Hypoxic pulmonary hypertension in the mast cell-deficient mouse

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Abstract
The mast cell was postulated to be involved in hypoxic pulmonary hypertension. The pulmonary vascular response was compared to hypoxia in mast cell-deficient mice (W/WV) with that in normal mice (BALB/c). Chronic exposure to 10% O2 (mean 31 days) increased right ventricular peak systolic pressure during room air breathing under anesthesia from 21 .+-. 2 to 48 .+-. 3 (SE) mm Hg in the normal mouse (n = 7) and from 22 .+-. 4 to 53 .+-. 4 mm Hg in the mast cell-deficient mouse (n = 6). Ten min of reexposure to 10% O2 increased right ventricular peak systolic pressure to 75 (n = 3, range 70-85) and 69 mm Hg (n = 4, range 66-82), respectively. Right ventricular hypertrophy occurred to the same degree in normal (n = 14) and mast cell-deficient mice (n = 14) with an increase in the ratio of right ventricular to left ventricular weight plus septum from 26.7 .+-. 3.2 to 41.9 .+-. 2.1% in the normal mouse and from 26.5 .+-. 3.2 to 39.8 .+-. 2.1% in the mast cell-deficient mouse. Pulmonary arteries also remodeled similarly in the mast cell-deficient and normal mice with hypertrophy and hyperplasia of smooth muscle, extension of smooth muscle into more peripheral vessels and apparent loss of peripheral small arteries. The fractional rise in hematocrit after chronic hypoxia in the normally anemic mast cell-deficient mice was the same as in the normal mice, although the final hematocrit was 45.6 .+-. 1.5 as opposed to 54.5 .+-. 0.6 (P < 0.01). In the mouse, mast cells do not seem to augment or clearly modulate hypoxic pulmonary hypertension. Histamine was not excluded as a mediator of hypoxic vasoconstriction, as histamine content of mast cell-deficient and normal mouse lungs was the same, indicating a non-mast cell source of lung histamine.

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