contraction between the body of the left ventricle and the papillary muscles, which leads to mitral regurgitation, rapid decompression of the left ventricle, and concentric hypertrophy. The importance of outflow tract obstruction and the possible contribution of excessive catecholamines within the heart in producing an abnormally powerful and rapid contraction of the left ventricle are debated.It is concluded that while lesions which produce eccentric hypertrophy do not usually involve the papillary muscles or cause subvalvar mitral regurgitation, disorders which cause obstruction to outflow and which are associated with concentric hypertrophy and with reduction in the size of the cavity in systole are often associated with papillary muscle disorder and thus with mitral regurgitation.
SummaryThe effect of white cells on platelet aggregation has been studied. White cells have little or no effect on nor-adrenaline induced clumping, produce disaggregation of ADP, 5HT and thrombin induced clumping, and first enhance and then reverse ATP induced clumping. The effects of white cells on clumping are similar to their effects on the clumping agents themselves, for they do not inactivate nor-adrenaline, but rapidly inactivate ADP, and produce a more active agent from ATP. In respect of the patient to patient variability in clumping activity, the amount of aggregation produced by ATP is very closely related to the white cell content of the PRCP, whereas the variations in ADP induced clumping must be due to other factors. The significance of these findings for the possible role of the platelet clumping agents in arterial thrombosis is discussed.
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