The American review of respiratory disease
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Am. Rev. Respir. Dis. · Aug 1988
Attenuation of acute lung injury in septic guinea pigs by pentoxifylline.
Pentoxifylline (PTXF), a drug demonstrated to improve intermittent claudication, is a methylxanthine that increases intracellular cyclic AMP (cAMP) and, unlike theophylline, has few side effects. Because increased cAMP levels have been associated with a decrease in lung injury, we examined the effects of PTXF on acute lung injury in a septic guinea pig model. Five groups of guinea pigs were studied over a period of 8 h. (Group I: saline control injected intravenously with 2 ml of saline; Group II: septic control injected intravenously with 2 x 10(9) Escherichia coli; Group III: E. coli septicemia plus PTXF bolus 20 mg/kg injected 5 min before E. coli injection; Group IV: E. coli septicemia plus PTXF continuous infusion, begun with bolus [20 mg/kg] followed by continuous infusion [20 mg/kg/h] started 60 min before injection of E. coli; Group V: PTXF continuous infusion [20 mg/kg/h] control). ⋯ Lung water (wet-to-dry ratio), the concentration ratio of 125I-labeled albumin in bronchoalveolar lavage (BAL) fluid to that in plasma (albumin index; AI), total cell count in BAL fluid, thiobarbituric-acid-reactive material (TBARM), and the lysosomal enzyme beta-glucuronidase (beta-G) were examined. Lung tissue was studied histologically to assess neutrophil accumulation. Our results showed that E. coli septicemia caused significant peripheral neutropenia and histopathologic evidence of neutrophil alveolitis associated with an increased ratio of TBARM and beta-G in BAL fluid as compared with those in plasma (TBARM BAL ratio and beta-G BAL ratio).(ABSTRACT TRUNCATED AT 250 WORDS)
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Am. Rev. Respir. Dis. · Aug 1988
Respiratory mechanics during the first day of mechanical ventilation in patients with pulmonary edema and chronic airway obstruction.
We investigated the early changes of respiratory mechanics in mechanically ventilated patients with acute respiratory failure (ARF): 8 patients after acute exacerbation of chronic airway obstruction (CAO), 8 patients with cardiogenic pulmonary edema (CPE), and 8 patients with adult respiratory distress syndrome (ARDS). The patients were studied within the first day from the onset of mechanical ventilation. ⋯ We found that: (1) acute exacerbation of CAO was characterized by high respiratory resistance (reflecting in part time-constant inequalities within the lung) and severe pulmonary hyperinflation, with "intrinsic" PEEP (PEEPi) up to 22 cm H2O (mean [SD], 13.5 [6.7] cm H2O); (2) PEEPi, even if not high, was present in almost all patients with pulmonary edema, averaging 3.8 and 3.0 cm H2O in ARDS and CPE, respectively; (3) respiratory resistance was increased in patients with CPE and ARDS who had no history of airway disease; (4) patients with ARDS were characterized also by low compliance (mean [SD], 0.035 [0.005] L/cm H2O) and high resistance, the latter also reflecting a substantial component caused by time-constant inequalities; (5) in all 24 patients, static respiratory compliance (and its reciprocal, elastance) was significantly correlated with the pulmonary oxygenation index, i.e., the PaO2/PAO2 ratio. We conclude that early assessment of respiratory mechanics in mechanically ventilated patients with ARF can provide better understanding of the patients' conditions as well as guidelines for therapeutic approach and weaning attempts.
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Am. Rev. Respir. Dis. · Aug 1988
Pulmonary vascular pressure-flow plots in canine oleic acid pulmonary edema. Effects of prostaglandin E1 and nitroprusside.
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 rectilinear in all experimental conditions. In control dogs (n = 8), PAP was increased over the entire range of Q studied, from 1 to 4 L/min.m2, 90 min after oleic acid 0.09 ml/kg, and remained so during 2 consecutive 5-point PAP/Q plots, each of them being constructed in about 30 min. ⋯ Systemic blood pressure was decreased by 21% after PGE1 and by 24% after NP. Neither drug affected Q nor blood gases after oleic acid. The results suggest that pulmonary hypertension secondary to oleic acid pulmonary edema may be due more to an increase in effective outflow pressure of the pulmonary circulation than to an increase in incremental vascular resistance, and that active vasoconstriction contributes to this type of pulmonary hypertension.