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Biomedical subjects

F W Cheney

Publications and source records attributed to F W Cheney.

At least 91 records · Page 5Linked to original sources
PubMed1980

Pulmonary arteriovenous shunts during halothane anesthesia in dogs.

The fraction of cardiac output flowing through pulmonary arteriovenous anastomoses (Qav/Qt) was measured in dogs during halothane anesthesia and compared with results obtained in normal awake dogs. Flow through arteriovenous anastomoses was measured using 99mTc-labelled polystyrene microspheres (50 microns diameter). The fraction of cardiac output perfusing pulmonary arteriovenous anastomoses during halothane anaesthesia was 4.1% (+/- SD 1.75) compared with 4.6% (+/- SD 0.73) in air-breathing awake control dogs. In spite of variations in arteriovenous shunt fraction, no significant relationship between the Qav/Qt and Qs/Qt was detected. These results suggest that pulmonary arteriovenous anastomases do not contribute significantly to the physiological shunt observed during halothane anaesthesia.

Anesthesia, Inhalation↗
PubMed1980

The effects of 50% oxygen on the resolution of pulmonary injury.

We studied the effects in dogs of long-term inhalation of 50% oxygen on an 8-day course of pulmonary injury caused by intravenous oleic acid. After lung injury, the experimental animals were placed in an environmental chamber where the inspired oxygen fraction (FIO2) was maintained at 0.5 (N = 12) or 0.21 (N = 12). Oleic acid caused a marked increase in venous admixture and a decreae in PaO2, which persisted at about the same concentration for 3 days after injury. These variables gradually returned toward preinjury values at 8 days. There was no significant difference in the clinical course, gravimetric lung water measurements, or lung histologic findings between oxygen-treated and air-breathing control animals. We concluded that 50% oxygen does not affect either the extent or resolution of lung injury induced by a sublethal dosage of oleic acid.

Animals↗
PubMed1979

Effects of methylprednisolone on experimental pulmonary injury.

We studied the effects of methylprednisolone on pulmonary function of unanesthetized dogs with oleic acid induced pulmonary edema observed over a four day period. Methylprednisolone (30 mg/kg) was administered to 11 dogs three and 24 hours after pulmonary injury. Eleven animals were untreated after pulmonary injury and served as controls. There was no difference between the two groups until 72 hours after injury, when the venous admixture of the steroid treated animals was 11 +/- 3% (SD) compared to 22 +/- 8% (p less than 0.001) in the untreated with respective PaO2 values of 76 +/- 6 torr and 64 +/- 8 torr (p less than 0.001). Light microscopic examination of the lungs 96 hours after injury revealed a marked proliferation of Type II pneumocytes in the methylprednisolone treated animals. We conclude that, in the oleic acid or fat embolism model of pulmonary injury, methylprednisolone significantly increases resolution of the pulmonary injury presumably by stimulation of active proliferation and maturation of Type II pneumocytes.

Animals↗
PubMed1979

Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung.

The effects of the mode of reinflation and of the duration of prior collapse on the development of unilateral pulmonary edema following reexpansion of collapsed lung were studied in a rabbit model simulating the human syndrome of "reexpansion pulmonary edema." The right lungs of rabbits were maintained in an atelectatic state for 0.5 h to 8 days, by injection of air into the pleural space. Reexpansion was achieved in 2 h by application of positive pressure to the airway while a chest tube was connected to underwater seal, or by application of negative pressure (-20 to -100 Torr) to a screened window in the partietal pleura. The lung surface pressures we actually applied by the two methods are not known. Animals were then killed and pulmonary edema was determined by wet-to-dry weight ratios. The incidence of unilateral pulmonary edema increased as the duration of prior collapse was increased (85% after 7--8 days; 17% after 3 days; and 0% after 0,5 h) when reinflated with -100 Torr applied to the pleural window. Although the incidence was less, it also occurred following the use of pleural window pressure less negative than -100 Torr, and after reinflation by positive airway pressure.

Airway Obstruction↗
PubMed1979

Effects of inspiratory flow pattern on gas exchange in normal and abnormal lungs.

To study the influence of inspiratory flow pattern on gas exchange in normal and abnormal lungs, 15 dogs were mechanically ventilated with the ascending or descending half of a rectified sine-wave flow pattern during pentobarbital anesthesia. Blood-gas status and cardiac output were monitored during each pattern. Pulmonary injury was induced in 9 animals by prior injection of oleic acid into the right atrium. Ventilation was with room air and zero end-expiratory pressure. Although no significant difference was seen between the patterns in animals with normal lung function (PaO2 greater than 85 Torr on the ascending pattern), the descending pattern resulted in a rise in PaO2 of about 10% (P less than 0.01) in animals with abnormal lung function (PaO2 less than 70 Torr on the ascending pattern). No significant difference in PaCO2 or cardiac output was detected when flow pattern was changed in any of the animals. We conclude that inspiratory flow pattern is not a significant factor when ventilating normal lungs, but may improve gas exchange significantly when severe ventilation-perfusion maldistributions exist.

Animals↗
PubMed1978

Effect of pulmonary microembolism on arteriovenous shunt flow.

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.

Animals↗
PubMed1978

Mechanical and chemical damage to lung tissue caused by meconium aspiration.

We investigated the effects of meconium on the lungs of an adult rabbit model to distinguish between mechanical obstruction of airways and chemical pneumonitis. After the rabbits were anesthetized and intubated, 20% human meconium in saline was instilled into the trachea. Arterial and mixed venous blood gases, functional residual capacity, cardiac output vascular pressures, calculated venous admixture, and pulmonary vascular resistance were measured. Sections of affected lung tissue were examined microscopically. The results were consistent with an early mechanical obstruction of airways with gradual development of chemical pneumonitis over 48 hours.

Airway Obstruction↗
PubMed1977

Sodium nitroprusside increases Qs/Qt in dogs with regional atelectasis.

This study investigated the effects of sodium nitroprusside (SNP) on arterial oxygen tension (Pao2), pulmonary shunt (Qs/Qt), and pulmonary vascular resistance (PVR) in the presence of atelectasis of one lung. Ten dogs were anesthetized, their tracheas intubated with a bronchial divider, and their lungs ventilated with IPPB with pure oxygen. Atelectasis of the left lung was produced by occluding the left side of the bronchial divider and ventilating the right lung. SNP was infused to decrease mean arterial blood pressure by 25%. Pao2 decreased from (mean value+/-1 SD) 134+/-75 to 77+/-23 torr (P less than 0.05) with SNP infusion. Qs/Qt increased from 30+/-7.0 to 39+/-6.0% (P less than 0.05), while cardiac output did not change significantly. PVR of the atelectatic lung decreased, while PVR of the ventilated lung was unchanged. The decrease in PVR in the atelectatic lung suggests that SNP decreases Pao2 and increases Qs/Qt by reversing the hypoxic pulmonary vasoconstriction. As a result, during SNP infusion, perfusion of the atelectatic lung was maintained while perfusion of the ventilated lung decreased.

Animals↗
PubMed1977

Mechanism of change in pulmonary shunt flow with hemorrhage.

In the presence of regional atelectasis, hemorrhage increases the pulmonary shunt fraction (Qs/Qt). We wanted to determine if the increase in Qs/Qt occurs due to inhibition of hypoxic vasoconstriction or due to hydrostatic effects associated with a collapsed lung and decrease in cardiac output. We compared the effects of hemorrhage on flow to a hypoxic lung (Qh) produced in two ways in anesthetized dogs. In six dogs atelectasis of one lung was produced by bronchial occlusion and in a second group of six dogs one lung was ventilated with 100% nitrogen. The other lung in each group was ventilated with 100% nitrogen. The other lung in each group was ventilated with 100% O2. Hemorrhage (20 ml/kg) had no effect on Qh/Qt in dogs with a nitrogen-ventilated lung suggesting that hemorrhage did not inhibit hypoxic vasoconstriction. In contrast, hemorrhage caused a marked increase in Qh/Qt in dogs with a collapsed lung because the flow to the inflated ventilated lung fell, while flow to the collapsed lung did not change. The increase in Qs/Qt in the dogs with atelectasis can be explained solely on the basis of mechanical effects produced by the differences in lung heights and alveolar pressures between ventilated and atelectatic lung.

Animals↗
PubMed1975

Variability of effect of positive end expiratory pressure.

Mechanical ventilation with positive end expiratory pressure (PEEP) has been reported to produce prompt improvement in oxygeneration when used to treat acute respiratory failure. Reports of the effect of PEEP on cardiac output have been conflicting. We studied 14 patients and found that, although mean values of arterial oxygen tension (PaO2) increased as PEEP increased, on eight occasions in the acute studies and three in the elective studies, it fell as PEEP was increased. On five occasions the fall in PaO2 was associated with an increased shunt. Arterial pressure did not, on the average, change at any level of PEEP, but in 13 of 30 measurements it fell by more than 20% and necessitated curtailment of the study at blood pressure levels of less than 50 torr. Since these effects of PEEP cannot be predicted, careful patient monitoring is essential when ventilation with PEEP is utilized.

Adult↗
PubMed1975

Pulmonary shunt: a comparison between oxygen and inert gas infusion methods.

Pulmonary shunt measurement was compared using the standard oxygen (Berggren) technique and a new multiple inert gas infusion (Wagner et al.) technique in 11 mongrel dogs with either regional atelectasis or diffuse pulmonary edema. Relative retentions of sulfur hexafluoride, ethane, cyclopropane, halothane, diethyl ether, and acetone were used to calculate intrapulmonary shunt. Relative dilution of oxygen (Berggren method) was used to calculate total right to left shunt. The two methods gave similar results in the range of 20-80%. At low shunts the oxygen method measured higher values. This is because of the greater relative importance of fixed extrapulmonary shunts at this level and, as well, error in the measurement of PO2. Both techniques are suitable for normal clinical use.

Acetone↗
PubMed1975

Comparison of the cardiopulmonary effects of subcutaneously administered epinephrine and terbutaline in patients with reversible airway obstruction.

The cardiopulmonary effects of epinephrine and terbutaline were compared in a doubleblind crossover study in 23 subjects with chronic obstructive airway disease. On each of three days each subject received a single subcutaneous dose of saline, 0.25 mg of epinephrine or 0.5 mg of terbutaline. Treatment with epinephrine produced significant increases in forced vital capacity (FVC), forced expiratory volume in one second (FEV-1), maximal expiratory flow rate (MEFR) and maximal mid-expiratory flow (MMEF). Terbutaline caused even more pronounced increases in all four parameters and exhibited a longer duration of action. Neither drug altered arterial pH, arterial oxygen pressure (PaO-2), or arterial carbon dioxide pressure (PaCO-2). With regard to cardiovascular effects, no alterations in either systolic or diastolic pressure were observed. Administration of epinephrine and terbutaline caused statistically significant increases in heart rate. The effect of terbutaline was more pronounced that that of epinephrine. In addition, terbutaline caused a heart rate-related depression of the T-wave of the lead 2 ECG. Neither drug altered any of the hematologic, hemochemical or urinary parameters monitored before and after treatment. Side effects were seen in eight subjects after administration of saline solution, in 13 subjects after epinephrine and in 19 subjects after terbutaline. None of these side effects was considered clinically serious and none required treatment. It is concluded from this study that subcutaneously administered terbutaline is a more effective bronchodilator than epinephrine.

Adult↗
PubMed1975

Effects of pattern of ventilation on pulmonary metabolism and mechanics.

Effects of three patterns of mechanical ventilation on pulmonary mechanics, lung phospholipid and surface activity were studied in the normal closed-chest dog. The patterns were continuous mechanical ventilation with: 1) tidal volume (VT)=15 ml/kg; 2) VT=15 ml/kg with 10 cm H2O positive end-expiratory pressure (PEEP); 3) VT=50 ml/kg. THE DOGS IN EACH GROUP WERE VENTILATED FOR 24 HOURS, WITH CAREFUL ATTENTION PAID TO MAINTENANCE OF NORMAL BLOOD GASES, FLUID BALANCE, AND CARDIAC OUTPUT. The animals were sacrificed and the lungs studied to determine pressure-volume curves, dry lung weight/wet lung weight ratios, phospholpid contents and surface activities. The results were compared with control values in acutely sacrificed unventilated dogs. No significant change from controls was found with any pattern of ventilation employed with the exception of the tendency for lungs ventilated with PEEP to retain fluid (decreased dry lung weight/wet lung weight ratio).

Animals↗