In cats anesthetized with pentobarbital, 188 direct microvascular pressure and diameter measurements were made of the tenuissimus muscle. The microvascular pressure in arterioles of 70 mum in diameter or larger was proportional to the systemic arterial pressure (PA). The arterioles with diameter-s ranging from 35 to 20 mum have been shown to be the principa-l source of arteriolar resistance regulating micropressures downstream. Across the capillary bed proper, the drop in pressures was about 15% of PA. Micropressures in the smallest venules (8-15 mum) averaged 24 mmHg and reflect closely capillary blood pressure. With a background of basic microvascular data, the vasodilatory mechanism of papaverine (P) and isoproterenol (IPR) in the skeletal muscle was analyzed. Administration of IPR decreases both arteriolar and venular pressure, while P infusion decreased the pressure in arterioles wider than 20 mum in diameter; however, in smaller arterioles there was a substantial elevation in micropressure. The data establish two basically different vasodilatory effects on the terminal vasculature: one with increased capillary pressure and fluid filtration (P), a second with a decrease in capillary pressure enhancing absorption (IPR).
The terminal lymphatics are a network of highly previous vessels that are distributed in a loose association with the blood capillary bed, in particular along with the collecting venules. The base-line pressure in these lymphatics is close to atmospheric, but after they converge to form valved collecting channels PL is increased with a pressure differential of 1-2 cmH20 built up across each valve. This increment in lymphatic pressure is clearly related to the presence of one-way valves, the contractile activity of the collecting channels, and the comparative impermeability of these channels. The pressure differential required to draw fluid from the interstitium into the lymphatics would appear to reside in the vasomotor activity of the collecting channels, although the data do not rule out changes in Pt coincident with net capillary filtration or absorption.
SUMMARY Information concerning the microcirculation has been obtained largely by intravital microscopy of selected tissues in the rat-skeletal muscle and splanchnic viscera, as well as in the cheek pouch of the hamster. The data for the most part pertain to the spontaneous form of hypertension in the SHR strain of rats and renovascular forms of the disease involving surgical manipulation of the kidney or its blood supply. Direct measurements of pressure and flow in exteriorized skeletal muscle preparations reveal a 2-to 3-fold increase in resistance to flow. An increase in resistance appears in the terminal arterioles and their precapillary branches as early as at 4 weeks of age for SHR animals and is progressively exacerbated in older more mature animals. The increase in microvascular resistance appears to develop as a consequence of neurogenic and humoral mechanisms which act initially on larger arterioles (50-100 /xm) and subsequently on the peripheral arterioles (15-25 /xm in diameter). The smaller arterioles not only show an increased tone under steady state conditions but what can be referred to as a functional rarefaction in which 30% to 50% of the precapillary extensions of the arterioles are shut off for varying periods from the active muscle circulation. Structural rarefaction (a reduced number of arterioles) is seen only in the late stages of the SHR syndrome and can account for a small portion of the increase in peripheral resistance. The cause and effect relationship between the microvascular changes and the associated elevation in systemic pressure cannot be unequivocally demonstrated in intravital preparations. Hypertension induced by different experimental modalities does not have a consistent microcirculatory counterpart, leading to the conclusion that depending on the precise mechanisms involved in the initiation of the syndrome, microcirculatory derrangements can arise as either initiating or secondary phenomena. Tissue pathology is uniformly associated with a reduction in arterial supply, and uneven distribution of blood and red cell hematocrit in the network proper. On the postcapillary side, there is a trend for venular tortuosity and distension.
Initial lymphatics are noncontractile and drain into collecting lymphatics with a smooth muscle intima, valves, and peristalsis, How does interstitial fluid enter the initial lymphatics?
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