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Biomedical subjects

J R Michael

Publications and source records attributed to J R Michael.

79 records · Page 5Linked to original sources
PubMed1984

Nifedipine inhibits hypoxic pulmonary vasoconstriction during rest and exercise in patients with cystic fibrosis and cor pulmonale.

Nifedipine has recently been reported to reduce pulmonary artery pressure and pulmonary vascular resistance during rest and exercise in adult patients with hypoxic pulmonary hypertension from chronic obstructive pulmonary disease. To determine whether nifedipine reduces pulmonary vascular resistance in patients with cor pulmonale from cystic fibrosis (CF), we studied 2 patients with severe CF lung disease during rest and exercise while breathing room air or receiving low-flow oxygen therapy. Nifedipine markedly lowered pulmonary vascular resistance and improved cardiac index and pulmonary pressure-flow relationships during all treatment conditions. Nifedipine did not substantially change arterial PO2, except for a slight decrease during exercise while receiving low-flow oxygen. Nifedipine, however, markedly increased oxygen delivery during rest and exercise. Both patients noted improved exercise tolerance with chronic nifedipine therapy. Nifedipine may be a useful adjuvant to supplemental oxygen in the treatment of patients with CF and cor pulmonale.

Adult↗
PubMed1984

Nifedipine inhibits hypoxic pulmonary vasoconstriction during rest and exercise in patients with chronic obstructive pulmonary disease. A controlled double-blind study.

To determine whether nifedipine reduces pulmonary artery pressure and pulmonary vascular resistance index during rest and exercise in patients with hypoxic pulmonary hypertension, we studied 6 clinically stable patients using a randomized, double-blind, crossover design. While patients were hypoxic, nifedipine significantly lowered mean pulmonary artery pressure during rest from (mean +/- SEM) 38 +/- 2 mmHg with placebo to 35 +/- 3 mmHg with nifedipine (p less than 0.01) and during exercise from 63 +/- 4 mmHg with placebo to 51 +/- 3 with nifedipine (p less than 0.01). During hypoxia nifedipine reduced pulmonary vascular resistance index during rest by 27% from 7.84 +/- 0.5 units with placebo to 5.71 +/- 0.6 units with nifedipine (p less than 0.02) and during exercise by 44% from 7.84 +/- 1 units with placebo to 4.37 +/- 1 units with nifedipine (p less than 0.001). Nifedipine when added to low flow oxygen reduced pulmonary vascular resistance index during rest by 16% from 6.15 +/- 0.8 units with oxygen to 5.14 +/- 0.5 units with oxygen plus nifedipine (p less than 0.007) and during exercise by 27% from 5.9 +/- 0.9 units with oxygen to 4.3 +/- 0.7 units with oxygen plus nifedipine (p less than 0.005). On room air nifedipine decreased PaO2 during rest by only 4 +/- 1 mmHg and did not decrease exercise PaO2. During oxygen therapy nifedipine decreased PaO2 during rest by 12 +/- 4 mmHg and during exercise by 8 +/- 3 mmHg. Nifedipine therapy, however, substantially increased oxygen delivery during rest and exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

Initial aminoglycoside levels in the critically ill.

Twenty-six consecutive patients admitted to the medical ICU with presumed sepsis or septic shock had their initial serum aminoglycoside level determined 1 h after completion of a 20-min infusion of tobramycin, 2 mg/kg. There was a poor correlation between the dose received and the measured aminoglycoside level; 59% of the patients had initial blood aminoglycoside concentrations below the recommended peak level of 5 micrograms/ml. An underestimation of the volume of distribution in critically ill patients best explains the low serum aminoglycoside levels produced by the currently recommended dosage schedule.

Aminoglycosides↗
PubMed1981

Acute pulmonary disease caused by phenytoin.

Acute pulmonary disease may occur as part of the hypersensitivity angitis produced by phenytoin sodium. The clinical features of the pulmonary involvement are fever, dyspnea, hypoxemia, and bilateral radiographic infiltrates. The pathologic process is an interstitial pneumonitis that appears reversible with cessation of the drug and treatment with corticosteroids.

Acute Disease↗
PubMed1979

Community-acquired acinetobacter pneumonia.

Acinetobacter calcoaceticus var anitratus, a nonfermentative grampnegative bacillus, has been infrequently reported as a cause of community-acquired pneumonia. In this paper we describe the course of six recent patients with community-acquired, bacteremic pneumonia due to this organism and review the six previously reported cases. Our experience suggests this organism is a more common cause of community-acquired pneumonia than previously thought. Acinetobacter pneumonia occurs in older persons with chronic disease, especially alcoholism. It is a fulminant illness with respiratory distress, hypoxemia, leukopenia and shock. Chest roentgenograms reveal a lobar or bronchopneumonic infiltrate which often becomes bilateral within 24 hours of admission to the hospital. Pleural effusions are common. The mortality rate is 43 per cent. Factors that predict a fatal outcome are granulocytopenia, empyema and therapy with inappropriate antibiotics. Therapy with appropriate antibiotics, especially carbenicillin and an aminoglycoside, increases survival.

Acinetobacter Infections↗
PubMed1976

Reversible renal failure and myositis caused by phenytoin hypersensitivity.

A 38-year old woman receiving phenytoin (diphenylhydantoin) noticed maculopapular erythema as the first manifestation of a syndrome that included acute renal failure and myositis in addition to fever, lymphadenopathy, exfoliative dermatitis, and hepatitis. Prednisolone sodium phosphate therapy resulted in resolution of this hypersensitivity reaction, and she recovered from renal insufficiency. The occurrence of renal failure and myositis in the spectrum of phenytoin hypersensitivity reactions is discussed, and the importance of a morbilliform rash in a patient receiving phenytoin is emphasized.

Acute Kidney Injury↗