Different types of aortic stenosis and simulation of their morphological-hydrodynamic interdependence--in vitro study with allografts and stenotic valve models.

Biological valves display a dependence of valve resistance and valve area on flow and a phase shift between systolic flow through the valves and pressure difference across the valves. The pressure-flow relations of stenosed valves raise questions about the "best measure of stenosis". There is a need for quantitative evaluation of the hydrodynamic performance of homografts and allografts. In the present paper, we report on in vitro studies of the hydrodynamic behavior of homografts from human donors, allografts from different animal species as well as three valve models. Valve model I was designed to simulate flow-dependence of valve area, valve model II was designed to simulate restricted valve opening independent of flow, and valve model III was designed to simulate a flow-dependent movement of valve root in flow direction. Among other aspects, the effect of increased viscosity of the test fluid on the pressure difference and the effects of water absorption by valve tissue on valve characteristics were investigated. The results of the present studies clearly indicate that any biological valve may be modelled as a serial connection of a model I type valve and a model II type valve. From the results, the dependence of the characteristic pressure-flow relationship of a valve on valve size and valve distensibility can be clearly seen and the clinical significance of the characteristic coefficients of the pressure-flow relationship of a valve can be elucidated. Further, it was shown that the characteristic phase shift between flow and pressure difference displayed by biological valves is due to their movable valve plane similar to that of valve model III.

Cerebral trauma-induced changes in corpus striatal dopamine receptor subtypes.

A device designed specifically for mild to severe concussions was used to produce quantitative experimental blunt brain injury in male Wistar rats. We have examined the effects of varying magnitudes of cerebral trauma on the maximal binding capacity (Bmax) of D1 and D2 dopamine (DA) receptors. The Bmax for each receptor subtype was obtained from Scatchard analyses of [3H]-SCH 23390 and [3H]Spiperone binding to striatal membrane. Anesthetized rats were injured--one, two, or three times--once every 24 h, with either a 68- or 268-g rubber-headed reflex hammer accelerated from a predetermined distance. Uninjured nonanesthetized (NA) and anesthetized (A) rats served as controls. No significant difference in receptor density was observed between NA and A rats for each receptor subtype. Immediately (0 h) following injury from the 68-g hammer weight, the density of D1 receptors decreased (50%), then increased (30%) above control levels by 24 h. The same pattern was observed with the 268-g hammer weight. Analysis of variance (ANOVA) showed that there was no overall effect of number of injuries or treatment on the density of D1 and D2 receptor subtypes. However, there was an interaction of both variables on the D1, but not D2, receptor subtype. Partial ANOVA for receptor densities after rats were injured either one, two, or three times showed that receptor density was altered only after the rats were injured one time. These results suggest that striatal DA D1 receptors are downregulated and then upregulated following isolated injury to the cerebral cortex.