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)

Peptic aspiration pneumonitis (Mendelson's syndrome) results when gastric acid is aspirated into the lung, as may occur during anesthesia. In the present study, 0.1 N HCl was insufflated via the endotracheal tube into pentobarbital-anesthetized dogs in an amount sufficient to cause severe pulmonary damage. At death, the thorax was opened, the lungs grossly examined, and either weighed and desiccated for determination of wet/dry lung weight ratios, rinsed with saline for removal of alveolar surface phospholipids, or homogenized for whole lung phospholipid determination. Gross appearance and wet/dry lung weight ratios indicated severe pulmonary edema. The surface tension values of the lung wash were elevated over control values. Lysophophatidyl-choline (LPC) showed a striking increase over control values. Because LPC is a potent hemolytic agent which builds up in the lung following this pulmonary insult, and because increased hemorrhaging gradually develops following experimental acid insufflation, it is concluded that LPC is most probably causally related to the hemorrhagic pneumonia of Mendelson's syndrome.
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PMID:Aspiration pneumonitis and pulmonary phospholipids. 99 55

Immediate attention must be given to the respiratory system of the heroin abuser; then he should be given naloxone HCl. Search for evidence of use of additional drugs, which may compound problems. Pulmonary edema, aspiration pneumonia and pulmonary embolization are the most common complications. Infections, particularly endocarditis, and cardiac arrhythmia also occur with heroin overdose. Hepatitis is common. Treatment must include not only attention to the presenting symptoms but also referral to a rehabilitation center when possible.
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PMID:Treating heroin overdose. 112 10

The effect of the beta-agonist, ritodrine HCl, was studied on cardiac output (CO) and pulmonary lymph flow (QL) in sheep. Increased CO is associated with an increase in pulmonary QL in sheep during exercise. Isoproterenol increases CO but has not been shown to increase pulmonary QL. Ritodrine HCl was chosen because of its association with pulmonary edema when used to halt premature labor in pregnant women. Unanesthetized sheep received an intravenous infusion of ritodrine in increasing doses over 4 h up to a maximum of 6.3 micrograms/kg/min. Pulmonary pressure increased 2 mmHg after 1 h and returned to baseline by hours 3 and 4 with no change in left atrial pressure or lymph to plasma protein ratio. Pulmonary QL increased by 61% and CO by 80% at hour 3 of infusion (ritodrine dose 5.4 micrograms/kg/min) and remained at this level. Pulmonary QL and CO (normalized to baseline) correlated, r = 0.72, p less than 0.001, but there was no correlation between pulmonary QL and calculated microvascular pressure. Although an increase in pulmonary microvascular endothelium permeability with concurrent pulmonary vasodilation can not be completely ruled out, it appears from this study that beta-agonist therapy with ritodrine increases pulmonary QL by a CO related recruitment of microvessels.
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PMID:Effects of ritodrine infusion on hemodynamics and lung lymph in awake sheep. 180 92

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14

The effect of pulmonary injury induced by aspiration of HCl on plasma atrial natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration. Rats were housed individually in metabolic cages and were given a constant infusion of sodium solution via catheters chronically inserted into the jugular vein. Plasma ANP levels were elevated at 3 and 24 h after tracheal injection of 0.2 ml of 0.1 N HCl via the cricothyroid membrane. Urine volume and urinary sodium excretion increased during the first 24 h after acid aspiration. However, this increase was reduced by the injection of anti-ANP serum. Furthermore, the injection of anti-ANP serum resulted in a significant (P less than 0.05) increase in wet lung weight from a value of 0.74 +/- 0.06 (HCl aspiration with normal rabbit serum injection) to 0.83 +/- 0.07% of body weight. These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung.
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PMID:Release of ANP and its physiological role in pulmonary injury due to HCl. 213 26

Acute, diffuse lung injury, the principal lesion in ARDS, is often refractory to treatment. Recently, pretreatment with several pulmonary vasodilators that increase cAMP levels: isoproterenol, terbutaline, theophylline, and prostacyclin, was found to reduce the severity of lung injury in animal models. We have investigated the possible modulation of HCl-induced pulmonary edema in rats by VIP, a lung neuropeptide with potent vasodilator and cAMP-producing properties. The lungs of rats were perfused in situ at 10 ml/min with Krebs-4% albumin solution, and ventilated at constant tidal volume (6.5 ml/kg). Peak airway pressure (PAW), mean pulmonary arterial pressure (PPA) were measured throughout the experiment, and wet to dry lung weight ratio (W/D), afterwards. All animals were observed for one hour. In 6 rats receiving HCl only, 0.2 N-HCl was instilled intratracheally at 2 ml/kg. Four rats received 2 ml/kg of physiological saline intratracheally as control. In 6 other animals, VIP was infused into the pulmonary artery at 1 micrograms/kg/min, beginning 10 minutes before HCl and for the rest of the experiment. Another 6 rats were pretreated with atrial natriuretic peptide (ANP, atriopeptin II) just like the VIP group. Lungs of saline control animals showed little or no chage in PAW or PPA. With HCl alone, PAW increased immediately and continued to rise for the rest of the hour, reaching 500% of basal value at 30 minutes. PPA increased by 68% and W/D by 74% compared to saline-instilled lungs. In the VIP + HCl group, all abnormalities were significantly reduced relative to the HCl group. The rise in PAW was attenuated by 79% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vasoactive intestinal peptide (VIP) protects against acid-induced acute lung injury in isolated perfused rat lungs]. 281 Sep 67

Hemodynamic changes after intravenous application of 10 mg celiprolol-HCl (3-[3-acetyl-4-(3-tert-butylamino-2-hydroxy-propoxy)-phenyl]-1,1-diethyl urea hydrochloride. Selectol; in the following briefly called celiprolol) were investigated over an interval of 30 min in 15 patients with angiographically determined coronary heart disease and depressed left ventricular function (ejection fraction less than 60%, left ventricular end-diastolic pressure (LVEDP) greater than 12 mmHg). One patient suffered from severe left ventricular failure with lung edema and could not be evaluated. The heart rate was not influenced, the arterial pressure was significantly reduced (p less than 0.01), similarly LVEDP (p less than 0.001), and pulmonary pressure (p less than 0.01). Cardiac output and total peripheral resistance were not changed significantly. The hemodynamic working profile of celiprolol in patients with depressed left ventricular function is that of a beta 1-receptor blocker with a strong intrinsic sympathomimetic activity (ISA = Intrinsic Sympathetic Activity) and vasodilating properties--even on preload. The intravenous application of celiprolol in patients with severely depressed left ventricular function can cause pump failure.
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PMID:[Hemodynamic effects of intravenously administered celiprolol in patient with coronary heart disease and depressed left ventricular function]. 288 31

The aspiration of gastric acid causes pulmonary edema and hypoxemia. One approach to the management of this syndrome is to raise cardiac output (Qt) and O2 delivery (QO2) to ensure tissue oxygenation (VO2) at the risk of increasing the edema. Another approach reduces the edema by reducing pulmonary microvascular pressure (Pmv) at the risk of reducing QO2 and VO2. We compared these approaches in 24 anesthetized, ventilated dogs with pulmonary wedge pressure (Ppw), a clinical approximation of Pmv, of 12.5 mmHg. Before and again 1 h after endobronchial instillation of 0.1 N HCl, we measured Qt, QO2, VO2, venous admixture, and in vivo extravascular lung liquid. The dogs were then randomly divided into four equal groups: 1) 12.5 mmHg Ppw, high Qt; 2) 7.5 mmHg Ppw, intermediate Qt; 3) 4.5 mmHg Ppw, low Qt; and 4) 4.5 mmHg Ppw plus dopamine, intermediate Qt. Measured values were followed for 4 more h, after which the lungs were excised to compare wet weight-to-body weight ratios (W/B). When plasmapheresis reduced Ppw at 1 h, edema did not increase further and W/B of groups 2 (21 +/- 3), 3 (18 +/- 3), and 4 (22 +/- 3) were significantly less than in group 1 (27 +/- 3) (P less than 0.001). Although Qt decreased with Ppw, increased hematocrit and reduced venous admixture maintained QO2 in group 2 but not in group 3. In group 4 an intermediate Qt maintained QO2 even at 4.5 mmHg Ppw but edema increased to the group 2 level presumably because Pmv rose with Qt on dopamine. VO2 remained constant over time in each group. These data demonstrate that canine HCl-induced pulmonary edema, measured in vivo or gravimetrically, is very sensitive to reductions in Pmv. Moreover, the lowest Pmv (and QO2) was well tolerated because an O2 supply dependency of VO2 was not observed.
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PMID:Treatment of canine aspiration pneumonitis: fluid volume reduction vs. fluid volume expansion. 318 34

The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 +/- 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 +/- 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.
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PMID:Synthetic smoke with acrolein but not HCl produces pulmonary edema. 328 67

In canine pulmonary capillary leak induced by intravenous oleic acid, reducing pulmonary wedge pressure (Ppw) reduces pulmonary edema, venous admixture (Qva/Qt), and cardiac output (Qt). The authors tested the possibility that in another canine model of pulmonary capillary leak, that induced by endobronchial instillation of hydrochloric acid, nitroprusside would reduce Ppw and edema without reducing Qt or oxygen delivery (QO2). In 18 dogs, the authors measured extravascular lung water (EVLW) by thermal-dye dilution and the hemodynamic and gas exchange variables before and at intervals (1, 1.5, 3, and 5 h) after .1 N HCl bronchial infusion. By 1 h, HCl increased EVLW from 175 to 250 ml and Qva/Qt from 11 to 21%. Immediately after the 1-h measurements, the dogs were divided into three equal groups: six controls (C) were maintained with a Ppw of 12 mmHg, while plasmapheresis (P) or nitroprusside (NP) reduced Ppw to 5 mmHg for the next 4 h. EVLW continued to increase to 548 ml in C, but did not increase further in P and NP. Weights of lungs excised at 5 h confirmed that P and NP reduced edema by 50% in 4 h. In C, Qva/Qt increased, but there was no reduction in Qt or QO2. In contrast, plasmapheresis reduced Qva/Qt, Qt, and QO2. With nitroprusside, Qt and QO2 were maintained despite reduced Ppw at 1.5 and 3 h, and Qva/Qt did not decrease as in Group P. We conclude that plasmapheresis-induced reduction in Ppw reduces the pulmonary capillary leak and venous admixture following acid aspiration, but this has the potentially adverse effect of reducing cardiac output and oxygen delivery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of nitroprusside on pulmonary edema, oxygen exchange, and blood flow in hydrochloric acid aspiration. 330 Apr 29


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