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Biomedical subjects

J Schnader

Publications and source records attributed to J Schnader.

At least 19 recordsLinked to original sources
PubMed1996

Chronic pulmonary hypertension in sheep: temporal progression of lesions.

Scant data exist on the evolution of the lesions of pulmonary hypertension. This study establishes a model in sheep in which the left upper lobe (LUL) was rendered hypertensive by a systemic-pulmonary shunt while the rest of the pulmonary circulation remained normotensive. By examining lung tissue at 2 months and 1 1/2 years after shunting, we sought the temporal progression of pulmonary hypertensive lesions. In the hypertensive LULs (n = 5), many vascular lesions were seen in contrast to the absence of lesions in both the contralateral normotensive lungs (n = 5) and the "control" lungs from sheep which underwent thoracotomy without shunting (n = 5). Vascular necrosis and vasculitis were present after 2 months (P < 0.01) but disappeared after 1 1/2 years. In contrast, intimal thickening was present after 1 1/2 years (n = 2, P < 0.01) but not significantly after 2 months. These intimal lesions often demonstrated increased cellularity staining positively for factor VIII. Plexiform lesions were present at 2 months (P < 0.05) but were more profuse after 1 1/2 years (P < 0.01). These findings are consistent with an early vascular injury and a later remodeling or reparative process in hemodynamic pulmonary hypertension.

Animals↗
PubMed1993

Effects of nordihydroguaiuretic acid on sulfidopeptide leukotriene activity and hypoxic pulmonary vasoconstriction in the isolated sheep lung.

Sulfidopeptide leukotrienes have been proposed as mediators of hypoxic pulmonary vasoconstriction. We studied the effects of nordihydroguaiuretic acid (NDGA), a lipoxygenase inhibitor, on hypoxic pulmonary vasoconstriction and on immunoreactive leukotriene C4 (i-LTC4) levels in lung lymph, perfusate and bronchoalveolar lavage (BAL) fluid in isolated, indomethacin treated, sheep lungs perfused with blood at a constant flow of 100 ml/kg/min. The protocol consisted of two randomized periods with inspired 02 concentration either 28.2 or 4.2%. Five groups of lungs were studied with calculated NDGA concentrations of 0 to 1300 microM. At the end of each period, i-LTC4 was measured in lung lymph, perfusate and BAL. NDGA levels were also measured. Consistent with our previous findings (10), hypoxia did not increase i-LTC4 levels in lymph, perfusate or BAL fluid. Although NDGA decreased i-LTC4 in perfusate in a dose-dependent manner, it did so at concentrations which were ten times lower than those causing inhibition of hypoxic vasoconstriction. These NDGA concentrations also inhibited vasomotor responses to KCl, serotonin and PGF2 alpha suggesting nonspecificity. These observations are not consistent with mediation of hypoxic vasoconstriction by i-LTC4.

Analysis of Variance↗
PubMed1993

Pneumocystis carinii pleural effusion. Pathogenesis and pleural fluid analysis.

We present three new cases of Pneumocystis carinii in pleural effusions of patients with AIDS, bringing the total number of reported cases to six. In our patients, diagnosis was made by visualization of Pneumocystis in pleural fluid stained with Gomori methenamine silver. LDH was greater than 400, and pleural fluid to serum LDH ratio was greater than 1.0 in all cases at time of presentation. All six reported patients have been associated with aerosolized pentamidine, and five of the six had documented underlying Pneumocystis pneumonia. The sixth patient, which we report, presented with primary pleural infection with Pneumocystis. Although we could not document underlying pneumonia, we suspect it was present. Pneumocystis pleural disease appears to be an anatomic extension of smoldering subpleural Pneumocystis pneumonia, and prognosis is not worse than with pneumonia alone.

AIDS-Related Opportunistic Infections↗
PubMed1990

Effects of hypoxia on leukotriene activity and vasomotor tone in isolated sheep lungs.

To determine whether hypoxic pulmonary vasoconstriction was associated with release of sulfidopeptide leukotrienes (SPLTs) from the lung, we measured SPLT activity by bioassay (guinea pig ileum) and radioimmunoassay in lymph, perfusate, and bronchoalveolar lavage (BAL) fluid from sheep lungs (n = 20) isolated and perfused in situ with a constant flow of autologous blood (100 ml.kg-1.min-1) containing indomethacin (60 micrograms/ml). The protocol consisted of three periods, each at least 1 h in duration. In experimental lungs, inspired O2 concentration (FIO2) was 28.2% in periods 1 and 3 and 4.2% in period 2. In control lungs, FIO2 was 28.2% throughout. Hypoxia increased pulmonary arterial pressure but did not alter peak tracheal pressure, lung lymph flow, or weight gain measured during the last 30 min of each period. SPLT activity was greatest in lung lymph and least in BAL fluid. Hypoxia did not alter SPLT activity in any fluid. Similar results were obtained in lungs not treated with indomethacin (n = 15). These data do not support the hypothesis that hypoxic pulmonary vasoconstriction is mediated by SPLTs.

Animals↗
PubMed1988

Interaction of fatigue and hypercapnia in the canine diaphragm.

We studied 10 open-chest dogs and measured the pressure across the diaphragm (Pdi) in each period of the protocol during stimulation at frequencies of 1, 20, 50, and 80 Hz. Three ranges of arterial PCO2 (PaCO2) were examined: less than or equal to 26, 36-50, and greater than or equal to 89 Torr. The diaphragm was fatigued with repetitive phrenic stimulation (30 Hz). During the fatiguing activity, five of the animals were subjected to hypercapnia and the other five to hypocapnia. A frequency-Pdi curve was generated for each period in the protocol. The data show that 1) fatiguing to 50% of the initial Pdi value during hypercapnia was significantly more rapid than during hypocapnia; 2) both the prefatigue and postfatigue mean Pdi values over all interactions of frequency, fatigue, and PaCO2 were unaffected by the fatiguing environment (hypercapnia vs. hypocapnia); 3) the percent reduction of Pdi by hypercapnia was the same at all four frequencies; 4) hypocapnia did not alter either the pre- or postfatigue frequency-Pdi curve; and 5) one-half relaxation time, unaffected by PaCO2, was prolonged by fatigue. We conclude that the hypercapnic diaphragm has less endurance than the hypocapnic diaphragm and that although both fatigue and hypercapnia decrease Pdi, they appear to be separate entities working through different mechanisms.

Animals↗