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Biomedical subjects

R E Moon

Publications and source records attributed to R E Moon.

At least 37 records · Page 2Linked to original sources
PubMed1996

VA/Q abnormalities during gram negative sepsis.

Hypoxemia in bacterial sepsis develops by mechanisms which are incompletely understood. In this study, we measured pulmonary gas exchange in eight baboons to determine the causes of hypoxemia after infusion of live Escherichia coli (1 x 10(10) CFU/kg) followed by resuscitation with intravenous fluid. VA/Q distributions were measured periodically using the multiple inert gas elimination technique until death or for a maximum of 42 h. After E. coli infusion, dispersion of perfusion (logSDq) increased rapidly and a transient rise in dead space was observed at 6 h coinciding with systemic hypotension and acidosis. The intrapulmonary shunt developed later and reached 27 +/- 6% at 24 h. PaO2 began to decrease at 12 h and correlated with increases in intrapulmonary shunt and logSDq. There was no evidence of diffusion limitation. Lung edema was mild despite aggressive fluid resuscitation. Morphometric analysis of postmortem lungs revealed dramatic intravascular accumulation of granulocytes. There were increases in arithmetic mean thicknesses of epithelium and interstitium. These data indicate that gram negative sepsis with fluid resuscitation causes progressive hypoxemia, primarily due to the development of intrapulmonary shunt and very low VA/Q regions in the lung. The VA/Q abnormalities occur early and likely reflect ongoing cellular responses in pulmonary vasculature and smaller airways in sepsis.

Animals↗
PubMed1995

Treatment of cervical necrotizing fasciitis with hyperbaric oxygen therapy.

Hyperbaric oxygen therapy has significantly improved the management of necrotizing fasciitis of the extremities and trunk. Its role in cervical necrotizing fasciitis has not been fully evaluated. Historically, necrotizing fasciitis has been associated with considerable morbidity and mortality. This report discusses our experience with cervical necrotizing fasciitis in six patients treated from 1986 to 1993 who received hyperbaric oxygen therapy. All patients survived. In all cases infection was of probable odontogenic origin. Most patients in whom necrotizing fasciitis develops have identifiable risk factors; however, two patients in this series were previously healthy, and there was no relationship between hospital course and identified risk factors. Clinical presentation and microbiology are reviewed together with the rationale for hyperbaric oxygen therapy as an adjunct to broad-spectrum antibiotics and aggressive early surgical debridement.

Adult↗
PubMed1995

Artificial surfactant attenuates hyperoxic lung injury in primates. I. Physiology and biochemistry.

Prolonged exposure to O2 causes diffuse alveolar damage and surfactant dysfunction that contribute to the pathophysiology of hyperoxic lung injury. We hypothesized that exogenous surfactant would improve lung function during O2 exposure in primates. Sixteen healthy male baboons (10-15 kg) were anesthetized and mechanically ventilated for 96 h. The animals received either 100% O2 (n = 6) or 100% O2 plus aerosolized artificial surfactant (Exosurf; n = 5). A third group of animals (n = 5) was ventilated with an inspired fraction of O2 of 0.21 to control for the effects of sedation and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion distribution (VA/Q) was measured daily using a multiple inert-gas elimination technique. Positive end-expiratory pressure was kept at 2.5 cmH2O and was intermittently raised to 10 cmH2O for 30 min to obtain additional measurements of VA/Q. After the experiments, lungs were obtained for biochemical and histological assessment of injury. O2 exposures altered hemodynamics, progressively worsened VA/Q, altered lung phospholipid composition, and produced severe lung edema. Artificial surfactant therapy significantly increased disaturated phosphatidylcholine in lavage fluid and improved intrapulmonary shunt, arterial PO2, and lung edema. Surfactant also enhanced the shunt-reducing effect of positive end-expiratory pressure. We conclude that an aerosolized protein-free surfactant decreased the progression of pulmonary O2 toxicity in baboons.

Animals↗
PubMed1994

Natural surfactant and hyperoxic lung injury in primates. I. Physiology and biochemistry.

Surfactant dysfunction contributes to the pathophysiology of adult respiratory distress syndrome (ARDS), and we hypothesized that surfactant treatment would improve experimental ARDS produced by continuous exposure to hyperoxia. Twelve healthy male baboons (10-15 kg) were anesthetized, paralyzed, and mechanically ventilated with 2.5 cmH2O positive end-expiratory pressure (PEEP) for 96 h. Baboons were divided into three groups: 1) the O2 group (n = 5) received 100% O2, 2) the surfactant group (n = 5) received 100% O2 and aerosolized porcine surfactant, and 3) a control group (n = 2) was ventilated at fractional concentration of inspired O2 of 0.21 for 96 h to control for effects of anesthesia and mechanical ventilation. Hemodynamic parameters were obtained every 12 h, and ventilation-perfusion (VA/Q) distribution was measured daily by multiple inert gas elimination technique. PEEP was increased once or twice daily to 10 cmH2O for 30 min to study its effects on measurements of VA/Q. At the end of experiments, lungs were obtained for biochemical analysis. Prolonged hyperoxia resulted in progressive worsening in VA/Q, hemodynamic deterioration, severe lung edema, and altered surfactant metabolism. Surfactant administration increased disaturated phosphatidylcholine in lavage fluid but did not improve lung edema or gas exchange. In the surfactant group, however, the addition of 10 cmH2O PEEP resulted in a greater degree of shunt reduction than did 2.5 cmH2O PEEP (47 vs. 31% in the O2 group, P < 0.05). We conclude that aerosolized porcine surfactant did not prevent pulmonary O2 injury in baboons, but it potentiated the shunt-reducing effect of PEEP.

Aerosols↗
PubMed1994

Cerebral imaging of decompression injury patients with 18-F-2-fluoro-2-deoxyglucose positron emission tomography.

The objective assessment of the extent of cerebral insult and the effects of therapy in decompression injury patients has proven to be difficult by most imaging modalities. In this pilot study we evaluated the ability of 18-F-2-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) to identify metabolic brain abnormalities in decompression injury patients. Twenty-two patients who were evaluated at our institution for decompression accidents were evaluated with FDG-PET. Four of the 22 patients had no neurologic symptoms and no neurologic findings on clinical exam at the time of the FDG-PET study. No statistically significant correlations were found between the presence of symptoms and the demonstration of abnormalities on the PET study and no statistically significant correlation was found between the location of the decompression injury and the demonstration of abnormalities on the PET study. We conclude that FDG-PET imaging of the brain cannot reliably identify cerebral abnormalities in patients with decompression injuries and would be of limited benefit for monitoring therapy in patients with decompression illness.

Adult↗
PubMed1993

Effects of clenbuterol hydrochloride on pulmonary gas exchange and hemodynamics in anesthetized horses.

We evaluated the effects of clenbuterol HCl (0.8 micrograms/kg, of body weight, IV), a beta 2 agonist, on ventilation-perfusion matching and hemodynamic variables in anesthetized (by IV route), laterally recumbent horses. The multiple inert gas elimination technique was used to assess pulmonary gas exchange. Clenbuterol HCl induced a decrease in arterial oxygen tension (from 57.0 +/- 1.8 to 49.3 +/- 1.2 mm of Hg; mean +/- SEM) as a result of increased shunt fraction (from 6.6 +/- 2.1 to 14.4 +/- 3.1%) and ventilation to regions with high ventilation-perfusion ratios. In contrast, no changes in these variables were found in horses given sterile water. In horses given clenbuterol HCl, O2 consumption increased from 2.23 +/- 0.18 to 2.70 +/- 0.14 ml.min-1.kg-1, and respiratory exchange ratio decreased from 0.80 +/- 0.02 to 0.72 +/- 0.01. Respiratory exchange ratio and O2 consumption were not significantly modified in sterile water-treated (control) horses. Clenbuterol HCl administration was associated with increased cardiac index (from 57.4 +/- 4.0 to 84.2 +/- 6.3 ml.min-1.kg-1), decreased total peripheral vascular resistance (from 108.3 +/- 9.3 to 47.6 +/- 2.8 mm of Hg.s.kg.ml-1), and decreased pulmonary vascular resistance (from 31.3 +/- 3.8 to 13.6 +/- 0.7 mm of Hg.s.kg.ml-1). Our findings indicated that clenbuterol HCl may potentiate hypoxemia as a result of increased shunt fraction in horses anesthetized by the IV route, and caused changes in hemodynamic variables that were consistent with its ability to stimulate beta 2-adrenergic receptors.

Anesthesia, General↗
PubMed1992

Urinary vasopressin and aldosterone and plasma volume during a saturation dive to 450 m.

Urinary vasopressin (VP), aldosterone (ALDO), osmotic substances, sodium excretion, and plasma volume were assessed in 4 healthy male divers during 2 predive control days, 2 compression days, 6 days at 46 atm abs, and 26 days of decompression with stops at 37 and 27 atm abs. At pressure the ambient gas was trimix (0.5 atm abs O2:5% N2:remainder He). All urine was collected throughout the dive. Samples were divided into daytime (0700-1900) and nighttime (1900-0700). Indocyanine green dye dilution was used to determine plasma volume at predive 1, 46, and 24 atm abs. In agreement with previous dives at 31 atm abs, there was a decrease in VP excretion during compression lasting until return to 1 atm abs (P less than 0.05). Also similar to the shallower dives at 31 atm abs, the normal diurnal pattern of VP excretion, daytime higher than nighttime (P less than 0.05), disappeared at pressure. Urine osmolality showed alterations compatible with responses to VP. In contrast to previous studies at 31 atm abs, but in agreement with a previous study at 49.5 atm abs, there was no sustained increase in urinary ALDO excretion and only a transient natriuresis during the compression phase, followed by a reduced sodium excretion. In confirmation of earlier conclusions from indirect evidence, direct measurements of plasma volume indicated a reduction of about 20% (P less than 0.05) at 46 atm abs which remained reduced after decompression to 24 atm abs.

Adult↗
PubMed1992

Platelet count in deep saturation diving.

Platelet counts were measured in 10 divers during the course of 4 experimental deep dives (450 and 600 m) and different anticoagulants were tested. The use of sodium citrate as an anticoagulant was associated with artifactual thrombocytopenia, whereas ethylenediaminetetraacetic acid proved to be satisfactory. During one of the dives (450 m) the use of fluorocarbon to remove excess dissolved inert gas before decompression of the samples was systematically tested. Mean platelet count decreased from 272,600 +/- 29,400 mm-3 (mean +/- SD) on Day 7 (450 m) to 177,700 +/- 26,400 mm-3 on Day 12 (360 m). Platelet count had recovered to 209,900 +/- 20,700 mm-3 at the time of surfacing. Mean hematocrit (expressed in percent) increased from 44.7 +/- 2.2 predive to 59.4 +/- 2.0 on Day 7 (450 m) to 40.9 +/- 2.8 at the time of surfacing. These changes were statistically significant (P less than 0.05). Platelet counts on samples that had been degassed with fluorocarbon were not different from samples that had been decompressed without degassing.

Citrates↗
PubMed1992

Renal responses during a dry saturation dive to 450 msw.

Four subjects were compressed to a simulated depth of 450 msw (46 bar) for 37 days in the main research chamber of the German underwater simulator diving facility at the GKSS Research Center, Geesthacht. The ambient gas was trimix. Urine was collected at 0700, 1300, and 1900 h each day for analysis of Na+, K+, volume, osmolality, and creatinine. Urine, antidiuretic hormone (ADH), and aldosterone were analyzed separately. Daily fluid, Na+, and K+ intake were analyzed throughout the dive. The aim of the investigation was to confirm the existence of a diuresis and natriuresis which had been observed in earlier saturation dives to 31 atm abs using He-O2. A significant diuresis was observed during compression despite a decrease in fluid intake. After compression the diuresis decreased somewhat but remained significantly above precompression control levels during the entire hyperbaric exposure. No significant change in fluid intake was observed. Daily Na+ and K+ excretion increased significantly during compression, which was accompanied by a significant increase in nocturnal excretion of Na+ and K+. Daily intake of Na+ and K+ decreased throughout the dive. Daily urine ADH decreased immediately upon compression and was associated with a parallel decrease in urine osmolality. In contrast, urinary aldosterone excretion exhibited no change during the dive despite the increase in Na+ and K+ excretion and decrease in Na+ intake.

Aldosterone↗
PubMed1992

Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts.

We reviewed over 220 cases of acute carbon monoxide (CO) poisoning and now report on 17 patients whose poisoning occurred from the indoor use of propane-fueled forklifts. All patients in this series presented with neurologic symptoms or persistent headache and were given hyperbaric oxygen to resolve their symptomatology. We investigated the concentration of CO in the exhaust emissions of 12 propane-fueled forklifts used in various workplaces in our location. The average CO concentration in the exhaust during engine idling was 36,000 parts per million (3.6%). This value decreased slightly to 30,000 ppm (3.0%) at working engine speed. Measurements of exhaust flow indicate CO production rates of approximately 60 liters per minute at working engine speed. These quantities of CO constitute a significant occupational exposure risk to workers using propane-fueled forklifts in unventilated indoor environments.

Acute Disease↗
PubMed1991

Extubation after transsternal thymectomy for myasthenia gravis: a prospective analysis.

Recommendations concerning postoperative extubation after thymectomy for myasthenia gravis are presently based upon retrospective chart reviews. We present the results of a prospective investigation of time to extubation after thymectomy for 14 patients over a 12-month period based upon a protocol that included preoperative immunologic therapy, combined epidural and general anesthesia, postoperative epidural narcotic analgesia, and a standardized approach to discontinuation of ventilatory support. After a neurologist took measures to optimize preoperative neuromuscular function, all 14 patients received agents to produce lumbar epidural anesthesia and light general anesthesia. Muscle relaxants were avoided in all but one patient. Postoperative analgesia was initially maintained with epidural hydromorphone, then therapy was switched to patient-controlled intravenous morphine sulfate. Criteria for weaning from mechanical ventilation, first measured at the end of anesthesia, were partial pressure of oxygen (arterial) greater than or equal to 90 mm Hg (fraction of inspired oxygen = 0.40), partial pressure of carbon dioxide (arterial) less than or equal to 50 mm Hg, pH greater than or equal to 7.30, and respiratory rate less than or equal to 30 breaths/min. If these criteria were not met, ventilatory support was continued postoperatively with intermittent mandatory ventilation, and the patient was weaned gradually from this support. Criteria for extubation included meeting the criteria for weaning, vital capacity greater than or equal to 10 mL/kg, and inspiratory pressure better than -30 cm H2O. Criteria for reintubation included tachypnea (respiratory rate greater than 40 breaths/min), respiratory acidosis not due to narcotics, or vital capacity less than or equal to 8 mL/kg. The mean time to extubation was 9 hours (range, 0.75 to 25 hours). Mean preoperative vital capacity was 2.59 +/- 0.64 L (range, 1.90 to 4.20), which decreased approximately 50% to 1.19 +/- 0.39 L (range, 0.70 to 2.0) at the time of extubation. No patient required reintubation. Half of the patients required postoperative anticholinesterase therapy based upon serial neurologic examinations; there were no instances of cholinergic crisis. Thirteen patients returned to the ward on the first postoperative day, and one on the second day. Thirteen patients preferred epidural analgesia to patient-controlled analgesia. The time to extubation and average length of stay in an intensive care setting were markedly reduced compared to those reported in previous retrospective studies. We conclude that a multidisciplinary approach that optimizes neuromuscular function and decreases poststernotomy pulmonary insult will shorten the time to extubation and decrease the length of stay in the intensive care or recovery room after thymectomy.

Adolescent↗
PubMed1991

Venous gas emboli and complement activation after deep repetitive air diving.

Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.

Adult↗
PubMed1990

Barotrauma and air embolism in hyperbaric oxygen therapy.

A 69-year-old woman underwent hyperbaric oxygen therapy because of a nonhealing ulcer of her foot. During decompression, she developed a left-sided hemiplegia and confusion. Recompression resulted in transient neurologic improvement, but she eventually became comatose. Ventricular dysrhythmias developed and she died without regaining consciousness 17 h after onset of symptoms. An autopsy revealed diffuse interstitial pulmonary fibrosis with severe paracicatricial emphysema, chronic interstitial inflammation, and chronic bronchitis with abundant intrabronchial mucus. There was extensive multifocal ischemic injury of the cerebral cortex. The hippocampi, basal ganglia, and cerebellum were spared. Scattered acute myofiber necrosis was present in the heart. Clinical presentation and autopsy findings strongly support the diagnosis of air embolism and illustrate a potential risk of hyperbaric oxygen therapy in patients with preexisting pulmonary disease.

Aged↗