Blood cardioplegia serves as a bicarbonate donor to the myocardium during ischemia: effects of anoxia and hypercapnia on acid-base characteristics of blood cardioplegic solution.

OBJECTIVES: We investigated the alterations of acid-base characteristics of the blood cardioplegia (BCP) solution during aortic cross-clamping in hearts arrested with BCP and during in vitro-simulated ischemia. METHODS: Following aortic cross-clamping, the hearts of 40 patients undergoing cardiac surgery were intermittently infused with an 18°C BCP solution and finally with a 34°C BCP solution prior to aortic cross-clamp release. We measured the pH, partial CO(2) pressure (pCO(2)), [HCO(3)(-)], and [Cl(-)] of the coronary sinus effluent in the final BCP solution. The BCP solution was assessed under in vitro gassing at 34°C with 95% N(2) + 5% CO(2) (n = 6), 50% N(2) + 50% CO(2) (n = 3), or 100% CO(2) (n = 6). RESULTS: The coronary sinus effluent, compared with the preinfusion BCP solution, exhibited a significantly lower pH and a greater pCO(2) with no change in the [HCO(3)(-)] level. In vitro, the 95% N(2) + 5% CO(2) gassing (simulated hypoxia) group exhibited a slight increase in [HCO(3)(-)] with no change in pCO(2) or pH whereas the 50% N(2) + 50% CO(2) gassing and the 100% CO(2) gassing (simulated hypoxia and hypercapnia) groups exhibited a significant increase in [HCO(3)(-)] under high pCO(2)-induced acidification. CONCLUSIONS: Under anoxia and CO(2) retention during aortic cross-clamping, the BCP solution can be a bicarbonate donor to the myocardium.

[Simultaneous abdominal aortic replacement and thoracic stent-graft placement for multiple aortic aneurysms: report of a case].

Patients with aneurysmal disease involving both the thoracic and abdominal aorta have historically required simultaneous or sequential conventional operations. Staged operations were generally preferred, but we experienced that a patient had rupture of the second aneurysm after he finished initial treatment for the first aneurysm. We have implemented simultaneous operation using thoracic stent-graft placement. A 78-year-old male who had multiple aortic aneurysm involving both the thoracic and abdominal aorta underwent conventional abdominal aortic replacement with endovascular stent-graft placement into the distal arch of the thoracic aorta under fluoroscopic guidance. The stent-graft was composed of two units of self-expanding stainless-steel Z stent covered with an thin wall woven Dacron graft. Postoperative aortography showed no stent migration and no endoleak. Simultaneous abdominal aortic replacement and deployment of a thoracic stent-graft may be a valuable treatment option for these patients. However, careful long term follow up is necessary to prove the value and the effects of the endovascular treatment.

A new approach to the development of anti-ischemic drugs. Substances that counteract the deleterious effect of lysophosphatidylcholine on the heart.

Lysophosphatidylcholine (LPC) is an amphiphilic metabolite that can be produced from membrane-phospholipids by activation of phospholipase A2 (PLA2), and it accumulates in the heart during ischemia and reperfusion. It is known that LPC is an arrhythmogenic substance. Recent studies have revealed that LPC produces mechanical and metabolic derangements in perfused working rat hearts, and Ca(2+)-overload in isolated cardiac myocytes. Thus, LPC possesses an ischemia-like effect on the heart. LPC accumulated in the myocardium activates phospholipase A2, establishing a vicious circle; i.e. LPC itself has an ability to produce another LPC. Therefore, a drug that has an anti-LPC effect would protect or improve ischemia/reperfusion damage. This article will review the effect of LPC in relation to ischemia, and consider a possibility of developing new anti-ischemic drugs on the basis of the anti-LPC action.

Exogenous lysophosphatidylcholine increases non-selective cation current in guinea-pig ventricular myocytes.

Whole cell, patch-clamp studies were performed to examine the effect of lysophosphatidylcholine (LPC) on the membrane current in guinea-pig ventricular myocytes. The addition of 10 microM LPC to the external solution induced a membrane current which had a reversal potential of 0 mV. When Na+, the main cation in the external solution, was replaced by either K+, N-methyl-D-glucamine (NMG) or 90 mM Ca2+, LPC induced a current with the reversal potential near 0 mV, indicating that the current passed through a Ca2+-permeable non-selective cation channel. The order of the cationic permeability calculated from the reversal potential of the current was Cs+ > K+ > NMG > Na+ > Ca2+. Cl- did not pass through the LPC-induced channel. The LPC-induced current was not blocked by Gd3+ in the external solution, nor by the absence of Ca2+ in the pipette solution. In conclusion, LPC induces a Ca2+-permeable non-selective cation channel in guinea-pig ventricular myocytes.