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J F Moran

Publications and source records attributed to J F Moran.

At least 73 records · Page 4Linked to original sources

Hemodynamic effects of prolonged hyperoxia.

Experimental studies have consistently demonstrated the development of perivascular edema in the dog lung following prolonged exposure to 95% oxygen. This pathological change has been thought to result from capillary injury, but a direct effect secondary to left ventricular dysfunction has not yet been excluded. To evaluate the latter possibility, ten trained, awake dogs were prepared with monitoring of right and left atrial, systemic and pulmonary artery pressures, cardiac output, and mixed venous and arterial blood gases. Animals were exposed to an F1O2 greater than 0.95 for 48-70 hours. Radioactive 8-10 mu microspheres (141Ce, 51Cr, 85Sr, 46Sc) were injected into the left atrium at zero, six, 24, and 48 hours. PaO2 was 480 +/- 10 mm Hg during exposure, and the pulmonary shunt fraction increased from 11.3% to 16.9% (p less than 0.0001) during 70 hours. Left atrial pressure fell from 9 +/- 2 mm Hg to 3 +/- 3 mm Hg (p less than 0.0001), but cardiac output was constant at 2.7 +/- 0.1 l/min. Pulmonary arteriolar resistance increased from 183 +/- 20 dynes-sec-CM-5 to 791 +/- 30 at 70 hours (p less than 0.0001). Histologic sections of the lungs demonstrated the characteristic perivascular edema. Of particular interest was the fact that myocardial perfusion was significantly increased to all three layers of the ventricular wall at 24 and 48 hours. These data indicate that perivascular edema developing after exposure to high concentrations of oxygen is secondary to pulmonary capillary endothelial damage with no evidence that myocardial dysfunction occurs during this period.

Animals↗

Reversible pulmonary oxygen toxicity in the primate.

In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96--110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (PaO2 40 +/- 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (PaO2 89+/- 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrese in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air.

Animals↗

EKG of the month.

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Arrhythmias, Cardiac↗

EKG of the month.

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Arrhythmias, Cardiac↗

EKG of the month.

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Arrhythmias, Cardiac↗

EKG of the month.

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Arrhythmia, Sinus↗

EKG of the month.

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Atrial Fibrillation↗

EKG of the month.

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Arrhythmias, Cardiac↗

EKG of the month.

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Atrial Fibrillation↗

Regional pulmonary function during experimental unilateral pneumothorax in the awake state.

This study examines changes in regional pulmonary function during unilateral pneumothorax, immediately after, and 2 hours following re-expansion in awake dogs. Respiratory rate, tidal volume, physiologic dead space, arterial blood gases, and pulmonary shunt fraction were determined at each stage. Cardiac output (thermodilution), vascular pressures, and regional ventilation and perfusion (133Xe scans) were also measured. Chest roentgenogram confirmed the presence of UP. Respiratory rate increased 124 percent (p less than 0.01) during UP while alveolar ventilation remained unchanged. Pulmonary shunt fraction rose 93 percent (p less than 0.01) during UP, causing PaO2 to fall from 86 to 51 mm. Hg (p less than 0.01). PaCO2, pH, and cardiac output were not altered by UP. UP caused a relative underventilation of the collapsed lung (V/Q = 0.73 (p less than 0.01)) and an overventilation of the contralateral lung (V/Q = 1.74) (p less than 0.01). Immediately after re-expansion of the collapsed lung, all the above changes reverted to the control values. All variables remained unchanged 2 hours following complete re-expansion.

Animals↗

Refractory ventricular arrhythmia: the role of intraoperative electrophysiological study.

Thirty patients with drug refractory ventricular tachycardia (RVT) were studied between 1 week and 5 years after myocardial infarction with coronary agniography and left ventriculography. They were divided into four groups: (1) inoperable, five patients; (2, a) operated, with primary left ventricular failure, five patients; (2, b) operated with primary RVT, not mapped, 15 patients; (2, c) operated, with mapping, five patients. The mortality rate in group 1 was 100%, and in group 2, a it was 80%. In group 2, b, despite aggressive drug therapy and operation, including aneurysmectomy, coronary revascularization, and intra-aortic balloon pumping when appropriate, the mortality rate wad intraoperative mapping in group 2, c. Arrhythmogenic foci were identified and removed in four. There was one operative death (20%) and four patients are alive from 12 to 27 months after operation, three of whom are asymptomatic. Intraoperative epicardial mapping is an important adjunct to surgery for RVT.

Aged↗

EKG of the month.

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Arrhythmia, Sinus↗