Ganong's Review of Medical Physiology, 23rd Edition

604 SECTION VIIRespiratory Physiology

ganglia reduces pulmonary blood flow by as much as 30%.
The vessels also respond to circulating humoral agents. Sev-
eral of the receptors involved and their effect on pulmonary
smooth muscle are summarized in Table 35–4. Many of the
dilator responses are endothelium-dependent and presum-
ably operate via release of nitric oxide (NO).
Passive factors such as cardiac output and gravitational
forces also have significant effects on pulmonary blood flow.
Local adjustments of perfusion to ventilation are determined
by local effects of O 2 (or the lack of O 2 ). With exercise, cardiac
output increases and pulmonary arterial pressure rises pro-
portionately with little or no vasodilation. More red cells
move through the lungs without any reduction in the O 2 satu-
ration of the hemoglobin in them, and consequently, the total
amount of O 2 delivered to the systemic circulation is
increased. Capillaries dilate, and previously underperfused
capillaries are “recruited” to carry blood. The net effect is a
marked increase in pulmonary blood flow with few, if any,
alterations in autonomic outflow to the pulmonary vessels.
When a bronchus or a bronchiole is obstructed, hypoxia
develops in the underventilated alveoli beyond the obstruc-
tion. The O 2 deficiency apparently acts directly on vascular
smooth muscle in the area to produce constriction, shunting
blood away from the hypoxic area. Accumulation of CO 2
leads to a drop in pH in the area, and a decline in pH also pro-
duces vasoconstriction in the lungs, as opposed to the vasodi-
lation it produces in other tissues. Conversely, reduction of
the blood flow to a portion of the lung lowers the alveolar
PCO 2 in that area, and this leads to constriction of the bronchi
supplying it, shifting ventilation away from the poorly per-
fused area. Systemic hypoxia also causes the pulmonary arte-
rioles to constrict, with a resultant increase in pulmonary
arterial pressure.

FIGURE 35–21 Effects of decreasing or increasing the
ventilation/perfusion ratio (V

(^) A/Q

• ) on the PCO 2 and PO 2 in an
  alveolus. The drawings above the curve represent an alveolus and a
  pulmonary capillary, and the dark red areas indicate sites of blockage.
  With complete obstruction of the airway to the alveolus, PCO 2 and PO 2
  approximate the values in mixed venous blood (V


• 
  

  ). With complete
  block of perfusion, PCO 2 and PO 2 approximate the values in inspired
  air. (Reproduced with permission from West JB: Ventilation/Blood Flow and Gas
  Exchange, 3rd ed. Blackwell, 1977.)

  
  


• •

50

050100 150

_ O A

V

Decreasing VA/Q

Increasing VA/Q

Normal

PO 2 (mm Hg)

PCO

(mm Hg) 2

• •

TABLE 35–4 Receptors affecting smooth

muscle in pulmonary arteries and veins.

Receptor Subtype Response

Endothelium

Dependency

Autonomic

Adrenergic α 1 Contraction No

α 2 Relaxation Yes

β 2 Relaxation Yes

Muscarinic M 3 Relaxation Yes

Purinergic P2x Contraction No

P2y Relaxation Yes

Tachykinin NK 1 Relaxation Yes

NK 2 Contraction No

VIP? Relaxation?

CGRP? Relaxation No

Humoral

Adenosine A 1 Contraction No

A 2 Relaxation No

Angiotensin II AT 1 Contraction No

ANP ANPA Relaxation No

ANPB Relaxation No

Bradykinin B 1? Relaxation Yes

B 2 Relaxation Yes

Endothelin ETA Contraction No

ETB Relaxation Yes

Histamine H 1 Relaxation Yes

H 2 Relaxation No

5-HT 5-HT 1 Contraction No

5-HT1C Relaxation Yes

Thromboxane TP Contraction No

Vasopressin V 1 Relaxation Yes

Modified and reproduced with permission from Barnes PJ, Lin SF: Regulation of pul-

monary vascular tone. Pharmacol Rev 1995;47:88.