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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of regional hypoxic pulmonary vasoconstriction (HPV) on lobar flow diversion in the presence of hydrostatic pulmonary edema. Ten anesthetized dogs with the left lower lobe (LLL) suspended in a net for continuous weighing were ventilated with a bronchial divider so the LLL could be ventilated with either 100% O2 or a hypoxic gas mixture (90% N2-5% CO2-5% O2). A balloon was inflated in the left atrium until hydrostatic pulmonary edema occurred, as evidenced by a continuous increase in LLL weight. Left lower lobe flow (QLLL) was measured by electromagnetic flow meter and cardiac output (QT) by thermal dilution. At a left atrial pressure of 30 +/- 5 mmHg, ventilation of the LLL with the hypoxic gas mixture caused QLLL/QT to decrease from 17 +/- 4 to 11 +/- 3% (P less than 0.05), pulmonary arterial pressure to increase from 35 +/- 5 to 37 +/- 6 mmHg (P less than 0.05), and no significant change in rate of LLL weight gain. Gravimetric confirmation of our results was provided by experiments in four animals where the LLL was ventilated with an hypoxic gas mixture for 2 h while the right lung was ventilated with 100% O2. In these animals there was no difference in bloodless lung water between the LLL and right lower lobe. We conclude that in the presence of left atrial pressures high enough to cause hydrostatic pulmonary edema, HPV causes significant flow diversion from an hypoxic lobe but the decrease in flow does not affect edema formation.
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PMID:Hypoxic pulmonary vasoconstriction does not affect hydrostatic pulmonary edema formation. 355 36

A study of the blood oxygenation in pulmonary capillaries is made by considering the transport mechanisms of molecular diffusion, convection and the facilitated diffusion due to the presence of haemoglobin. The resistance offered by the pulmonary membrane on the transport of gases has been incorporated. The resulting system of coupled, non-linear partial differential equations is solved numerically. It is found that, in the immediate neighbourhood of the entry, the amount of dissolved O2 decreases. This decreases further as the resistance offered by the pulmonary membrane increases. The rate of oxygenation of blood increases as the permeability coefficient for O2 (PO) increases. It is shown that the ideally permeable case for both O2 and CO2 can be approximated by taking PO approximately 10 cm/s. Further, it is shown that the oxygen takes longest and CO2 is the fastest to attain equilibration. The equilibration length increases as the resistance offered by the membrane increases. Finally, some of the pulmonary diseases such as pulmonary oedema and fibrosis have been analyzed.
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PMID:A numerical model for blood oxygenation in the pulmonary capillaries--effect of pulmonary membrane resistance. 365 68

Hyperoxia and infused granulocytes act synergistically in producing a nonhydrostatic high-permeability lung edema in the isolated perfused rabbit lung within 4 h, which is substantially greater than that seen with hyperoxia alone. We hypothesized that the interaction between hyperoxia and granulocytes was principally due to a direct effect of hyperoxia on the lung itself. Isolated perfused rabbit lungs that were preexposed to 2 h of hyperoxia (95% O2-5% CO2) prior to the infusion of unstimulated granulocytes (under normoxic conditions) developed significant nonhydrostatic lung edema (P = 0.008) within 2 h when compared with lungs that were preexposed to normoxia (15% O2-5% CO2) prior to granulocyte perfusion. The edema in the hyperoxic-preexposed lungs was accompanied by significant increases in bronchoalveolar lavage (BAL) protein, BAL granulocytes, BAL thromboxane and prostacyclin levels, perfusate chemotactic activity, and lung lipid peroxidation. These findings suggest that the synergistic interaction between hyperoxia and granulocytes in producing acute lung injury involves a primary effect of hyperoxia on the lung itself.
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PMID:Mechanisms of interaction between oxygen and granulocytes in hyperoxic lung injury. 383 44

Eight rat lungs were perfused in an in vitro circuit with a blood-PS solution and then with a perfluorocarbon emulsion (perfluorotributylamine, FC-43). With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes in pulmonary artery pressure when F1,O2 was changed to 0.1, 0.06, 0.04, 0.03, 0.02 and zero with FI,CO2 of 0.05. The hypoxic response to an FI,O2 of 0.03, with the blood-PSS perfusate, was an increase from baseline pressure of 93.5 +/- 18% and, with the perfluorocarbon perfusate was 67.5 +/- 18%; these values were not significantly different (P greater than 0.2). A stimulus-response relationship was obtained with the FC-43 perfusate by plotting the response as a percentage of the maximum response (R%max) against the logarithm of the alveolar oxygen tension. The equation for the linear portion of the response was R%max = 257.9-140.2 X log (10) PA,O2 and r = 0.78. The PA,O2 corresponding to half of the maximum response (ED50) was 30.4 mmHg. The present study demonstrated that HPV is maintained in isolated rat lungs perfused with an FC-43 emulsion. The stimulus-response relationship as well as the ED50 with the FC-43 is similar to earlier results with blood perfusate. Lung oedema was not found after perfusion with the FC-43 emulsion.
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PMID:Hypoxic pulmonary vasoconstriction in isolated rat lungs perfused with perfluorocarbon emulsion. 406 Nov 15

Little is known of the effect of chronic renal failure (CRF) on ventilatory regulation. In 38 subjects (19 healthy, 19 with CRF before and after dialysis), we performed measurements of ventilation (VE) and occlusion pressure (P0.1) while the subjects were breathing air and hypercapnic gas mixtures. The results have shown that (1) during air ventilation, CRF patients exhibited lower values of VE and P0.1, which returned to normal after dialysis; (2) during hypercapnic ventilation, CRF patients had the same response as healthy subjects for VE but higher P0.1; hemodialysis induced an upward shift of the CO2 response curve in CRF patients. A twofold mechanism is probably involved: pulmonary edema, which reduces lung elasticity, and neuromuscular hypoexcitability, both implying a stronger central command.
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PMID:Ventilatory and occlusion pressure responses to hypercapnia in patients with chronic renal failure. 643 71

We studied a 58-year-old woman during an acute episode of cardiac pulmonary edema complicated by carbon dioxide (CO2) retention. As pulmonary wedge pressure became greater, metabolic production of CO2 increased by 38 ml/min and minute ventilation by 1.53 L; by contrast, alveolar ventilation remained unchanged due to a concomitant rise in physiologic dead space and, as a result, arterial CO2 tension increased up to 61 mm Hg. With treatment, all these variables returned to baseline values. Subsequent measurement of mouth occlusion pressure (p 0.1) during a CO2 rebreathing trial showed that neuromuscular inspiratory drive response to CO2 was preserved, but that ventilatory response was markedly reduced, presumably because of the severe restrictive and obstructive ventilatory defect and of the loss of inspiratory muscle force demonstrated in the patient. We conclude that CO2 retention in cardiac pulmonary edema involves a combination of: (1) increased CO2 production, (2) rise in physiologic dead space, and (3) severe respiratory mechanical impairment.
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PMID:The mechanism of CO2 retention in cardiac pulmonary edema. 643 53

Lung prostaglandins (PGs) play a key role in normal pulmonary vascular regulation. We investigated PG metabolism during edema formation following paraquat-induced damage with an isolated perfused rat lung preparation. Lungs perfused with paraquat (PQ), 1 X 10(-7) M to 1 X 10(-2) M, showed significant increases in PGF2 alpha prior to detectable functional and pathological changes (increases in airway resistance, vascular resistance, and edema). No changes in PGE were observed. PGF2 alpha in perfused lungs showed a dose-related response following PQ exposure (up to 300% increase over control values). Lungs perfused with PQ and ventilated with high oxygen (95% O2-5% CO2) instead of air-5% CO2 showed a dramatic potentiation in the selective increase of PGF2 alpha, with levels reaching over 1 ng/ml (a 2600% increase over control values). The addition of exogenous PGF2 alpha to the perfusate without PQ initiated edema in a dose-related fashion, indicating the potential of PGF2 alpha as a causative agent in lung edema formation from PQ injury. The addition of ibuprofen (a nonsteroidal anti-inflammatory agent) to the perfusion medium blocked endogenous release of PGF2 alpha in lungs linked to oxidant-induced edema. These data show that in the perfused lung: (1) PQ caused a selective increase of PGF2 alpha; (2) this selective increase occurred prior to the onset of edema; (3) exogenous PGF2 alpha alone induced pulmonary edema; and (4) ibuprofen, in doses which blocked PGF2 alpha, also prevented edema formation.
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PMID:Selective action of prostaglandin F2 alpha during paraquat-induced pulmonary edema in the perfused lung. 657 98

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

Utilizing a fluid percussion device, we measured the physiological effects of brain trauma in cats exposed to controlled levels of injury. Concussive brain injury at 3-4 atm of intensity led to profound elevations of the mean systemic arterial blood pressure from 128 +/- 26 to 229 +/- 33 mmHg, left ventricular end-diastolic pressure from 4 +/- 2 to 24 +/- 15 mmHg, and pulmonary wedge pressures (PWP) from 5 +/- 3 to 27 +/- 17 mmHg and a relatively moderate increase in intracranial pressure (ICP) from 6 +/- 3 to 38 +/- 31 mmHg (all P < 0.001). Pulmonary edema was evidenced by a significant increase in lung tissue wet-to-dry weight ratios to 3.74 +/- 0.81 as compared with a control group of 2.29 +/- 0.23 (P < 0.001). There was poor correlation between wet-to-dry weight ratios and PWP. Approximately 60% of all spontaneously breathing animals become permanently apneic within 6 min after injury, while the remaining 40% developed transient apnea. Arterial O2 or CO2 pressure alterations, in contrast to pretreatment with phentolamine did not affect the hemodynamic or edemogenic response to trauma. Phentolamine did not block the apneic response or increase in ICP. Comparative studies using intravenous levarterenol without trauma produced responses similar to trauma. Concussive brain injury of 3-4 atm results in pulmonary edema, apnea, sympathetically mediated peripheral vasoconstriction and left ventricular failure effect.
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PMID:Physiological effects of controlled concussive brain trauma. 677 80

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.
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PMID:Ventilatory response in patients with acute lactic acidosis. 680 Jul 2


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