Distribution of lung vascular resistance after chronic systemic-to-pulmonary shunts

Abstract

Congenital cardiac shunts produce pathological lesions on the arterial side of the lung vasculature. We examined the effects of chronic shunts (14.2 +/- 1.2 mo) in 10 young dogs, between the left subclavian and the left lower lobe (LLL) artery, on pulmonary vascular pressure and flow (P-Q) relationships, segmental resistance with arterial and venous occlusion (AVO), and sensitivity to drugs. At final thoracotomy, mean LLL pulmonary arterial pressure (Ppa) was 23.2 +/- 4.3 mmHg compared with 11.9 +/- 0.9 in the right lung (P less than 0.05); two animals had LLL Ppa of 41 and 48 mmHg. The LLL artery and vein were cannulated, and pressure-flow (P-Q) and AVO measurements were made and compared with previous control LLL (n = 11) and contralateral right lower lobe (RLL, n = 5). Responses to serotonin, histamine, and vasodilators (diltiazem and isoproterenol) were evaluated. Comparisons of morphometric measurements were made between LLL and RLL. We found a significant increase in arterial resistance as measured with AVO and a hypersensitivity to serotonin in the shunt LLL, without changes in total pulmonary vascular resistance or P-Q measurements; vasodilators had a small effect only in the hypertensive lobes. Our data suggest that chronic shunts to the pulmonary circulation increase arterial resistance and sensitivity to serotonin, even in the absence of discernible morphometric changes, and that vasoconstriction may be an important precursor to the development of morphological lesions.

Pulmonary Hypertension in Hemodialysis Patients

“…Medical conditions with shunting of blood from the left to the right side of the heart and increased cardiac output and pulmonary blood flow, such as congenital heart disease, are well recognized as possible causes of PH. 5,6 Excess mortality rates due to cardiovascular disease in end-stage renal disease (ESRD) patients had been described by epidemiological and clinical studies. It accounts for approximately 50 percent of deaths in dialysis patients.…”

Pulmonary Vein Total Occlusion Following Catheter Ablation for Atrial Fibrillation

“…Both the pulmonary venous and arterial systems are well known to be interrelated (10 -13). It has been shown that sudden occlusion of a pulmonary vein is soon followed by gradual decline and then cessation of the arterial flow to the affected segment (12,14). This is caused by a decline in the arteriovenous gradient as well as compression by the developing tissue edema (10).…”

“…As a consequence, the involved alveoli are affected by the resulting ischemia and surrounding edema, leading to atelectasis, infarction, or susceptibility to infections (15). With the resulting alterations in pulmonary hemodynamics, redistribution of blood flow occurs with opening of vascular channels or neovascularization in which tissue hypoxia is known to play a role (12,14). Hence, the venous drainage of the affected segment becomes mainly dependent on the ipsilateral veins draining the healthy lobes.…”

The relationship between arteriovenous fistula blood flow rate and pulmonary artery pressure in hemodialysis patients

“…The major mechanisms for the development of PH are an increase in pulmonary BFR and pulmonary vascular resistance [13,14]. Both mechanisms are involved in patients with chronic renal failure.…”