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Biomedical subjects

F W Cheney

Publications and source records attributed to F W Cheney.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1989

Effect of regional alveolar hypoxia on gas exchange in dogs.

We studied the effects of left lower lobe (LLL) alveolar hypoxia on pulmonary gas exchange in anesthetized dogs using the multiple inert gas elimination technique (MIGET). The left upper lobe was removed, and a bronchial divider was placed. The right lung (RL) was continuously ventilated with 100% O2, and the LLL was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Whole lung and individual LLL and RL ventilation-perfusion (VA/Q) distributions were determined. LLL hypoxia reduced LLL blood flow and increased the perfusion-related indexes of VA/Q heterogeneity, such as the log standard deviation of the perfusion distribution (log SDQ), the retention component of the arterial-alveolar difference area [R(a-A)D], and the retention dispersion index (DISPR*) of the LLL. LLL hypoxia increased blood flow to the RL and reduced the VA/Q heterogeneity of the RL, indicated by significant reductions in log SDQ, R(a-A)D, and DISPR*. In contrast, LLL hypoxia had little effect on gas exchange of the lung when evaluated as a whole. We conclude that flow diversion induced by regional alveolar hypoxia preserves matching of ventilation to perfusion in the whole lung by increasing gas exchange heterogeneity of the hypoxic region and reducing heterogeneity in the normoxic lung.

Animals↗
PubMed1988

Peer reviewer agreement for major anesthetic mishaps.

In a study of peer reviewer agreement for major anesthetic mishaps, 42 anesthesiologists performed a standardized peer review of 48 reports of anesthetic mishaps obtained from a national data base. The peer review group exhibited agreement (P less than 0.0001) for judgments on the appropriateness of clinical care, the presence or absence of human error, and the role of better monitoring in prevention of the mishap. Personal attributes of the reviewers (eg, type of practice, length of time in practice, and previous experience with mishap review) did not appear to influence agreement. The study findings suggest a highly favorable environment for the development of broadly recognized standards of care in anesthesiology.

Anesthesia↗
PubMed1988

Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors.

Fourteen cases of sudden cardiac arrest in healthy patients who received spinal anesthesia were discovered in a preliminary review of 900 closed insurance claims for major anesthetic mishaps. All patients were resuscitated from the intraoperative cardiac arrest, but six suffered such severe neurologic injury that they died in hospital. Of the eight survivors, only one exhibited sufficient neurologic recovery to allow independence in daily self-care. In view of the unexpected nature of the cardiac arrests, as well as the ultimate severity of injury, these cases were analyzed in detail to determine whether there were recurring patterns of management that may have contributed to the occurrence or outcome of these anesthetic mishaps. Two patterns were identified. The first was the intraoperative use of sufficient sedation to produce a comfortable-appearing, sleep-like state in which there was no spontaneous verbalization. Cyanosis frequently heralded the onset of cardiac arrest in patients exhibiting this degree of sedation, suggesting that unappreciated respiratory insufficiency may have played an important role. The second pattern appeared to be an inadequate appreciation of the interaction between sympathetic blockade during high spinal anesthesia and the mechanisms of cardiopulmonary resuscitation. Prompt augmentation of central venous filing through the use of a potent alpha-agonist and positional change might have improved organ perfusion, shortened the duration of cardiac arrest, and lessened the degree of neurologic damage.

Adult↗
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

Anaesthesia and the law: the North American experience.

The professional liability climate in the United States can best be described as tempestuous in most areas of the U.S. The major strategy of organized anaesthesia and the professional liability insurance industry is to attempt to reduce patient injury. In the unlikely eventuality that human error and equipment failure in anaesthesia can be eradicated, some patient injury will inevitably still occur. For this reason tort reform is necessary, and alternatives to the tort system need to be developed to compensate injured parties adequately without bankrupting the medical system.

Anesthesiology↗
PubMed1987

Effects of breathing 80% oxygen on water and albumin accumulation in oleic acid-injured rabbit lungs.

This study was done to determine whether breathing 80% oxygen would enhance edema formation in oleic acid (OA) lung injury. Rabbits breathed air (n = 51) or 80% oxygen (n = 51) for 1 to 7 days after OA lung injury (0.09 ml/kg iv). Control groups breathed 80% oxygen (n = 37) or room air (n = 8) without OA injury. Pulmonary vascular permeability was assessed by measuring 131I-albumin (RISA) concentration in extravascular, extracellular lung water (EVECW) relative to plasma (RISAL/RISAPL). EVECW (ml/g dry lung) was measured by 24Na, and total lung water (TLW) by wet/dry weight (g/g dry lung). Air-breathing control values were 4.53 +/- 0.25 (SD) for TLW and 0.40 +/- 0.09 for RISAL/RISAPL. In the air-breathing OA group, TLW and RISAL/RISAPL increased to 8.32 +/- 0.85 and 0.93 +/- 0.16, respectively, 2 h after OA (p less than .001) but by 24 h, were equal to air-breathing controls. TLW and RISAL/RISAPL in the oxygen treated OA group did not differ from the air breathing OA group on days 2 through 7 inclusive, suggesting that 80% oxygen had no effect on edema formation in the OA-injured lung. Breathing 80% oxygen alone, without OA injury, significantly (p less than .005) increased TLW and RISAL/RISAPL on days 5 and 6. Thus, preexisting lung injury had a protective effect against edema formation from a high fraction of inspired oxygen.

Albumins↗
PubMed1987

Hemodynamic effects of rapidly evacuating prolonged pneumothorax in rabbits.

Clinical observations suggest that systemic hypotension may be caused by rapid evacuation of persistent pneumothorax. This observation has not been substantiated experimentally and the mechanism(s) are unknown. In this study, we measured systemic hemodynamic parameters in rabbits before and for 2 h during negative pressure evacuation of a right-sided pneumothorax of 7-9 days duration. Three groups of animals were studied: 10 rabbits breathed room air and were hypoxemic during pneumothorax (hypoxemic pneumothorax = HP); 10 rabbits breathed 40% O2-60% N2, which prevented arterial hypoxemia during pneumothorax (supraoxemic pneumothorax = SP); seven normal control animals were untreated during this time period (NC). Pneumothoraces in HP and SP were evacuated by negative pressure applied to the right pleural space for 2 h while animals were anesthetized and mechanically ventilated. The NC group was anesthetized and ventilated without prior pneumothorax. Serial hemodynamic measurements were made before and during pleural suction.(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

Effect of spontaneous sighs on arterial oxygenation during isoflurane anesthesia in humans.

The presence, frequency, and volume of spontaneous sighs was evaluated in 21 (ASA 1-2) supine patients aged 44 +/- 15.2 (SD) yr, during isoflurane-nitrous oxide anesthesia. Before induction the inspiratory capacity of each patient was determined. After induction of anesthesia and tracheal intubation patients breathed spontaneously except for three manual inflations to each patient's predetermined inspiratory capacity at the beginning and end of surgery. Arterial blood gas tensions were measured before and 5 min after each set of mechanical deep breaths and each hour during surgery, the mean duration of which was 2 +/- 0.09 hr. Spontaneous sighs occurred in 13 of 21 patients. The average frequency was 6 +/- 4 sighs/hr. At FIO2 = 0.5, nonsighing patients had an initial PaO2 of 229 +/- 59 mm Hg and sighers had an initial PaO2 of 162 +/- 57 mm Hg (P less than 0.05). Arterial oxygen did not change in sighing patients during the course of surgery, while in nonsighing patients the PaO2 decreased from the initial value of 229 +/- 60 mm Hg to 170 +/- 63 mm Hg (P less than 0.05). Mechanical deep breaths administered at the end of surgery produced no improvement in oxygenation in either sighers or nonsighers. The presence or absence of sighs did not correlate with PaO2 or PACO2. Though the results suggest that spontaneous sighs in some patients may function to help maintain arterial oxygenation, all patients maintained their PaO2 while breathing spontaneously under general anesthesia in the supine position.

Adult↗
PubMed1986

Effect of furosemide on fully established low pressure pulmonary edema.

It has been shown that furosemide, via nondiuretic vascular effects, reduces pulmonary shunt and lung water during the development of oleic acid permeability edema. We studied this effect in a fully established stable model of oleic acid permeability edema. Sixteen anesthetized mongrel dogs, mechanically ventilated with a FIO2 of 0.5, were studied 24 hr after induction of pulmonary capillary leak by intravenous oleic acid (0.06 cc/kg). After stabilization of pulmonary capillary wedge pressure (PCWP) in the range of 0.5-3 mm Hg, bilateral ureteral ligation was performed. Furosemide (2 mg/kg) was then administered intravenously to eight dogs (treated group). An equivalent volume of saline was given to eight control dogs (control group). Pulmonary artery (PAP) and capillary wedge pressures (PCWP), thermodilution cardiac output (Qt), thermal dye lung water (LW), venous admixture (Qva/Qt), arterial and mixed venous blood gases (PaO2, MVO2) were then measured at hourly intervals for 4 hr. During this period of time, central hemodynamics (PCWP, PAP, Qt) remained stable in both groups. Indices of gas exchange and edema formation (Qva/Qt, LW, PaO2) did not change significantly in either control or treated animals. We conclude that furosemide, previously shown to reduce pulmonary shunt and lung water in the early phase of oleic acid permeability edema, does not have any effect once the pulmonary injury is well-established.

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

Extracellular fluid volume during pneumothorax and hypoxemia in rabbits.

This study was designed to test the hypothesis that persistent pneumothorax of greater than or equal to 6 days duration causes a decrease of extracellular fluid volume (ECF). Such changes are of interest as they may be causally related to persistent hypotension that has occurred in humans following pneumothorax evacuation. Experiments were done in rabbits to determine the effect on ECF of persistent pneumothorax with or without systemic hypoxemia. Animals were divided into four treatment groups: 1) pneumothorax with hypoxemia [fractional concentration of O2 in inspired gas (FIO2) = 0.21, n = 30], 2) pneumothorax without hypoxemia (FIO2 = 0.40, n = 25), 3) hypoxemia alone (FIO2 = 0.14, n = 11), and 4) normal controls (FIO2 = 0.21, n = 15). Measurements of ECF were made in the base-line control state and after 6 days of treatment using the dilution volume of thiocyanate sodium as an estimate of ECF volume. We found a reduction of ECF in 53% of animals with pneumothorax plus hypoxemia (range -47% to +13%) and in 54% of animals with hypoxemia alone (range -26% to +25%). ECF declined in only 7% of normal controls and 20% of animals with pneumothorax without hypoxemia. Arterial O2 tensions after 6 days of treatment were 58 +/- 12.6, 141 +/- 28, 60 +/- 5.1, and 97 +/- 9.3 Torr (mean +/- SD) in groups 1-4, respectively. The results suggest that pneumothorax with hypoxemia or hypoxemia alone may contribute to depletion of ECF, but this response is variable and unpredictable in individual animals.

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↗