We evaluated the effects of cilostazol, a selective inhibitor of cyclic adenosine monophosphate phosphodiesterase, on the pial vessels of adult cats subjected to endothelial damage followed by middle cerebral artery occlusion. Six cats were treated with cilostazol and four with 30% JVVV-dimethylfonnamide in 70% saline (solvent). The brain surface was irradiated with ultraviolet rays through a cranial window for 3 minutes to selectively damage the endothelium of the pial vessels in both groups. Beginning 32 minutes after termination of the irradiation, the middle cerebral artery was occluded for 30 minutes. Thirty minutes before occlusion, intravenous infusion of 30 /ig/kg/min cilostazol or 0.1 ml/kg/min solvent was begun and continued until the end of the study. Before occlusion, the infusion of cilostazol induced a significant (p<0.05) dilatation while the infusion of solvent produced no significant changes in the diameter of the pial arteries. The pial veins of solvent-treated cats showed significant (p<0.05) constriction during occlusion, whereas cilostazol-treated cats exhibited only mild constriction of the pial veins. The formation of platelet thrombi after occlusion was significantly (p<0.05) inhibited in the pial veins of cilostazol-treated compared with solvent-treated cats. Similarly, the microcirculation of the pial veins was effectively restored after reopening of the middle cerebral artery in cilostazol-treated compared with solvent-treated cats. Our data suggest that cilostazol is an effective antithrombotic agent as well as a potent vasodilator acting on vascular smooth muscle. (Stroke 1989;20:668-673)

A 73-year-old male was hospitalized for cerebral bleeding in his thalamus and complained of chest pain during his hospitalization. During the heart attack, the ECG showed an ST-segment depression in leads II, III, and aVF. A thulium cardiac scintigram showed an inferior redistribution, indicating the presence of coronary heart disease. The patient had a history of hypertension and hypercholesterolemia, but no history of bronchial asthma or esophageal problems. Three months later, the patient was transferred to the cardiology department and a cardiac catheterization was scheduled. A plain chest roentgenogram showed a bilateral aortic notch at the level of aortic arch, indicating possible congenital abnormalities ( Figure 1). A computed tomography scan and magnetic resonance imaging revealed a double symmetric aortic arch in both the left and right sides (Figure 2 and 3). The catheterization revealed a double aortic arch with advanced 3-vessel coronary artery disease. The patient underwent aortocoronary bypass surgery. The postsurgical course was uneventful and the patient was discharged (Figure 4). Double aortic arch or aortic ring is a congenital abnormality. In most cases, this abnormality is diagnosed in childhood because of symptoms related to esophageal or tracheal obstruction, and surgical correction usually yields a good prognosis. Sporadic cases have been reported in adult patients, who are usually diagnosed after complaining of asthma-like symptoms or swallowing difficulties because of the compression of the trachea or esophagus by the abnormal aortic arches. Case reports of elderly patients are rare, especially symptom-free cases. The patient's double aortic arch was defined accidentally when he began suffering from cerebral bleeding and his coronary heart disease became symptomatic. In this particular case, the trachea and esophagus were placed in the middle of the aortic ring without compression, because the right and left aortic arches were almost the same size and the inner space of the ring was large enough to fit them both inside. DisclosuresNone.

We investigated the change in the instantaneous diastolic left coronary pressure-flow relation (DPFR) when the pressure surrounding the heart (SHP), right heart pressure (RHP), and left heart pressure (LHP) were systematically varied. Eight excised and maximally vasodilated canine hearts placed in an air-tight chamber were used. To obtain a capacitance-free DPFR, coronary perfusion pressure was slowly decreased (about 2 mm Hg/sec) during a prolonged diastole. The zero-flow pressure (Pf = 0) and the slope of the DPFR were analyzed. The mean values of the slope did not change significantly throughout the interventions. The mean value of Pf = 0 in the control state (SHP = RHP = LHP = 0 mm Hg) was 6.0 +/- 2.0 mm Hg (mean +/- SD, n = 8), significantly higher than the venous outflow pressure, RHP (p less than 0.001), and the other two pressures (p less than 0.001). When SHP was raised to 15 and 30 mm Hg, while the other pressures remained at 0 mm Hg, the mean values of Pf = 0 increased to 20.9 +/- 2.4 and 35.6 +/- 3.1 mm Hg (p less than 0.001 and p less than 0.0005, respectively, vs. control). The mean values of Pf = 0 when only RHP was elevated to 15 and 30 mm Hg were 16.0 +/- 1.5 and 29.3 +/- 1.5 mm Hg (p less than 0.001 and p less than 0.0005 vs. control). On elevation of LHP to 15 and 30 mm Hg, the mean values of Pf = 0 were 12.0 +/- 2.8 and 17.3 +/- 3.6 mm Hg (p less than 0.01 and p less than 0.01 vs. control). When both SHP and LHP were almost evenly elevated to about 15 and 30 mm Hg, the mean values of Pf = 0 were raised to 22.0 +/- 2.9 and 35.3 +/- 3.2 mm Hg, respectively. These mean values were not significantly different from those when only SHP was elevated to the comparable levels. The observation that Pf = 0 exceeded RHP in the control state and that RHP, which was elevated above the preceding Pf = 0, was identical with the present Pf = 0 supports the vascular waterfall mechanism when RHP is low. Furthermore, the evidence that the degree of DPFR shift was almost linearly dependent on the SHP level rather than on the LHP level indicates that the pressure on the epicardial side is one of the factors that determines the pressure at the top of the vascular waterfall.

We evaluated the effect of a stable synthetic prostacyclin analogue, TRK-100, on the microcirculatory derangement occurring in feline pial vessels with endothelial damage after middle cerebral artery occlusion. Fifteen adult cats were divided into an untreated group (Group 1, n = 8) and a treated group (Group 2, n = l). Thirty minutes after 10 minutes of ultraviolet irradiation, which selectively damaged endothelium in the pial vessels, the middle cerebral artery was occluded in both groups and maintained for 30 minutes. In Group 2, 50 ng/ kg/min TRK-100 was continuously infused intravenously following ultraviolet irradiation. In both the pial arteries and veins, platelet aggregate adhesion to the endothelium with subsequent thrombus formation was significantly (/?<0.01 and /><0.05, respectively) inhibited during middle cerebral artery occlusion in Group 2 compared with Group 1. Similarly, blood flow stasis in the pial veins was effectively prevented in Group 2 during occlusion. Furthermore, the pial artery diameter returned to the control level during the late period of occlusion, whereas in Group 1 the pial artery remained constricted. Our data suggest that TRK-100 can prevent microcirculatory derangement in the acute stage of ischemic stroke. {Stroke 1988; 19:1267-1274)

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