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Biomedical subjects

F W Cheney

Publications and source records attributed to F W Cheney.

At least 73 records · Page 4Linked to original sources
PubMed1986

Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax.

Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and anuria after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure, disseminated intravascular coagulation, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.

Adult↗
PubMed1985

Endogenous plasma proteins in edematous lungs and alveolar fluid in rabbits.

In this study, we compared two methods of differentiating hydrostatic and permeability types of pulmonary edema. The first method entailed measurement of protein concentrations directly in samples of alveolar fluid (AF); the second method was an indirect technique in which protein concentration in extravascular extracellular water (EVECW) was calculated on the basis of separate measurements of the quantity of protein in the lung and the volume of EVECW. The concentration of albumin (Alb) and gamma-G-globulin was measured in EVECW and alveolar fluid in excised edematous rabbit lungs. Edema was caused by elevation of left ventricular end-diastolic pressure to 25 Torr (hydrostatic edema, HE) or by intravenous oleic acid, 0.09 ml/kg (permeability edema, PE). The volume of distribution of Na+ was utilized as a measure of EVECW in the lung. Protein concentration in EVECW and AF relative to plasma (EV/PL and AF/PL, respectively) was compared in the two types of edema. The EV/PL was 0.61 +/- 0.12 (SD) for Alb in He compared with 1.18 +/- 0.47 in PE (P less than 0.02). The AF/PL was 0.54 +/- 0.12 and 1.25 +/- 0.33 in HE and PE, respectively (P less than 0.001). There was good correlation between EV/PL and AF/PL for Alb (r = 0.74, P less than 0.001) but not for gamma-G-globulin. Thus EV/PL for Alb, AF/PL for Alb, and gamma-G-globulin all differentiated hydrostatic from permeability edema.

Animals↗
PubMed1985

Effect of vasodilator treatment on the resolution of oleic acid injury in dogs.

Diffuse pulmonary injury is accompanied by reduction of blood flow to injured areas because of local pulmonary vasoconstriction, vascular thrombosis, and vascular obliteration. To assess whether reduced pulmonary arterial blood flow might produce relative ischemia in injured areas and consequent potentiation of the injury, we studied the effects of vasodilator treatment in a dog model of diffuse alveolar damage. Twenty-five awake dogs with arterial and pulmonary arterial catheters in place were given 0.08 ml/kg oleic acid, a dose that produces a diffuse lung injury that largely resolves over a 1-wk period. Ten of the animals were treated with minoxidil, a potent vasodilator and inhibitor of hypoxic pulmonary vasoconstriction. Observations were made for a total of 96 h. At 24 h, treated animals had lower pulmonary vascular resistance (207 +/- 85 versus 348 +/- 136 dyne X s X cm-5, p less than 0.01) but higher venous admixture (30 +/- 10% versus 18 +/- 12%, p less than 0.05) and thermodilution-measured lung water (17 +/- 8 ml/kg versus 9 +/- 2 ml/kg, p less than 0.05). However, by 96 h, there were no differences between the 2 groups in any measured parameters of hemodynamic status, gas exchange, or histologic examination. We conclude that pulmonary vasodilation increased blood flow to injured areas but did not affect eventual resolution of the injury.

Animals↗
PubMed1984

Reflex responses to positive end-expiratory pressure.

When positive end-expiratory pressure (PEEP) is applied to rabbits there is a large depression of cardiac output. The authors investigated the baroreceptor and lung stretch reflex responses to PEEP in rabbits to determine if reflex responses are important in causing the depression of cardiac output which occurs with PEEP. With PEEP there was a depression of cardiac output and blood pressure, no change in heart rate, and an increase in systemic vascular resistance. The responses to PEEP were similar after vagotomy and after a large dose of atropine, but, after treatment with phenoxybenzamine, blood pressure was lower during PEEP and systemic vascular resistance did not increase. The data suggests that lung stretch response is not an important factor in the cardiovascular response to PEEP in rabbits.

Animals↗
PubMed1984

Pathophysiological patterns of resolution from acute oleic acid lung injury in the dog.

Lungs of mongrel dogs with permanent tracheostomies and implanted systemic pulmonary arterial catheters were injured by intravenous infusion of oleic acid (0.09 mg/kg). Injury resulted in extensive, multifocal, and nonrandomly distributed lung damage. Awake dogs were studied during a control period and 1, 4, and 7 days following injection of oleic acid. Standard gas exchange measurements, the inert gas elimination technique, and subsegmental bronchoalveolar lavage (BAL) were used. Five oleic acid dogs and two saline control dogs were killed after each study period for morphological evaluation. Control dogs did not develop significant gas exchange abnormalities but did have localized inflammatory reactions at the lavage site. The oleic acid dogs developed significant shunt at day 1 with resolution of shunt by day 7. The multifocal sites of oleic acid injury were virtually identical in appearance at a given time interval; they consisted of alveolar cell necrosis with varying amounts of hemorrhagic inflammatory exudation at day 1 followed by a proliferative reparative reaction resulting in substantial restoration of alveolar structure at day 7. BAL showed a suppurative inflammatory response with hemorrhage on day 1 and an increased number of macrophages by day 7. The oleic acid model of acute diffuse lung injury demonstrates several pathophysiological alterations that could be compared with pathomorphological changes during the acute injury phase and during the subsequent reparative phase.

Animals↗
PubMed1984

Effect of hydralazine on cardiac output and venous admixture in experimental lung injury.

The mechanism by which hydralazine increases venous admixture (QVA/QT) in the setting of lung injury was investigated in a canine model of noncardiogenic pulmonary edema. Permeability pulmonary edema was produced by administration of oleic acid, 0.08 ml/kg given intravenously to 9 mongrel dogs. After stabilization of lung injury, hydralazine was administered intravenously in a loading dose of 1 mg/kg and followed by a constant infusion at 0.05 mg/kg/h. To control for the effect of increased cardiac output (QT) on QVA/QT, a balloon catheter was placed in the inferior vena cava, and stepwise inflation of the balloon was used to impede venous return and maintain QT at predrug levels. Prior to inflation of the balloon catheter, administration of hydralazine produced a 51% decrease in total systemic resistance (TSR) and a 23% decrease in mean arterial pressure (Pa). In contrast, pulmonary vascular resistance (PVR) showed no significant change, and mean pulmonary artery pressure (Ppa) increased 47%. Cardiac output increased from 3.4 +/- 0.3 to 5.5 +/- 0.4 L/min (mean +/- SEM; p less than 0.01) after administration of hydralazine, and QVA/QT increased from 23 +/- 7 to 35 +/- 5% (p less than 0.05). Mean arterial oxygen tension (PaO2) showed no significant change. Inflation of the balloon in the inferior vena cava after hydralazine administration reduced QT to 3.1 +/- 0.4 L/min and QVA/QT to 28 +/- 4%. Neither of these values differed significantly from the prehydralazine levels. Similarly, values for Ppa and PVR after hydralazine administration plus balloon inflation did not differ significantly from predrug levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of methylprednisolone on resolution of acid-aspiration pneumonitis.

We studied the effects of methylprednisolone sodium succinate on the pulmonary function of unanesthetized dogs for four days after aspiration of 1.5 to 2.0 mL/kg of 0.1N hydrochloric acid. Methylprednisolone sodium succinate (30 mg/kg) was administered to nine dogs at 2, 8, and 24 hours after acid aspiration. Nine animals were untreated after aspiration and served as controls. Acid aspiration caused significant increases in venous admixture and reductions in Pao2 in both groups of animals. These changes persisted for 96 hours after aspiration. There were no differences in cardiac output, venous admixture, and blood gas values between treated and untreated animals at any time. At death there were no differences between groups in amounts of lung water or histologic characteristics. We concluded that methylprednisolone administered after hydrochloric acid aspiration does not affect resolution of the injury.

Animals↗
PubMed1983

Effects of pulmonary blood flow and mixed venous O2 tension on gas exchange in dogs.

The authors investigated whether the increases in venous admixture and intrapulmonary shunt which occur with increases in cardiac output (Qt) results from an effect mediated by mixed venous PO2 (PVO2) or an effect mediated by the increase in pulmonary blood flow. Using a veno-venous bypass system thay were able to alter PVO2 independent of variations in Qt and vice versa. During room air ventilation of dogs with normal lungs at constant Qt, an increase in PVO2 from 33 +/- 7 (mean +/- SD) to 54 +/- 9 mmHg (P less than 0.05) resulted in a decrease in venous admixture from 22 +/- 11 to 13 +/- 4% (P less than 0.05). During room air ventilation of normal dogs at a constant PVO2, raising Qt from 2.16 +/- .53 to 3.49 +/- 0.91 l/min (P less than 0.05) increased venous admixture from 10 +/- 5 to 16 +/- 5% (P less than 0.05). During oxygen ventilation in these two groups of dogs, changes in PVO2 and Qt had no effect on shunt. During oxygen ventilation of dogs with significant shunts from oleic-acid-induced pulmonary edema, independent increases in either PVO2 or pulmonary blood flow resulted in increased shunt. At constant Ot, an increase in PVO2 from 30 +/- 8 to 52 +/- 3 mmHg (P less than 0.05) resulted in an increase in shunt from 39 +/- 12 to 43 +/- 12% (P less than 0.05). When PVO2 remained constant, increasing Qt from 1.97 pm 0.42 to 3.61 +/- 0.50 l/min (P less than 0.05) resulted in an increase in shunt from 47 +/- 17 to 53 +/- 15% (P less than 0.05). The authors conclude that during oxygen ventilation, normal dogs have shunts which are unaffected by changes in blood flow or PVO2. Increases in pulmonary blood flow increase venous admixture during room air ventilation, while increases in PVO2 decrease venous admixture during air ventilation. In edematous lungs, increases in either PVO2 or pulmonary blood flow increase shunt.

Animals↗
PubMed1983

The effects of prophylactic expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory airway pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome (ARDS) or if it also affects the resolution of their lung injury. The present investigation was performed to determine whether expiratory positive airway pressure (EPAP), a form of PEEP, is prophylactic in preventing the lung injury induced by oleic acid in dogs or in enhancing its resolution. Arterial and mixed venous blood gases and functional residual capacity (FRC) were measured in 14 pairs of mongrel dogs with indwelling catheters and permanent tracheostomies. One member of each pair was treated with 10 cm H2O EPAP through a valve attached to the tracheostomy tube. Both dogs received 0.06 ml/kg oleic acid intravenously at hour 0. Measurements were made at three, 12, and 24 hours, when EPAP was discontinued, and over the next six days. Five dog pairs were sacrificed at 72 hours; the other surviving animals were sacrificed at 168 hours. FRC was higher at three, 12, and 24 hours in dogs receiving EPAP than in the untreated dogs. The arterial oxygen tension (PaO2) was higher and the venous admixture (Qva/Qt) was lower at three and 12 hours in the dogs receiving EPAP than in the untreated dogs. However, after 24 hours, no differences were noted between the two groups in FRC, PaO2, Qav/Qt, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histology. It is concluded that EPAP improves gas exchange during its administration, but has no demonstrable prophylactic effect on the resolution of lung injury in the oleic acid model of human ARDS.

Animals↗
PubMed1983

The effects of hemodilution during pulmonary edema in dogs.

Because of their multiple medical problems, patients with the adult respiratory distress syndrome (ARDS) often develop anemia. In order to determine the effects of a low hemoglobin concentration on gas exchange in such patients, the authors studied the effects of isovolemic hemodilution in the dog oleic acid model of ARDS. Twelve splenectomized dogs with oleic acid-induced pulmonary edema and a consequent venous admixture of 31% +/- 5% (mean +/- SEM) (FIO2 = 0.21) underwent two-stage isovolemic hemodilution with Hetastarch followed by retransfusion of the withdrawn red cells. This resulted in hemoglobin levels at each stage of 12.7 +/- 0.7 g/100 ml, 9.1 +/- 0.6 g/100 ml, 6.5 +/- 0.5 g/100 ml, and 10.1 +/- 0.5 g/100 ml (mean +/- SEM). Oxygen transport fell from 363 +/- 25 ml/kg/min to 219 +/- 17 ml/kg/min (p less than 0.001) at maximum hemodilution during air ventilation and from 383 +/- 79 ml/kg/min to 292 +/- 91 ml/kg/min (p less than 0.001) during oxygen ventilation. Since oxygen consumption remained constant throughout the hemoglobin range studied, decreased hemoglobin resulted in declines in P-VO2. Hemodilution with Hetastarch did not affect intrapulmonary shunt or venous admixture despite the significant increase in cardiac output associated with hemodilution.

Air↗
PubMed1983

Hydralazine does not inhibit canine hypoxic pulmonary vasoconstriction.

Clinical experience with hydralazine has led to conflicting data concerning its effect on the pulmonary vasculature. We studied the effects of hydralazine on the hypoxic pulmonary vasoconstrictor response in 9 dogs challenged with inhalation of 10% oxygen in the presence and absence of hydralazine. Prior to administration of the drug, hypoxia increased cardiac output from 174 +/- 13 to 209 +/- 21 ml/kg/min (p less than 0.05) and pulmonary artery pressure from 9 +/- 1 to 19 +/- 1 mmHg (p less than 0.05). After hydralazine, cardiac output rose during normoxia to 275 +/- 30 and during hypoxia to 305 +/- 34 ml/kg/min (p less than 0.05). Pulmonary artery pressure continued to respond to hypoxia, rising from 11 +/- 1 to 21 +/- 1 mmHg (p less than 0.05) in the presence of hydralazine. Hydralazine reduced pulmonary vascular resistance during normoxia from 173 +/- 14 to 136 +/- 13 dynes X s X cm-5 (p less than 0.05) but even after the drug, pulmonary vascular resistance rose sharply during hypoxia. There was no significant difference in the response to hypoxia of pulmonary artery pressure or pulmonary vascular resistance after hydralazine when compared with that before hydralazine. In a second set of 6 dogs, we repeated these experiments but volume-depleted the dogs after the administration of hydralazine to prevent the passive pulmonary vasodilation that occurs because of the rise in cardiac output with the drug. We again found no inhibition of hypoxic pulmonary vasoconstriction by hydralazine. Finally, we administered sodium nitroprusside to 4 dogs using the same model and found a significant inhibition of hypoxic pulmonary vasoconstriction. Hydralazine, unlike nitroprusside, does not inhibit the pulmonary vascular response to hypoxia.

Animals↗
PubMed1982

Extravascular, extracellular water in rabbit lung using Na and sucrose indicators.

We compared the volume of the pulmonary extravascular, extracellular water space using sodium and sucrose indicators in 8 normal and 11 edematous rabbit lungs by steady-state techniques. The volume of the extravascular, extracellular space (EVECW), expressed in milliliters per gram dry lung, was determined from the volume of distribution of 24Na, [3H]sucrose, or total sodium in 1) supernatant solutions obtained by centrifugation of homogenized lung or 2) intact lung fragments. There was no significant difference in EVECW measured in normal lungs [24Na 1.88 +/- (SD) 0.31; [3H]sucrose 1.84 +/- (SD) 0.27] or edematous lungs [24Na 4.78 +/- (SD) 1.44; [3H]sucrose 4.41 +/- (SD) 1.33] when comparing supernate solutions of homogenized lungs. Similarly, there was no significant difference between the volumes of distribution (EVECW) of these two isotopes when measured in intact fragments of normal lung [24Na 2.08 +/- (SD) 0.28; [3H]sucrose 1.68 +/- (SD) 0.37]. The volume of EVECW measured in supernates was less than in fragments with both isotopes. Washing the centrifuged tissue pellet and adding the wash activity to the initial supernate activity yielded results that were equal to the fragment technique. The failure to detect significant differences between 24Na and [3H]sucrose spaces in the lung suggests that the contribution on intracellular sodium to the measurement of lung water is small and relatively insignificant, at least within the confines of this experiment.

Animals↗
PubMed1982

The effects of expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome or also affects the resolution of their lung injury. We examined the effects of expiratory positive airway pressure (EPAP), a form of PEEP, on 13 pairs of spontaneously breathing mongrel dogs with permanent tracheostomies that were subjected to acute lung injury from oleic acid. One member of each pair was treated with 10 cm H2O EPAP by means of a special valve attached to its tracheostomy tube; the other member breathed through the tracheostomy tube alone. The EPAP was applied 3 h after an intravenous injection of 0.06 ml/kg oleic acid and continued for a total of 21 h. Functional residual capacity (FRC) was increased to preinjury values in the EPAP-treated dogs at 3, 12, and 24 h compared with that in the untreated dogs. The PaO2 was higher and the venous admixture (Qva/QT) was lower in the EPAP-treated dogs compared with that in the untreated dogs at 3 and at 12 h. However, over the 7 days after removal of EPAP no significant differences were noted between the 2 groups in FRC, PaO2, Qva/QT, inert gas elimination profiles, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histologic features. We conclude that EPAP improves gas exchange during its administration but has no demonstrable effect on the resolution of lung injury induced by oleic acid in dogs.

Animals↗
PubMed1981

Pulmonary gas exchange effects of nitroglycerin in canine edematous lungs.

The authors determined the effects of nitroglycerin on pulmonary edema induced by oleic acid injury. Measurements of venous admixture (QVA/Qt) and shunt (Qs/Qt) using both oxygen and inert-gas-elimination methods were done before, during, and after nitroglycerin infusion, first during air ventilation and then during ventilation with 100 per cent oxygen. Nitroglycerin reduced mean blood pressure (MAP) approximately 30 per cent (P less 0.01) during both air and oxygen ventilation. During air ventilation, nitroglycerin caused PVR to decrease by 29 per cent (P less than 0.01) but caused no change in PVR during oxygen ventilation. Pa02 decreased from 64 +/- 8 torr (mean +/- SD) to 55 +/- 9 torr (P less than 0.01) with nitroglycerin infusion during air ventilation. The decrease in Pa02 was primarily due to an increase in QVA/Qt which increased from 28 +/- 12 per cent to 36 +/- 14 per cent (oxygen method) (P less than 0.05). Similarly, the inert gas QVA/Qt increased from 31 +/- 10 to 37 +/- 14 per cent (P less than 0.05). During oxygen ventilation, the effect of nitroglycerin on gas exchange was similar in direction but less in magnitude. These results provide evidence that nitroglycerin may cause significance impairment of pulmonary gas exchange when abnormal lung function is present and FI02 is low. The mechanism is most likely due to inhibition of hypoxic pulmonary vasoconstriction.

Air↗
PubMed1981

Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits.

In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a 24Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

Animals↗