An arterial and venous microcannulation technique was developed for circulatory studies in the cat gastrocnemius muscle which, based on detailed morphological and functional observations of the microvascular arrangement, seems to permit continuous recordings of pressure in arterioles (diameter approximately 25 microns) and capillary pressure. These variables in combination with measurements of arterial and venous pressure and blood flow provided a means of continuous simultaneous recordings of total as well as segmental resistances in defined sections of the vascular bed, viz. in large arterial vessels (diameter greater than 25 microns), arterioles (less than 25 microns), and on the venous side. This new technique was applied to a study of the site(s) of autoregulatory reactions along the vascular bed evoked by changes of arterial pressure over the range 50-150 mmHg. The results indicated that active autoregulation mainly occurred within arterioles smaller than about 25 microns. In larger arterial vessels concomitant moderate active smooth muscle adjustments barely balanced out the pressure-induced passive calibre changes, and the venous vessels did not seem to contribute actively to autoregulation, but exhibited a passive change in postcapillary resistance (Rven). The described pattern of response results in quite effective autoregulation of blood flow and capillary pressure (PC). The observed passive Rven change, via its effect on the pre- to postcapillary resistance ratio, seems to explain the fact that autoregulation of PC can be more efficient than flow autoregulation. The study also provided quantitative data for the level of active intrinsic vascular tone in defined consecutive sections of the muscle vascular bed at normal arterial pressure and for segmental redistributions of tone evoked by pressure alterations.

A venous microcannulation technique applied to the cat gastrocnemius muscle was developed which, based on morphological and functional demonstrations of anastomotic connections between two supplying segmental vascular circuits at the level of capillaries and/or post-capillary venules, seems to permit continuous recordings of hydrostatic pressure (denoted Pcvenule) transmitted from such anastomoses, that is, from a site close to the main fluid exchange vessels. For validity tests, such Pcvenule recordings were compared with simultaneous estimates of capillary pressure (Pc) with the isogravimetric technique (Pciso) and, further, with data for experimentally evoked changes of Pc derived from volumetric recordings of net transvascular fluid flux divided by the capillary filtration coefficient (delta Pcvol). Simultaneously obtained data for Pcvenule and Pciso showed close agreement, and the Pcvenule and Pcvol data showed a highly significant linear correlation over a wide range of Pc changes. These results indicate that reliable estimates of Pc can be obtained with the Pcvenule method. It allows for continuous Pc recordings without interfering with normal vascular reactivity and can be applied to non-isogravimetric conditions and combined with simultaneous observations of whole-organ transvascular fluid exchange. At normal arterial and venous pressures and vascular tone, Pcvenule averaged 16.2 +/- 0.2 mm Hg, at which a Starling fluid equilibrium prevailed, and increased with decreasing vascular tone, resulting in net transvascular fluid filtration.

The controversial hypothesis that capillary pressure (Pc) is autoregulated in response to arterial pressure (PA) alterations was tested in sympathectomized cat skeletal muscle by studying the relation between Pc and PA under conditions of well preserved vascular tone and reactivity, during papaverine-induced maximal vasodilatation (passive vascular bed), and during impaired vascular reactivity caused by preparatory surgery, or by low dose isoproterenol administration. The latter states resembled such under which Pc autoregulation unintentionally seems to have been studied previously. Capillary pressure was assessed with the Pcvenule method for continuous direct pressure recordings from capillaries/postcapillary venules (Mellander et al. 1987) and simultaneously derived from observed net transvascular fluid flux divided by CFC. Resistances in the whole vascular bed and in its pre- and postcapillary segments (Ra and Rv) were determined from recordings of blood flow, PA, Pc, and PV. During preserved vascular reactivity, Pc was found to be virtually constant, that is, almost perfectly autoregulated, over the PA range from 50 to 180 mmHg, whereas in the passive vascular bed there was a direct linear relation between Pc and PA (y = 0.137x + 11.69; r = 0.97). The delta Pc/delta PA ratio was about 1/70 in the normal reactive, and 1/7 in the passive, vascular bed, implying an increase in Pc by 1 mmHg for every 70 mmHg and every 7 mmHg increase in PA, respectively. Capillary pressure autoregulation was explained by precise adjustments of Ra/Rv in relation to PA elicited by myogenic and metabolic regulatory mechanisms. This protective reaction against plasma loss during increased PA was abolished during maximal vasodilation, and was much impaired by surgical trauma, partly via a beta-adrenergic inhibitory effect, and by isoproterenol, in turn causing gross transcapillary fluid fluxes. The latter findings might explain failing Pc autoregulation in some previous studies undertaken under seemingly similar conditions.

An attempt was made to assess, from a large sample (n = 567), the normal level of hydrostatic capillary pressure (Pc) in resting skeletal muscle and the extent of Pc regulation as effected by strictly graded activation of metabolic and adrenergic control mechanisms over the entire physiological range of vascular tone. With the use of a new whole-organ technique, Pc towards the venous end of the capillary was continuously recorded at constant arterial pressure (100 mmHg) and under simultaneous observations of total regional vascular resistance (RT), precapillary resistance (Ra) and post-capillary resistance (RV). In the control state with a Starling fluid equilibrium, a venous pressure of 7 mmHg and normal vascular tone (RT = 19.1 +/- 0.3 PRU), Pc averaged 16.7 +/- 0.3 mmHg. Graded metabolic dilatation (muscle exercise), decreasing RT to a minimum value of 1.7 PRU, caused progressive increase in Pc up to 32 mmHg and consequent fluid filtration. Conversely, graded adrenergic constriction, increasing RT to a maximum of 100 PRU, caused a progressive decrease in Pc down to 10 mmHg and consequent fluid absorption. The relation between Pc and RT was highly non-linear, Pc increasing more steeply the more RT approached low values, and was described by the power function: Pc = 36.43 x RT-0.27 (r = -0.79, P less than 0.001). The resistance ratio, Rv/Ra (the main determinant of Pc), and vascular tone (RT) showed a similar non-linear relation. Regulatory change of Rv/Ra was mainly accomplished by active change of Ra, but a pronounced Rv decrease (venodilatation) occurred in the lowest RT range, exerting a protective function against excessive increase in Pc and detrimental plasma fluid loss.

The sympathetic nervous control of the vascular bed of cat gastrocnemius muscle was studied with a new whole-organ technique which permits simultaneous, continuous and quantitative measurements of capillary pressure (Pc), capillary fluid exchange and resistance reactions in the whole vascular bed and in its three consecutive sections: large-bore arterial vessels (greater than 25 microns), arterioles (less than 25 microns) and veins. The results demonstrated a distinct neural control of all three consecutive vascular sections, graded in relation to the rate of nerve excitation up to maximum at 16 Hz. Stimulation at high rates, which in the steady state caused an average rise of overall regional resistance from 15.3 to 120 PRU (7.8-fold increase), thus raised large-bore arterial vessel resistance from 8.8 to 64 PRU (7.3-fold increase), arteriolar resistance from 4.5 to 49 PRU (10.9-fold increase) and venous resistance from 2.0 to 7 PRU (3.5-fold increase). The rate of resistance development (PRUs-1) of the sympathetic constrictor response was much higher in the arteriolar than in the other sections, which indicates that the neural control is especially prompt and efficient in the arterioles. A passive component was shown to contribute to the described responses only on the venous side, but in no case by more than 10% of the total sympathetic venous resistance response, which thus is mainly active. Of special functional importance was that the new technique provided information about the adrenergic control of Pc in absolute figures. From the control value of 19 mmHg, graded sympathetic stimulation caused a graded decline in Pc, at maximum constriction by about 7 mmHg. This resulted in marked net transcapillary fluid absorption, in turn increasing plasma volume.