The controversial problem concerning the unusual haemodynamics of the deranged circulation during increased hydrostatic tissue pressure (PT) was elucidated by detailed studies of arterial, capillary and venous functions in cat skeletal muscle exposed to graded experimental changes of PT over a wide range. 2. The results indicated that the impaired circulatory state in skeletal muscle during raised tissue pressure is characterized by the following train of events: (a) a primary partial passive compression of the most distal part of the venous system due to negative vascular transmural pressure selectively at this site, in turn leading to the prompt development of a distinct 'venous outflow orifice resistance' graded in relation to the PT rise; (b) a consequent reduction of blood flow graded in relation to this resistance increase; (c) a rise in intramuscular venous pressure proximal of the 'venous outflow orifice' by the same extent as the PT increase; (d) transmission of the raised venous pressure to more proximal vessels in relation to the prevailing segmental resistance ratios; (e) a consequent maintenance of clearly positive transmural pressures in all vascular sections proximal to the 'venous outflow orifice', preventing collapse of these vessels; (f) maintenance of a largely normal capillary filtration coefficient and functional capillary surface area; and (g) an increase in capillary pressure by approximately 85% of the PT rise which reduces the rate of net transcapillary fluid absorption to about one-seventh of that expected from the PT rise per se. 3. Previous concepts of a 'vascular waterfall phenomenon', a capillary collapse, or an arteriolar 'critical closure phenomenon' did not seem to be valid for the skeletal muscle circulation during increased PT. 4. The rate of net transcapillary fluid flux per unit PT change was much smaller during positive than negative PT, since capillary pressure rose considerably when PT was increased above control, but was largely unchanged when PT was decreased below control. 5. Possible ways to improve the circulatory state in conditions with an oedema-induced tissue pressure rise are discussed.
