Increased lung lymph transport without heart failure after coronary ligation in sheep

Abstract

Pulmonary edema frequently accompanies acute myocardial infarction (MI). We measured pulmonary arterial (PAP), left atrial (LAP), and aortic pressures (AP),lung lymph flow (QL), and clearance of total serum protein and each of eight protein fractions in five anesthetized sheep before and after coronary artery ligation. After a stable base line of 1 h, ligation produced significant increases in LAP, QL, and clearance of total protein and four protein fractions, but no significant changes in PAP, AP, or lymph-to-plasma total protein concentration ratio (CSL/CSP). Variables returned to pre-MI levels within 2 h after occlusion. The ratio of wet to dry lung weight measured 2 h after ligation was within normal limits. Two sheep in which the time course of postligation LAP was duplicated by left atrial balloon inflation showed no change in QL. The QL changes seen cannot be caused by LAP increase alone without substantial decrease in CSL/CSP. Increased QL with high CSL/CSP is typical of increased lung vascular permeability, which is a plausible explanation of our results.

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

“…Dogs after coronary ligation have higher gravimetric lung water than control dogs with comparable P mv (Spath and Gee, 1979). Lung lymph flow and pulmonary protein clearance in anesthetized sheep rises shortly after coronary ligation despite minimal change in P mv (Collins et al, 1979).…”

“…Although several laboratories have reported similar conclusions using different methods (Massion et al, 1976;Gee et al, 1978;Collins et al, 1979), the mediator(s) of this rise in permeability has not been identified. Berger and co-workers (1976) have shown that after coronary ligation in the anesthetized dog, there is release of prostaglandins E and F from the ischemic myocardiium.…”

“…Recently, several investigators have presented evidence that microvascular hypertension is not the sole explanation for pulmonary edema after coronary ligation in dogs (Gee et al, 1978;Spath and Gee, 1979), cats (Massion et al, 1976(Massion et al, , 1978, and sheep (Collins et al, 1979). These authors suggest that post-MI puimonary edema in part results from increased pulmonary microvascular permeability.…”

Remote preconditioning lessens the deterioration of pulmonary function after repeated coronary artery occlusion and reperfusion in sheep

“…During reperfusion, specific myocardial enzymes (presumably leaked from damaged or necrotic tissue) and inflammatory cytokines 14 are being washed out and reach the lungs, 15 which might lead to lung injury. A series of acute experimental studies 5,[16][17][18] has demonstrated that coronary artery occlusion and reperfusion resulted in pulmonary edema, evidenced by an increase in extra-vascular lung water. Increased pulmonary microvascular permeability is suggested as one of the possible mechanisms.…”

High-Altitude Pulmonary Edema

“…the possible neurogenic component to HAPE, 14 as both cerebral and pulmonary edema of high altitude may coexist; 39 3. the possible role of endogenous opiatesas naloxone, the opiate receptor antagonist, prevents the increased lung lymph flow secondary to intracranial hypertension in sheep; 31 and 4. myocardial ischemia without overt heart failure. 6 With this continued search for mechanism(s) causing HAPE comes the hope that the prevention and cure for the condition will also be found. Nevertheless, it still seems likely that cautious ascent to altitude will remain the best preventative measure and rapid descent once HAPE develops, the best cure.…”