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Biomedical subjects

M J Bishop

Publications and source records attributed to M J Bishop.

At least 73 records · Page 4Linked to original sources
PubMed1989

Delivery efficiency of metered dose aerosols given via endotracheal tubes.

The authors studied the efficiency of delivery of the inhaled bronchodilator metaproterenol when delivered via an endotracheal tube (ETT) using a metered dose inhaler (MDI). They found that the percentage of drug exiting the ETT varied with tube size, ranging from 3.0 +/- 1.9 for a 6.0 mm ETT to 6.5 +/- 4.4 for a 9.0 mm ETT (mean +/- SEM, P less than 0.05). The efficiency of delivery was also affected by whether the MDI was activated before or after initiation of gas flow through the ETT, with activation into a flowing stream significantly more efficient. The authors conclude that an MDI can deliver a dose of drug to the trachea, but delivery efficiency is lower than reported for MDI delivery in spontaneously breathing patients.

Administration, Inhalation↗
PubMed1989

Regional alveolar hypoxia does not affect air embolism-induced pulmonary edema.

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema resulting from venous air embolization. Anesthetized dogs had the left upper lobe removed and a double-lumen tube placed so that right lung and left lower lobe (LLL) could be ventilated independently. Air was infused into the femoral vein for 1 h during bilateral ventilation at an inspiratory O2 fraction (FIO2) of 1.0. After cessation of air infusion the LLL was then ventilated with a hypoxic gas mixture (FIO2 = 0.05) in six animals and an FIO2 of 1.0 in six other animals. Lung hydroxyproline content was measured as an index of lung dry weight. LLL bloodless lobar wet weight-to-hydroxyproline ratio was 0.33 +/- 0.06 mg/micrograms in the animals exposed to LLL hypoxia and 0.37 +/- 0.03 mg/micrograms (NS) in the animals that had a LLL FIO2 of 1. Both values were significantly higher than our laboratory normal values of 0.19 +/- 0.01 mg/micrograms. We subsequently found in four more dogs exposed to global alveolar hypoxia before and after air embolism that the air injury itself significantly depressed the hypoxic vasoconstrictor response. We conclude that regional alveolar hypoxia has no effect on pulmonary edema formation due to air embolism. The most likely reason for these findings is that the air embolism injury itself interfered with hypoxic pulmonary vasoconstriction.

Animals↗
PubMed1989

Lack of alveolar O2 during lung reperfusion does not decrease edema formation.

We previously reported that pulmonary arterial occlusion for 48 h followed by 4 h of reperfusion in awake dogs results in marked edema and inflammatory infiltrates in both reperfused and contralateral lungs (Am. Rev. Respir. Dis. 134: 752-756, 1986; J. Appl. Physiol. 63: 942-950, 1987). In this experiment we study the effects of alveolar hypoxia on this injury. Anesthetized dogs underwent thoracotomy and occlusion of the left pulmonary artery. Twenty-four hours later the dogs were reanesthetized, and a double-lumen endotracheal tube was placed. The right lung was continuously ventilated with an inspiratory O2 fraction (FIO2) of 0.35. In seven study animals the left lung was ventilated with an FIO2 of 0 for 3 h after the left pulmonary artery occluder was removed. In six control animals the left lung was ventilated with an FIO2 of 0.35 during the same reperfusion period. Postmortem bloodless wet-to-dry weight ratios were 5.87 +/- 0.20 for the left lower lobe and 5.32 +/- 0.12 for the right lower lobe in the dogs with hypoxic ventilation (P less than 0.05 for right vs. left lobes). These values were not significantly different from the control dog lung values of 5.94 +/- 0.22 for the left lower lobe and 5.11 +/- 0.07 for the right lower lobe (P less than 0.05 for right vs. left lobes). All values were significantly higher than our laboratory normal of 4.71 +/- 0.06. We conclude that reperfusion injury is unaffected by alveolar hypoxia during the reperfusion phase.

Animals↗
PubMed1988

Dimethylthiourea does not ameliorate reperfusion lung injury in dogs or rabbits.

We previously demonstrated that in vivo reperfusion of a dog lung after 48 h of pulmonary arterial (PA) ischemia results in pulmonary edema with a significant infiltrate of polymorphonuclear leukocytes. We hypothesized that the injury resulted from production of hydroxyl radical by activated neutrophils. In the current study, we attempted to prevent the injury in both dogs and rabbits with dimethylthiourea (DMTU), a scavenger of hydroxyl radical. After 48 h of left PA occlusion in 18 dogs, DMTU was administered to 9 animals and 9 were not treated. The occlusion was then released, and the dogs were killed 4 h later. Reperfusion resulted in a drop in leukocyte count and left lung edema, but there was no difference between treated and untreated animals. The wet-to-dry ratios of the lungs in the treated group were 5.76 +/- 0.44 (SE) on the reperfused left side and 4.50 +/- 0.06 (P less than 0.05) on the right side. In the untreated groups the comparable ratios were 5.73 +/- 0.31 and 4.92 +/- 0.10 (P less than 0.05 for right vs. left). Histological examination revealed significant differences between the right and left lungs in the extent of intra-alveolar granulocytes and macrophages but did not reveal differences between the treated and untreated animals. To ensure that neither the model nor the lack of response to DMTU was species specific, we then developed a rabbit model of reperfusion edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Hypoxic pulmonary vasoconstriction does not affect hydrostatic pulmonary edema formation.

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.

Blood Pressure↗
PubMed1987

Effect of regional alveolar hypoxia on permeability pulmonary edema formation in dogs.

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.

Animals↗
PubMed1987

Lung reperfusion in dogs causes bilateral lung injury.

Occlusion of the pulmonary arterial circulation to a lung for prolonged periods has been reported to result in only minimal alterations in lung morphology. We studied the effects of 48 h of pulmonary arterial occlusion followed by 4 h of reperfusion in 18 awake dogs. Because of evidence in other organ systems of O2 radical generation, during reperfusion, nine of the animals were randomly assigned to receive allopurinol, a xanthine oxidase inhibitor, and vitamin E, an antioxidant. Reperfusion resulted in marked edema and inflammatory infiltrates in the reperfused lung but also caused mild edema and inflammation in the contralateral continuously perfused lung. Electron microscopy demonstrated lysis of both capillary endothelial and alveolar epithelial cells bilaterally, with the frequency of cell injury greater on the reperfused side. During reperfusion, body temperatures rose dramatically from 39.4 +/- 0.1 to 40.6 +/- 0.2 degrees C (P less than 0.05) and marked leukopenia developed. There were no differences in any hemodynamic, gas exchange, or morphometric measurements between allopurinol-treated dogs and untreated animals. We conclude that reperfusion causes local and distant injury which does not appear to be mediated by xanthine oxidase-produced O2 radicals.

Allopurinol↗
PubMed1987

Carbon dioxide excretion via bronchopleural fistulas in adult respiratory distress syndrome.

Expired gas and gas leaked via thoracostomy tubes was collected in nine patients with the adult respiratory distress syndrome (ARDS) and bronchopleural fistulas. Mean minute ventilation in the group was 23.9 +/- 7.5 L/min with 31 +/- 23 percent of the gas escaping via the leak. Carbon dioxide was present in the leaked gas in every patient, with the fraction of CO2 excreted via the leak highly correlated with the fraction of minute ventilation exiting via the leak (r = 0.86, p less than 0.005). Mean concentration of CO2 in leaked gas was 1.3 +/- 0.5 percent. We conclude that some of the gas leaked via a bronchopleural fistula in such patients participated in gas exchange.

Barotrauma↗
PubMed1987

Comparison of high-frequency jet ventilation with conventional mechanical ventilation for bronchopleural fistula.

In seven patients with acute respiratory failure and a bronchopleural fistula, the authors compared gas exchange and volume of gas lost via the chest tube during conventional mechanical ventilation (CV) and high-frequency jet ventilation (HFJV). After the initial comparison, patients were randomized to HFJV or CV, unless one mode of ventilation was clearly superior based on preestablished criteria. In six of the seven patients, oxygenation deteriorated after the switch from CV to HFJV. The ratio of PaCO2 to FI02 declined from 227 +/- 167 to 133 +/- 100 (mean +/- SD, P less than 0.05), and the PaCO2 increased from 47 +/- 13 to 56 +/- 18 mm Hg (P less than 0.05). The mean chest tube leak did not change significantly. Randomization of the mode of ventilation was not performed in any patient because CV was superior by a priori criteria. We conclude that when acute respiratory failure is complicated by a bronchopleural fistula, HFJV with mean airway pressures comparable to those provided during conventional ventilation does not provide satisfactory gas exchange.

Acute Disease↗
PubMed1986

Maximum likelihood alignment of DNA sequences.

The optimal alignment problem for pairs of molecular sequences under a probabilistic model of evolutionary change is equivalent to the problem of estimating the maximum likelihood time required to transform one sequence to the other. When this time has been estimated, various alignments of high posterior probability may be written down. A simple model with two parameters is presented and a method is described by which the likelihood may be computed. Maximum likelihood estimates for some pairs of tRNA genes illustrate the method and allow us to obtain the best alignments under the model.

Animals↗
PubMed1986

Effects of lobar pulmonary blood flow on the evolution of oleic acid lung injury in dogs.

We studied the effects of interruption of the pulmonary blood flow to the left diaphragmatic lung lobe on the evolution of canine oleic acid lung injury. We compared the morphology and edema of the left diaphragmatic lobe, whose pulmonary artery was ligated immediately after oleic acid injury, with the right diaphragmatic lobe, in which the blood supply was intact. The injury plus ligation resulted in hypoxemia and pulmonary hypertension with PaO2 falling from 98 +/- 4 to 72 +/- 21 torr (P less than 0.05) and pulmonary artery pressure increasing from 11 +/- 3 to 18 +/- 4 mm Hg (P less than 0.05). Animals were sacrificed 48 hr following the injury. Morphological examination of right and left lobes showed no consistent differences although wet/dry ratios indicated significantly greater edema (P less than 0.01) for the right diaphragmatic lobes (7.66 +/- 1.23) than the left (6.80 +/- 0.59). Both right and left lobes were substantially more edematous than our laboratory normal value of 4.74 +/- 0.54 (P less than 0.001 for both). We conclude that interruption of pulmonary arterial blood flow protects against edema formation in oleic acid injury but does not alter the morphologic evolution of the injury.

Animals↗
PubMed1986

Vasodilators worsen gas exchange in dog oleic-acid lung injury.

The authors studied the effects of vasodilator treatment with either hydralazine or minoxidil on gas exchange and lung water accumulation over a 5-h period in canine oleic acid-induced pulmonary edema. Thirty dogs were given intravenous oleic acid 1 day prior to study to produce a stable, diffuse lung injury. On the day of study, one group of animals was given minoxidil, a potent systemic and pulmonary vasodilator. A second group was given hydralazine, a potent systemic vasodilator but weak pulmonary vasodilator, and a third group was not treated. Hemodynamic and gas exchange variables were assessed prior to treatment, and again after 5 h of treatment. Both drugs caused an increase in cardiac output and a decrease in peripheral vascular resistance. Minoxidil increased venous admixture from 17 +/- 4 to 55 +/- 6% (P less than 0.05), whereas hydralazine-treated dogs had a smaller increase, from 26 +/- 5 to 47 +/- 6% (P less than 0.05), and untreated animals did not show a significant change. Lung water increased 27 +/- 12% in the untreated animals over the course of the study, 43 +/- 18% in the hydralazine animals, and 60 +/- 16% (P less than 0.05 vs. untreated) in the minoxidil animals. The authors conclude that adverse effects may result from peripheral vasodilators in animals with permeability pulmonary edema, but the extent and severity of these effects may vary, depending on the drugs' effects on the pulmonary circulation.

Animals↗
PubMed1986

Reperfusion of ischemic dog lung results in fever, leukopenia, and lung edema.

Pulmonary artery obstruction results in minimal parenchymal abnormalities in normal lung and diminishes edema formation in dog lungs injured by oleic acid. We tested the hypothesis that reperfusion of ischemic regions would result in significant injury in normal lung and would ablate the protective effect of ischemia in oleic acid injury. The pulmonary artery of the left diaphragmatic lobe was occluded for 48 h in 12 oleic-acid-injured and 10 normal animals. Observations made immediately before reperfusion and for 4 h after reperfusion in the awake dogs indicated that reperfusion resulted in systemic abnormalities in both groups of animals, including a rise in temperature, a fall in cardiac output, and a marked drop in circulating leukocytes. In uninjured animals, the reperfused lobe demonstrated an elevated wet-to-dry weight ratio of 5.70 +/- 0.13 compared with 4.42 +/- 0.06 for the right diaphragmatic lobe (p less than 0.05). Histologic examination revealed edema and white cell infiltrates in the alveoli of the reperfused lobe in uninjured animals. In injured animals, there was no difference in either wet-to-dry ratios or morphologic aspects between the lobes. The results demonstrate both a local and systemic toxic effect of reperfusion in normal animals and ablation of the partial protective effect of pulmonary artery occlusion in oleic-acid-injured animals.

Animals↗