In this paper, we report the purification and partial characterization of human platelet aggregation factor form the extracelular products (ECP) of Streptococcus mitis (S. mitis) isolated from a patient with Kawasaki disease (KD). Platelet aggregation reaction was carried out using platelet-rich plasma (PRP) and washed platelets suspended in ACD-PBS. The aggregation factor was disignated as S. mitis-derived human platelet aggregation factor (Sm-hPAF). The results obtained were as follows.
1) Sm-hPAF was isolated by chromatography on DEAE-Sepharose CL-6 B, hydroxyapatite and Superdex 75 columns. The purified Sm-hPAF showed a single band upon SDSpolyacrylamide gel electrophoresis (SDS-PAGE) and molecular weight of approximately 66 kDa on SDS-PAGE. The isoelectric point (0) of Sm-hPAF was 8.5, and Sm-hPAF showed an absorption peak at 278 nm on absorption spectra. When the platelet aggregation activity of the Sm-hPAF was compared with that of ECP, the specific aggregation activity of Sm-hPAF was significantly increased (up to 28-fold). Sugars were not found in Sm-hPAF. The sequence of the first 15 amino-terminal amino acid residues were ^H-Asp-Glu-Gln-Gly-Asn-Arg-Pro-Val-Glu-Thr-Glu-Asn-Ile-Ala-Arg. The platelet aggregation activity of Sm-hPAF was inactivated by heating at 45C for 10 min.
2) PGE₂ was released from platelets after incubation for 10 min with Sm-hPAF in a dose-dependent fashion. Platelet aggregation by the Sm-hPAF was totally inhibited by either PGE, or GRGDS, but these reagents did not inhibit the platelet aggregation by collagen.
3) Histological examination of the rabbit skin sites showing an early reaction revealed increased dilatation of the veins and capillaries with cellular infiltration in the perivascular space of the dermis. Hyperplasia of the endothelial cells was noted. Degeneration of the vascular walls was observed in the later stages of the reaction. Aggregation of red cells in the vascular endothelium was also observed. Sm-hPAF was capable of producing vasculitis.
4) Twenty (76.9%) platelet-rich plasma samples (PRP) derived from 26 healthy human volunteers reacted with Sm-hPAF, but the remaining 6 PRPs were not reactive. Preliminarystudy suggests the existence of an inhibitory factor in plasma from nonreactive donors.

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The evolution of neuronal damage in various regions during ischemia and in early recovery was investigated morphologically using hyperglycemic and normoglycemic Wistar rats.
Hyperglycemia (20-35, μmol/ml plasma) was achieved with the infusion of glucose (i. v.) prior to ischemia. Forebrain ischemia (10 minutes) was induced by bilateral common carotid artery occlusion and hypotension. Normoglycemic rats were fasted prior to ishcemia. Ischemic changes of neurons were quantified by a five-point scale in the caudoputamen (CPu), globus pallidus (GP), hippocampus CA 1 (CA 1), parietal cortex (Par), and substantia nigra reticulata (SNR) during ishcemia and for 90 minutes after recirculation.
In the hyperglycemic group, (1), CPu, CA 1 and Par ; severely damaged neurons were seen at 60-90 minutes after recirculation. (2) GP; there was little neuronal damage. (3) SNR; immediately after recirculation damaged neurons were observed, and more damage was observed at 90 minutes post recirculation. In the normoglycemic group, no prominent neuronal damage was observed in any region.
Hyperglycemia exacerbated ischemic neuronal damage after reperfusion. The evolution of neuronal damage was similar in the CPu and Par regions, but was different in the GP and SNR regions.

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This study was performed to investigate whether or not α-adrenergic stimulation exerts a chronotropic effect on the heart. Isolated right atria of rats were used. Phenylephrine (10^-5-10^-4 mol/l), an a-agonist, did not affect the rate of the atrial beat under treatment with propranolol (1 x 10^-6 mol/l), a β-blocker. When the atrial rate was increased to approximately double by treatment with isoproterenol (1 x 10^-8 mol/l) or forskolin (1 x 10^-6 mol/l), phenylephrine at the same doses significantly reduced the rate by about 6%. This effect was blocked by phentolamine (1 x 10^-6 mol/l). These results suggest that α-adrenoceptors function to reduce heart rate in the atria, of which rate is raised through intracellular cAMP activity.

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To clarify the relationship between diabetes mellitus (DM) and fatal ventricular arrhythmias, such as ventricular tachycardia (VT), in patients with ishcemic heart disease, signal-averaged electrocardiograms were recorded in 107 patients with DM and/or myocardial infarction (MI). During the acute stage of MI (within 6 weeks of onset), patients with DM had significantly greater amplitude in the last 40 msec of filtered QRS as compared to those without DM (69.1±55.1 vs 33.9.±17.5, μV, p<0.01), thus signifying a lower incidence of late ventricular potential (LP) and VT.
We therefore investigated the incidence of VT in 257 consecutive patients with acute MI (74 with DM, 183 without DM). Although there was no significant difference in the incidence of VT between the two groups, a subgroup with congestive heart failure (CHF, Killip II) in the DM group had a significantly lower incidence of VT than a subgroup with CHF but not DM (18.5% vs 41.9%, p<0.05).
It is concluded that patients with DM have a lower incidence of LP and VT during the acute stage of MI.

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