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The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

Recent reports have indicated that vascular responsiveness can be altered by exogenously administered or endogenously released prostaglandins. Furthermore, in certain tissues inhibitors of prostaglandin synthesis have been shown to limit the increase in blood flow in response to bradykinin and to enhance the reduction in blood flow in response to angiotensin and norepinephrine. These findings suggest an important local circulatory role for prostaglandins. We attempted to implicate further prostaglandins in local blood flow regulation by examining the effects of indomethacin (IND) and 5,8,11,14-eicosatetraynoic acid (ETA), inhibitors of prostaglandin synthesis, on microvascular arteriolar responses to bradykinin, prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), histamine, norepinephrine, and angiotensin. Male Wistar rats were anesthetized with sodium pentobarbital, and their cremaster muscle was exteriorized and prepared for in vivo microscopic observation of microvessels. Changes in arteriolar luminal diameters in response to topical administration of vasoactive agents were quantified with an image-shearing measuring eyepiece in conjunction with a television microscope and recorder. Local administration of IND or ETA significantly reduced the arteriolar dilation elicited by bradykinin, whereas the responses to PGE1 and PGE2 remained unaltered. Responses to histamine, although somewhat reduced, were not significantly different from control. Vasoconstrictor responses of arterioles elicited by norepinephrine and angiotensin were potentiated by IND or ETA administration. These results indicate that prostaglandins synthetized in skeletal muscle microcirculation in situ (1) mediate, in part, vasodilator responses to bradykinin and (2) modulate vasoconstrictor responses to angiotensin and norepinephrine. Thus, these findings support the hypothesis that prostaglandins are local regulators of microvascular responsiveness.

Several studies implicate endogenously synthesized prostaglandins in the mediation of reactive hyperemic responses in the coronary, renal, and skeletal muscle circulations. We sought additional evidence to involve locally released prostaglandins in the mediation of reactive hyperemia in skeletal muscle at the level of the microcirculation. The cremaster muscle of pentobarbital-anesthetized Wistar-strain rats was prepared for direct in vivo observation and measurement of postocclusive responses of single arterioles. Responses of individual arterioles were reproducible over a 3-h test period. The postocclusion increase in diameter and the duration of response were dependent upon the duration of the occlusion. Repetitive occlusions did not influence arteriolar responsiveness to vasoactive substances. Indomethacin and 5-8-11-14-eicosatetraynoic acid, inhibitors of prostaglandin synthesis, did not affect resting arteriolar diameters; however, both drugs decreased the maximum increase in diameter and duration of the vasodilator response following release of the arteriolar occlusion. These findings suggest that in this microcirculatory bed, prostaglandins contribute little to resting vascular tone; in contrast, temporary arteriolar occlusion elicits the local release of dilator prostaglandins which contribute to the reactive hyperemic response.

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