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Segmental vascular resistance in postobstructive pulmonary vasculopathy.

R P Michel¹, T S Hakim, D Petsikas

¹Department of Pathology, McGill University, Montreal, Quebec, Canada.

Journal of Applied Physiology (Bethesda, Md. : 1985)

|September 1, 1990

Summary

Chronic pulmonary arterial ligation in dogs significantly increases pulmonary vascular resistance, primarily due to arterial medial muscle thickening. This condition causes hypersensitivity to serotonin and histamine, impacting blood flow regulation.

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Area of Science:

Pulmonary Hypertension Research
Vascular Biology
Cardiovascular Physiology

Background:

Chronic unilateral pulmonary arterial ligation is a model for studying pulmonary arteriopathy.
This condition leads to increased bronchial collateral flow (Qbr).

Purpose of the Study:

To investigate the effects of chronic unilateral pulmonary arterial ligation on pulmonary vasculature.
To analyze changes in pulmonary and bronchial circulation and vascular resistance.

Main Methods:

Pulmonary artery ligation in seven dogs, followed by pump perfusion of the left lower lobe (LLL) after 120 days.
Measurement of pulmonary arterial flow (Qpa) and bronchial flow (Qbr).
Pressure-flow (P-Q) curve analysis with arterial and venous occlusion, and administration of serotonin and histamine.

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Main Results:

Ligated lobes showed a higher P-Q curve slope (33.4 mmHg.l-1.min) compared to controls (15.9 mmHg.l-1.min).
Increased arterial resistance (22.4 mmHg.l-1.min) was the main contributor, linked to medial muscle thickening and LLL volume loss.
Marked arterial hypersensitivity to serotonin and mild venous hypersensitivity to histamine were observed.

Conclusions:

Postobstructive vasculopathy significantly elevates pulmonary vascular resistance, predominantly upstream of bronchial circulation entry.
The bronchial circulation may play a role in mitigating excessive resistance increases in specific pulmonary segments.