:[Respiratory and circulatory changes after the intratracheal infusion of bile acids in dogs]. 258 10

A 27-year old man was admitted with a right-sided pneumothorax of 2-3 weeks duration. A chest tube was inserted and connected to an underwater seal drainage system without the application of external suction. Three hours later, the patient developed unilateral re-expansion pulmonary oedema and severe hypotension. Active management consisted of ventilating the patient with the addition of PEEP, and the administration of liberal amounts of fluids, including plasma and gelatin solution. The mechanism of re-expansion pulmonary oedema is different from that of cardiogenic pulmonary oedema, and the treatment consequently different. The cause of the hypotension may be due to hypovolaemia, from rapid pooling of fluid within the thorax, pre-existing volume depletion and myocardial depression. One must specially be aware of this possible complication when the pneumothorax is large and of more than 3 days, and it is to be stressed that suction should never initially be used in the treatment of a pneumothorax.
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PMID:Life threatening re-expansion hypotension and pulmonary oedema following treatment of a pneumothorax. 261 7

Patients who undergo peripheral vascular surgery are at increased risk for postoperative cardiac events and are difficult to assess preoperatively because of limitations on their activity. We prospectively studied 176 consecutive eligible patients undergoing elective vascular surgery to determine the value in predicting a postoperative cardiac event of preoperative electrocardiographic monitoring to detect myocardial ischemia. Of the 176 patients, 32 (18 percent) had 75 episodes of monitored ischemic ST-segment depression preoperatively (of which 73 were asymptomatic), and 13 (7 percent) met strict criteria for major postoperative cardiac events, including 1 with a fatal myocardial infarction, 3 with nonfatal infarctions, 4 with unstable angina, and 5 with ischemic pulmonary edema. Of the 32 patients with ischemia before their operations, 12 had postoperative events (univariate relative risk, 54; 95 percent confidence interval, 7.2 to 400). Only 1 postoperative event occurred among 144 patients who did not have preoperative ischemia. The sensitivity of preoperative ischemia was 92 percent, the specificity 88 percent, the predictive value of a positive result 38 percent, and the predictive value of a negative result 99 percent. In multivariate analyses, preoperative ischemia was the most significant correlate of postoperative cardiac events and remained a statistically significant independent correlate even after we had controlled for all other preoperative factors (multivariate relative risk, 24.4; 95 percent confidence interval, 6.8 to 88). These preliminary data suggest that preoperative electrocardiographic monitoring to detect episodes of myocardial ischemia is a useful method for assessing cardiac risk in patients who undergo elective vascular surgery. In particular, the absence of ischemia during monitoring indicates a very low risk.
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PMID:Correlation between preoperative ischemia and major cardiac events after peripheral vascular surgery. 279 5

Strain 13 guinea pigs inoculated subcutaneously with Pichinde virus developed fever, lost body weight, decreased water and food consumption, and died at 14 +/- 0.6 days. After FPL-55712, a leukotriene D4 antagonist, was administered beginning on PID (post-inoculation day) 3 for 18 days, the magnitude of body weight loss decreased and food intake increased, despite a persistent fever. The treated guinea pigs also survived significantly longer than infected animals receiving placebo injection (21 vs 14 days). Using guinea pig ileum bioassay and radioimmunoassay, we detected significant levels of plasma leukotrienes in Pichinde virus-infected guinea pigs on PID 11 and possibly PID 14. These findings strongly suggest that leukotrienes play a role in the pathogenesis of arenavirus infection and may account in part for the observed cardiac depression, pulmonary edema, and eventual death.
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PMID:Evidence for the involvement of sulfidopeptide leukotrienes in the pathogenesis of Pichinde virus infection in strain 13 guinea pigs. 302 93

Acute respiratory failure after hepatic resection, especially in case of concomitant liver dysfunction, is the most troublesome postoperative complication. In order to clarify the pathophysiological mechanism of acute respiratory failure, EVLW (extravascular lung water) was measured by double indicator dilution method in canine model. Mongrel dogs underwent laparotomy and the common bile duct was ligated and divided. After 6 weeks, EVLW was significantly elevated compared with that of normal dogs (p less than 0.05). From 4 hours after 70% hepatic resection dextran-40 was loaded to increase PWP (pulmonary wedge pressure). EVLW was increased accompanying the elevation of PWP in all groups, but in the group with biliary obstruction EVLW was significantly increased for the same elevation of PWP. These results suggest that permeability of pulmonary capillary was highly increased after hepatic resection in biliary obstruction group. Pulmonary edema in this canine model seems to resemble ARDS in human and the pathophysiological mechanism was thought to be related with depression of RES phagocytic function, activation of complement system and pulmonary vascular plugging by aggregates of degenerating granulocytes and endothelial injury. Gabexate mesilate blocked the increase of the lung vascular permeability and was thought to be effective to protect the lung from postoperative acute respiratory failure.
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PMID:[Acute respiratory failure after hepatic resection in canine biliary obstruction model]. 314 48

Patients with noncardiogenic pulmonary edema requiring ventilatory assistance are usually supported with CPPV using positive end-expiratory pressure (PEEP), but CPPV requires endotracheal intubation and may decrease cardiac output (QT). The purpose of this study was to examine thoracoabdominal continuous negative pressure ventilation (CNPV) using external negative end-expiratory pressure (NEEP). The effects on gas exchange and hemodynamics were compared with those of CPPV with PEEP, with the premise that CNPV might sustain venous return and improve QT. In 6 supine, anesthetized and paralyzed dogs with oleic-acid-induced pulmonary edema, 30 min of CNPV was alternated twice with 30 min of CPPV. Positive and negative pressure ventilation were carefully matched for fractional inspired oxygen concentration (FIO2 = 0.56), breathing frequency, and tidal volume. In addition, we matched the increase in delta FRC obtained with the constant distending pressures produced by both modes of ventilation. An average of -9 cm H2O of NEEP produced the same delta FRC as 10.8 cm H2O of PEEP. Gas exchange did not differ significantly between the 2 modes. However, QT was 15.8% higher during CNPV than during CPPV (p less than 0.02). Mixed venous oxygen saturation also improved during CNPV compared with that during CPPV (58.3 versus 54.5%, p less than 0.01). Negative pressure ventilation using NEEP may be a viable alternative to positive pressure ventilation with PEEP in the management of critically ill patients with noncardiogenic pulmonary edema. It offers comparable improvement in gas exchange with the advantages of less cardiac depression and the possible avoidance of endotracheal intubation.
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PMID:Hemodynamic effects of external continuous negative pressure ventilation compared with those of continuous positive pressure ventilation in dogs with acute lung injury. 331 Jul 73

We wished to determine the role of hypoxic chemosensitivity in high-altitude pulmonary edema (HAPE) by studying persons when ill and upon recovery. We studied seven males with HAPE and seventeen controls at 4,400 m on Mt. McKinley. We measured ventilatory responses to both O2 breathing and progressive poikilocapnic hypoxia. Hypoxic ventilatory response (HVR) was described by the slope relating minute ventilation to percent arterial O2 saturation (delta VE/delta SaO2%). HAPE subjects were quite hypoxemic (SaO2% 59 +/- 6 vs. 85 +/- 1, P less than 0.01) and showed a high-frequency, low-tidal-volume pattern of breathing. O2 decreased ventilation in controls (-20%, P less than 0.01) but not in HAPE subjects. The HAPE group had low HVR values (0.15 +/- 0.07 vs. 0.54 +/- 0.08, P less than 0.01), although six controls had values in the same range. The three HAPE subjects with the lowest HVR values were the most hypoxemic and had a paradoxical increase in ventilation when breathing O2. We conclude that a low HVR plays a permissive rather than causative role in the pathogenesis of HAPE and that the combination of extreme hypoxemia and low HVR may result in hypoxic depression of ventilation.
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PMID:Abnormal control of ventilation in high-altitude pulmonary edema. 336 41

Two fatal cases of Japanese pieris poisoning in goats are reported. The clinical symptoms of the two animals consisted in vomiting, salivation, excitation and depression. Despite rumenotomy and symptomatic treatment, the goats died within four days after the onset of the symptoms. Pulmonary oedema accompanied by lobular aspiration pneumonia was found to be present in one goat at autopsy. Hyperaemia, pulmonary oedema and acute tubular nephrosis were observed in the other animal.
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PMID:[Pieris japonica pieris poisoning in 2 goats]. 337 72


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