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Effects of pulmonary edema on regional blood volume and red blood cell transit time. Comparison of high pressure and oleic acid-induced edema.

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The present study was designed to determine the effects of pulmonary vascular pressure, vascular injury, and pulmonary edema on regional blood volume (Vr) and regional red blood cell (RBC) transit time (Tr) in the lung. The experiments were carried out in 15 dogs. Six served as controls, six had

Does indomethacin affect shunt and its response to PEEP in oleic acid pulmonary edema?

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We assessed hemodynamics, lobar perfusion, and shunts at base line 1.5 h after unilobar oleic acid edema, 15 min after indomethacin (10 mg/kg iv), and 15 min after positive end-expiratory pressure (PEEP) (10 cm) in 10 dogs. In 10 additional dogs (control) the same measurements were made but no

Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.

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The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and

Alveolar surface area-to-lung volume ratio in oleic acid-induced pulmonary edema.

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It is unknown how the in vivo alveolar surface area-to-volume ratio (S/V) changes in low-pressure pulmonary edema. Here, the S/V is the area of the air-tissue interface per unit total volume (air plus tissue). We hypothesized that in oleic acid (OA)-induced edema inactivation of the pulmonary

Effects of inhaled prostacyclin as compared with inhaled nitric oxide in a canine model of pulmonary microembolism and oleic acid edema.

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OBJECTIVE Recently, it has been shown that the inhalation of nitric oxide (NO) and of prostacyclin (PGI2) elicits selective pulmonary vasodilation in a canine model of pulmonary hypertension induced by hypoxic pulmonary vasoconstriction. The present study was designed to investigate whether inhaled

Comparison of venous admixture during high-frequency ventilation and conventional ventilation in oleic acid-induced pulmonary edema in dogs.

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High-frequency jet ventilation (HFJV) was compared with conventional ventilation ventilation during oleic acid-induced pulmonary edema in dogs. HFJV, when combined with positive end-expiratory pressure (PEEP), returned arterial PO2 (PAO2) and venous admixture to preoleic acid levels, even with tidal

Dependence of shunt on cardiac output in unilobar oleic acid edema. Distribution of ventilation and perfusion.

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OBJECTIVE In acute respiratory failure, increased cardiac output (Qt) increases shunt (Qs/Qt). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region. METHODS Oleic acid edema was induced in

[Effects of continuous negative extrathoracic pressure ventilation (CNETPV) on gas exchange and hemodynamics in dogs with oleic-acid-induced pulmonary edema].

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To investigate usefulness of continuous negative extrathoracic pressure ventilation (CNETPV) as a method of respiratory care for pulmonary edema, we compared effects of CNETPV on gas exchange and hemodynamics with those of CPPV in dogs with oleic-acid-induced pulmonary edema. End-expiratory negative

Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis.

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In mammals, oleic acid (OA) induces pulmonary edema (PE), which can initiate acute lung injury (ALI) and lead to acute respiratory distress syndrome (ARDS). Pulmonary surfactant (PS) plays a key role in a broad range of treatments for ARDS. The aim of the present investigation was to assess changes

Respiratory muscle blood flow in oleic acid-induced pulmonary edema.

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If respiratory muscle blood flow (RMBF) demands in pulmonary edema are large enough, an imbalance between supply and demand could lead to respiratory muscle failure. Therefore, to determine the magnitude of RMBF in this condition we produced pulmonary edema by injecting oleic acid into the pulmonary

Catalase pretreatment attenuates oleic acid-induced edema in isolated rabbit lung.

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Because reactive O2 metabolites have been demonstrated to be potent mediators of vascular dysfunction and are synthesized by lung tissue, their involvement as mediators of oleic acid (OA)-induced pulmonary edema in the isolated Krebs-perfused rabbit lung was assessed. Injection of OA (0.1 ml) into

Cardiovascular and blood gas responses to ketanserin in canine pulmonary edema induced by oleic acid.

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This study was performed to determine the cardiovascular and respiratory effects of ketanserin, a specific 5-HT2 antagonist, following oleic acid lung injury in anesthetized dogs. Following intravenous administration of oleic acid (0.1 ml/kg) to a control group (N = 7), systemic blood pressure

Inhibition of angiotensin-converting enzyme by perindopril diacid in canine oleic acid pulmonary edema.

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To test the hypothesis that angiotensin II could be a mediator of acute lung injury, we studied the effects of perindopril diacid, a new angiotensin-converting enzyme inhibitor, on hemodynamics, blood gases, lung mechanics, and extravascular lung water (EVLW). Twenty-four dogs were anesthetized,

Pulmonary vascular pressure-flow plots in canine oleic acid pulmonary edema. Effects of prostaglandin E1 and nitroprusside.

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We investigated the effects of prostaglandin E1 (PGE1) and of sodium nitroprusside (NP) on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in 24 pentobarbital-anesthetized and ventilated dogs with pulmonary hypertension secondary to oleic acid lung injury. The PAP/Q plots were

Failure of indomethacin to prevent or ameliorate oleic acid pulmonary edema in the dog.

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The possibility that prostaglandin synthesis inhibition might favorably inhibit the development of animal adult respiratory distress syndrome models was investigated in two groups of dogs; one group was pretreated with indomethacin 3 mg/kg. Both groups received oleic acid 0.15 mg/kg. Measurements of

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