Biomedical subjects

M DeFrancisis

Publications and source records attributed to M DeFrancisis.

3 recordsLinked to original sources

PubMed1993

Positive end-expiratory pressure-induced, calcium-channel-mediated increases in pulmonary vascular resistance in neonatal lambs.

OBJECTIVES: a) To study the dose response of the calcium-channel-mediated increases in pulmonary vascular resistance with different levels of positive end-expiratory pressure; b) to study the reversibility of the calcium-channel mediated increases in pulmonary vascular resistance after discontinuation of positive end-expiratory pressure; and c) to study the effect of cyclooxygenase and lipoxygenase inhibition on the calcium-channel mediated increases in pulmonary vascular resistance. DESIGN: A prospective, multiexperimental, dose response study. SETTING: Laboratory setting in a university hospital. SUBJECTS: Twenty-three 4- to 10-day-old neonatal lambs. INTERVENTIONS AND MEASUREMENTS: Lungs of neonatal lambs were isolated in situ, and perfused at a constant flow rate, and ventilated at a fixed tidal volume and rate. Mean pulmonary arterial pressure responses to the application and discontinuation of four levels (3.7, 7.4, 11, and 14.7 mm Hg) of positive end-expiratory pressure were studied before and after calcium-channel blockade with verapamil (5 mg) (n = 12). In addition, the mean pulmonary arterial pressure response to 11 mm Hg of positive end-expiratory pressure was studied before and after inhibition of cyclooxygenase with indomethacin (10 mg/kg) (n = 6) and lipoxygenase with diethylcarbamazine (100 mg/kg) (n = 5). RESULTS: The magnitude of the calcium-channel-dependent mean pulmonary arterial pressure response 4 mins after the application of positive end-expiratory pressure was dose related (2.1, 3.0, 4.1, and 5.5 mm Hg with 3.7, 7.4, 11.0, and 14.7 mmHg positive end-expiratory pressure, respectively) and entirely reversible on discontinuation of positive end-expiratory pressure with a time course of 2 to 4 mins. Neither indomethacin nor diethylcarbamazine affected the pulmonary arterial pressure responses to positive end-expiratory pressure. Airway pressure changes with positive end-expiratory pressure were not affected by verapamil, indomethacin, or diethylcarbamazine. CONCLUSIONS: The calcium-channel-mediated pulmonary arterial pressure responses with positive end-expiratory pressure, applied during continuous positive pressure breathing, occur even at low levels of positive end-expiratory pressure, are dose dependent, and are not abolished by treatment with indomethacin or diethylcarbamazine.

Airway Resistance↗

PubMed1991

Cardiac output during liquid (perfluorocarbon) breathing in newborn piglets.

BACKGROUND AND METHODS: Liquid ventilation using perfluorocarbons is a new technique for ventilation of infants with restrictive lung disease. However, this method of ventilation has been shown to impair cardiac output (Qt) in several animal species, casting doubt as to its feasibility. This study tested whether Qt could be maintained during liquid breathing by intravascular volume expansion. Seven piglets were carefully hydrated, instrumented for continuous Qt measurement, and subjected to 2 hr of liquid breathing. PaCO2 was maintained at 40 to 50 torr (5.3 to 6.7 kPa), and PaO2 greater than 80 torr (greater than 10.7 kPa). Additional colloid was given during liquid breathing if Qt decreased to less than 90% of preliquid breathing values. RESULTS: Four piglets maintained Qt throughout the liquid breathing trial with maintenance fluids only. Three piglets each required one 10 mL/kg fluid bolus for Qt 82% to 89% of the baseline value, after which Qt rapidly increased to greater than 90% of baseline. Oxygen consumption and serum lactate levels remained normal throughout liquid breathing. CONCLUSION: Qt is readily maintained during liquid breathing in properly hydrated animals.

Animals↗

PubMed1991

Perfluorocarbon-associated gas exchange.

BACKGROUND AND METHODS: Liquid ventilation with oxygenated perfluorocarbon eliminates surface tension due to pulmonary air/fluid interfaces, and improves pulmonary function and gas exchange in surfactant deficiency. In liquid ventilation, perfluorocarbon is oxygenated, purged of CO2, and cycled into and out of the lungs using an investigational device. A new approach, perfluorocarbon-associated gas exchange, uses a conventional ventilator and combines features of liquid ventilation and continuous positive-pressure breathing. In 13 normal piglets, a volume of perfluorocarbon equivalent to the normal functional residual capacity (30 mL/kg) was instilled into the trachea, left in situ, and volume-regulated gas ventilation (FIO2 1.0) was resumed. For 1 hr, perfluorocarbon was continuously bubble-oxygenated within the lungs, where it directly participated in gas exchange. RESULTS: PaO2 and PaCO2 averaged 401 +/- 51 and 40 +/- 4 torr (53.6 +/- 6.8 and 5.3 +/- 0.5 kPa), respectively. Peak airway pressure during perfluorocarbon-associated gas exchange (22 +/- 2 cm H2O at 1 hr) and during continuous, positive-pressure breathing (23 +/- 4 cm H2O) were nearly identical. Venous oxygen saturation and pH were normal (73 +/- 8% and 7.43 +/- 0.05, respectively, at 1 hr). CONCLUSIONS: Perfluorocarbon-associated gas exchange was uniformly well tolerated, and its efficiency approached that of continuous positive-pressure breathing. Applications of perfluorocarbon technology to lung disease may not be limited by existing instrumentation.

Animals↗