Frogs were sensitized with the same antigens as shown in report-I. After a period of 2〜3 weeks, the isolated frog's heart, which was fixed after Straub's method, was perfused with (1:50,000) solution of rabit myocardial phosphatid. The amplitude of heart contraction was not increased by the test solution in all sesitized groups, but increased in the non-sensitized group.

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In this communication, the author has studied the correlation between electrocardiographic and pathologic findings in 14 cases of coexistent infarction in the anterior and posterior walls of the left ventricle. One or more electrocardiograms, consisting of the multiple unipolar precordial leads (Wilson), the unipolar limb leads (Goldberger), the standard limb leads, and the Nehb's leads were obtained in most cases, and the standard limb leads, from three to five CF leads and the Nehb's leads were taken in few cases. The age of these cases ranged from 52 to 78 except in one case of 22 years old. Of 14 cases, the autopsy revealed that one case had a recent infarction and the other 13 cases had healed infarctions, but electrocardiogram was obtained in the relatively acute stage in at leaset 3 of these 13 case. the cases were classified into the following three groups, according to the distribution of the lesion at autopsy: (1) the infarction in which the so-called anteroseptal infarction involving the anterior free wall and the anteroseptal portion of the left ventricle, and at least the anterior portion of the interventricular septum, extended into the apical portion of the posterior wall of the left ventricle in 5 cases; (2) the large infarction, involved the interventricular septum (at least the anterior portion), and the anteroseptal portion, the anterior free wall, the lateral wall and the posterior wall of the left ventricle, and extending around the almost entire circumference of the left ventricle in 7 cases; (3) the infarction, involved the anterior free wall, the lateral and posterior walls of the left ventricle, and did not extended into the interventricular septem or extended into only the small posterior portion of the interventricular setpum in 2 cases. In the case of anteroposterior infarction, the lesion in the anterior free wall and the anteroseptal portion of the left ventricle, and the interventricular septum was manifested by signs of infraction in the unipolar precordial leads in all cases and the infarction in the lateral wall of the left ventricle was also demonstrated by the diagnostic or suggestive change of infarction in one or more of Leads V_5, V_6, V_7 and _aV_L in most cases (in 7 of 9 cases), but it was only 3 out of 14 cases, that the standard and unipolar limb leads displayed the sign of posterior infarction. Causes for the absence of the diagnostic pattern of posterior infarction under these circumstances, seem mainly to be the limitation of the posterior infarct to less than apical one-third of the posterior wall in 11 cases, and the horizontal position of heart in many cases. In 5 of 7 cases with extensive infarction involved the anteroseptal portion, anterior free wall, lateral wall and posterior wall of the left ventricle, and the interventricular septum, and in one case with infarction in the anterior free wall, lateral wall and posterior wall of the left ventricle and the posterior portion of the interventricular septum, Lead _aV_R displayed a high R wave and disappearance or decrease of a normal Q wave. The standard limb leads were of very limited value in the diagnosis of coexsistent anteroposterior infarction. None of all 14 cases could be diagnosed as anteroposterior infarction from the findings of the standard limb leads. In only 3 of them, the standard limb leads just indicated the sign of anterior infarction, and in another 3, these leads only displayed the sign of posterior infarction.

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