The effects of intracellular Ca

An 87-year-old woman was admitted to our hospital on an emergency basis with atypical chest pain and dyspnea. She had a continuous precordial murmur. Electrocardiogram showed no evidence of myocardial ischemia, but chest X-ray showed marked enlargement of the cardiac silhouette and an abnormal calcified vascular structure. Computed tomography of the chest revealed large abnormal masses next to the heart. Two-dimensional echocardiography showed enlargement of the main trunk of the left coronary artery and 2 giant saccular aneurysms. Abnormal diastolic inflow to the main pulmonary trunk was also observed by color flow imaging. These findings were supported by data obtained using magnetic resonance imaging and transesophageal echocardiography. Based on the above findings, we diagnosed this case as a coronary artery fistula originating from the proximal left anterior descending artery associated with 2 giant saccular aneurysms draining into the pulmonary artery. To our knowledge, this is the oldest patient ever reported with such an anomaly. This case emphasizes that a good prognosis is possible even with a very pronounced visible structural abnormality.

Intracellular pH (pHi) after the NH+4 pulse addition and its removal were measured in isolated alveolar type II cells (ATII cells) using BCECF fluorescence. In the absence of HCO(-3), the NH+4 pulse addition increased pHi (alkali jump) and its removal decreased pH(i) (acid jump) to the control level (no overacidification). This pHi change was induced by reaction 1 (NH3 + H+ <--> NH+4). However, in the presence of HCO(-3), the NH+4 pulse removal decreased pHi (acid jump) with overacidification. The extent of overacidification was decreased by acetazolamide (a carbonic anhydrase inhibitor), bumetanide (an inhibitor of Na+/K+/2Cl(-) cotransporter [NKCC]), and NPPB (an inhibitor of Cl(-) channel). The NH+4 pulse addition led to the accumulation of NH+4 in ATII cells via reaction 1 and NKCC, and the NH+4 pulse removal induced reaction 2 (NH+4 + HCO(-3) --> NH3 + H+ HCO(-3)) in addition to the reversal of reaction 1. Thus, NH+4 that entered via NKCC reacts with HCO(-3) (reaction 2) to produce H+, which induces overacidification in the acid jump. After the overacidification, the pH(i) recovery consisted of a rapid recovery (first phase) followed by a slow recovery (second phase). The first phase was inhibited by NPPB, glybenclamide, amiloride, and an Na+-free solution, and the second phase was inhibited by DIDS, MIA, and an Na+-free solution. Both phases were accelerated by a high extracellular HCO(-3) concentration. These observations indicate that the first phase was induced by HCO(-3) entry via Cl(-) channels coupled with Na+ channels activities, and that the second phase was induced by H+ extrusion via Na+/H+ exchanger and by HCO(-3) entry via HCO(-3) cotransporter. Thus, in ATII cells, HCO(-3) entry via Cl(-) channels is essential for recovering pHi after overacidification during the acid jump and for removing NH+4 that entered via NKCC from ATII cells, suggesting HCO(-3)-dependent NH3 excretion from lungs.

No abstract