In blood vessels in the systemic circulation, the plasmalemmal Na+/H+ exchanger has been implicated in a variety of cellular functions, including the regulation of intracellular pH (pHi) and cell volume, and the response to smooth muscle mitogens. The role of this transport system in pulmonary vascular smooth muscle has not been explored. The present study examined the characteristics of Na+/H+ exchange in cultured guinea pig pulmonary artery smooth muscle cells. These cells were subjected to an acid load, and the recovery from acid loading was monitored using the fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). In the absence of HCO3-, pHi recovery from acid loading was dependent on external Na+ and was inhibited by the Na+/H+ exchange inhibitor dimethylamiloride (DMA) (recovery rate was reduced from 54.4 +/- 5.5 to 12.8 +/- 2.0 mmol H+/liter.min). This exchanger was also active in the presence of HCO3-; DMA reduced resting pHi and slowed the rate of recovery from acid loading in HCO3- buffers. However, in the presence of HCO3-, other transport systems, presumably HCO3-/Cl- exchange, also contribute to the regulation of pHi. In HCO3- buffers, the rate of recovery from acid load averaged 40.8 +/- 1.8 mmol H+/liter.min. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of HCO3-/Cl- exchange, slowed this recovery to 25.5 +/- 1.6 mmol H+/liter.min. A combination of DIDS and DMA further slowed the recovery to 19.7 +/- 1.5 mmol H+/liter.min. These findings indicate that the Na+/H+ exchanger plays a significant role in the regulation of pHi in pulmonary artery smooth muscle cells, even in HCO(3-)-containing buffers.

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Intracranial brain abscess was produced in three monkeys by embolization of a small pledget of polyvinyl alcohol (PVA) soaked in a broth of Staphylococcus aureus. Imaging of the chronic stable abscess was performed on the General Electric 8800 CT unit (Milwaukee, Wis.) and a 1.4 T superconducting small bore imaging system. Magnetic resonance imaging included saturation recovery, inversion recovery, and spin echo techniques. MR imaging was also performed after paramagnetic enhancement using gadolinium-DPTA (Gd-DTPA). Our results show that paramagnetic enhancement with T1-weighted imaging adds specificity and enables rapid assessment of abnormalities of the blood-brain barrier. T2-weighted imaging without paramagnetic enhancement was very sensitive in defining areas of abnormality in the brain but in our experiment lacked specificity. T2-weighted imaging with Gd-DTPA demonstrated no obvious change in the appearance of the lesion. The combination of T1-weighted Gd-DTPA and T2-weighted imaging appeared complementary in our experiment, and these images correlated well with the pathologic findings.