Screen filtration pressure and pulmonary hypertension

Abstract

A series of experiments was devised to test the resistance to flow through the lungs of blood samples with different screen filtration pressures (SFP). The pulmonary artery and left atrial presures were measured in dogs rendered acutely hypotensive by rapid bleeding, and in others subjected to severe soft tissue trauma. Following acute hypotension the SFP always increased before and more markedly in the pulmonary artery than it did in femoral artery or vein blood. In other dogs similar measurements were made in normotensive dogs perfused with blood having a high screen filtration pressure. In each of these series of experiments the pulmonary artery pressure and difference between it and the left atrial pressure increased when the blood of the animal developed a high SFP (during hypotension and after trauma), or when high SFP blood was infused into the animal. It was suggested that the high SFP was due to adhesive and aggregated blood cells, especially platelets and leukocytes, and that these aggregates had occluded numerous blood conduits of the lungs.

Acute Changes in Adhesive Platelet Count and Pulmonary Hemodynamics in Tourniquet Shock of Dogs

“…Neither the present report, nor papers by other authors [4,18,31] consider sufficiently that other parameters such as diminished flow, acidosis, and low Po2 contribute to an increase in PVR in shock.…”

“…An obstruction of the pulmonary vascular bed by platelet aggregates [1,18,31], or a vasoconstriction by releasing vasoactive substances out of plate lets [3,29,32], cannot be excluded as a cause for the increase in PVR. However, the amount of changes of resistance and platelet count is not closely correlated.…”

“…An influence of blood platelets and platelet aggregates on pulmonary hypertension after hemorrhage was first reported by H issen and Swank [18]. Ljungqvist et al.…”

“…An increase in pulmonary vascular resistance (PVR) is a common finding [11,15,18,19,33] and it is believed that this rise in PVR is a major pathophysiolo gical index for late pulmonary complications [2,11,15,19,31].…”

“…[26] demonstrate a remarkable amount of platelet trapping in the lung in experimental traumatic shock. Increased adhesive ness of blood platelets in shock presumably causes platelet aggregates and a rise of PVR either by mechanical obstruction [1,18,31] or by releasing vasoactive substances [29,31,32].…”