Deciphering "integrated Chinese and Western medicine" in the rural Lijiang basin: state policy and local practice(s) in socialist China.

Based on ethnographic research during an eighteen-month period in 1989-90, this article explores the rural practice of "integrated Chinese and Western medicine" (integrated medicine) in southwest China's Lijiang basin. Integrated medicine is a consciously formulated hybrid medical practice that was introduced by Chairman Mao during the Cultural Revolution as the cornerstone of national health policy. It was originally envisioned as the epistemological handmaiden of the "cooperative health care" system (of "barefoot doctor" fame). The relationship between the respective People's Republic of China (PRC) practices of "Chinese medicine" and "Western medicine" embedded in integrated medicine is explored here on two levels. Integrated medicine is analyzed both as a state policy and as an everyday practice engaged in by village practitioners and lay villagers alike. During the Maoist period, integrated medicine in the rural Lijiang basin was particularly receptive to local interpretation and experimentation by "the masses." This local license in interpreting state policy represented a point of contrast between integrated medicine and other state-sanctioned medical practices. During the ensuing first decade of the post-Mao period, a popular cultural influence on integrated medicine persisted. Integrated medicine is thus examined here both in terms of how state/urban/elite agencies have enacted processes of "syncretism from above" as well as how local/rural/peasant agencies have enacted processes of "syncretism from below" in shaping it as a therapeutic practice. Rural Lijiang basin explanatory models reveal a pattern whereby afflictions are classified according to either "medicine of systematic correspondence" criteria or "stigmatized affliction" criteria. Both types of criteria reflect distinctive interpretations and appropriations of theories rooted in Chinese therapeutic practices and "Western medicine," respectively. The rural basin practice of integrated medicine thus reflects a local appropriation and mediation of state policy, and provides some insight into the nature of a "circularity" that operates between local (or popular) knowledge and state policy in the PRC.

Inhibition of lipid deposition in the hypercholesterolemic rat by clentiazem, a calcium channel blocker.

We studied the effects of clentiazem, a calcium channel blocker (1) on the accumulation of lipid in the aorta, (2) on the level of plasma lipids, and (3) on the number of adherent intimal monocytes and foam cells. Seventy Wistar rats were assigned to one of the following groups: (1) regular diet, (2) an atherogenic diet consisting of regular chow with 2% cholesterol, 1% cholic acid, and 0.5% thiouracil (CCT), (3) CCT supplemented with 5 mg/kg/day clentiazem, and (4) CCT with 25 mg/kg/day clentiazem. Animals were sacrificed after 6 or 12 weeks of diet. Aortas were studied by light microscopy after staining with oil red O (ORO) and/or hematoxylin. ORO staining was quantified in both abdominal and thoracic regions of the aorta. The aortas of the clentiazem groups demonstrated significantly less ORO staining than CCT diet controls in thoracic aorta after 6 weeks and abdominal aorta after 12 weeks. There was no significant difference in the plasma lipid concentrations. The clentiazem-treated groups had fewer numbers of adherent monocytes and foam cells. We conclude that clentiazem inhibits lipid deposition in cholesterol-fed rats without lowering plasma lipid concentrations and that the number of intimal monocytes and foam cells is decreased in the presence of this calcium antagonist.

Metabolism of kadsurenone and 9,10-dihydrokadsurenone in rhesus monkeys and rat liver microsomes.

The metabolism of the PAF antagonists kadsurenone and tritium-labeled 9,10-dihydrokadsurenone was studied in rhesus monkeys and rat liver microsomes. The monkey metabolites of the two drugs were isolated as their glucuronide conjugates from the urine of iv dosed males. The metabolites from both monkey and microsomal metabolism were purified by reverse phase HPLC and identified by spectral (NMR, UV, and mass spectrometric) analysis. The principal pathway of biotransformation of the tritium-labeled 9,10-dihydrokadsurenone in monkeys was hydroxylation of the C-5 propyl side chain to give two metabolites, 10-hydroxy-9,10-dihydrokadsurenone and 9-hydroxy-9,10-dihydrokadsurenone. These compounds were excreted as glucuronides. Microsomal incubation of tritium-labeled 9,10-dihydrokadsurenone yielded the 10-, 9-, and 8-hydroxy-9,10-dihydrokadsurenone as major metabolites. Kadsurenone was also metabolized at the C-5 side chain, an allyl group. The monoglucuronide of 9,10-dihydroxykadsurenone was isolated from monkey urine. Spectral analysis was not definitive as to the site of conjugation, and the structure of the metabolite was assigned as the C-10 conjugate. A major metabolite of rat liver microsomal incubation of kadsurenone was 9,10-dihydroxykadsurenone.