Autoregulation of capillary pressure and filtration in cat skeletal muscle in states of normal and reduced vascular tone

Abstract

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.

Effect of blood pressure on plasma volume loss in the rat under increased permeability

“…As the hydrostatic capillary pressure increases with increase in arterial pressure, it can be expected that an increase in arterial pressure will increase the loss of plasma fluid and proteins to the interstitium via the large pores. This would occur especially under conditions of depressed autoregulation, which is common during sepsis and SIRS or following trauma, as there will be a larger variation in hydrostatic capillary pressure with variation in arterial pressure [13]. This hypothesis offers a therapeutic strategy to reduce the need for blood volume substitution in critically ill patients by decreasing an unnecessarily high arterial pressure and, if confirmed, the results would also support the 2-pore theory for transvascular exchange of fluid and proteins.…”

Sympathetic, parasympathetic and enteric regulation of the gastrointestinal vasculature in rainbow trout (Oncorhynchus mykiss) under normal and postprandial conditions

“…The presence of TTX-insensitive autoregulatory mechanisms in combination with the anesthesia could contribute (Mellander et al, 1987), and also the fact that the gastrointestinal tract seems poorly autoregulated, at least in mammals . Another possible explanation is that the denervation of the gastrointestinal tract leads to a subsequent increase in the resistance of the remaining vasculature (Kremer and Wright, 1932).…”

Influence of pressure alterations on tone and vasomotion of isolated mesenteric small arteries of the rat.

“…This myogenic response may play a role in the autoregulation of flow (Johnson, 1980(Johnson, , 1986 and capillary pressure (Mellander, Oberg & Odelram, 1964;Mellander, Maspers, Bjornberg & Andersson, 1987). Much evidence in favour of a role in autoregulation comes from whole-organ studies.…”