Synovial fluid as a matrix of selection in the detection of beta-adrenergic agonist drugs in carcases and fresh meat.

Previous papers have supported the hypothesis that beta-agonist drugs could accumulate in those tissues with a high content of mucopolysaccharides. Based on our preliminary findings, between October and December 1993 we randomly sampled 534 samples of synovial fluids drawn from the knee joint of fresh carcasses. After a preliminary extraction able to break down the water domains of mucopolysaccharides and the interactions between the matrix and the drugs, samples were concentrated on diatomaceous earth and then screened on two different ELISA plates. We confirmed the structure of suspected fluids by GC-MS (HFBA derivatization), according to EC criteria. Of the 57 samples screened as positive (10.6% of the total), 51 (9.5%) were fully confirmed, while for six it was not possible to identify the drug. The results suggest that the analysis of synovial fluids is an adequate tool to monitor the misuse of beta-adrenergic drugs in animal production, especially when target organs such as liver and kidney are not available for sampling.

Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension.

We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 +/- 1.6 (mean +/- SE) to 101 +/- 1.4 mm Hg (p less than 0.01), and mean pulmonary artery pressure from 21 +/- 0.59 to 17 +/- 1.05 mm Hg (p less than 0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 +/- 0.85 to 29 +/- 0.72 U/m2 (p less than 0.01) and from 4.3 +/- 0.17 to 3.8 +/- 0.18 U/m2 (p less than 0.01), respectively. Indapamide did not change cardiac index (CI) (3,311 +/- 61.6 vs. 3,325 +/- 72.1 ml/min/m2), heart rate (HR) (75 +/- 1.7 vs. 75 +/- 9 beats/min), mean rate of left ventricular ejection index 140 +/- 2.04 vs. 139 +/- 1.99 ml/s/m2, and stroke index (44 +/- 5.6 vs. 43 +/- 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 +/- 0.6 to 5 +/- 0.5 mm Hg (p less than 0.05). Body weight, 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.