Convulsive seizures induced by N-methyl-D-aspartate microinjection into the mesencephalic reticular formation in rats.

Effects of microinjections of a single 2 or 10 nmol dose of N-methyl-D-aspartate (NMDA) into the unilateral mesencephalic reticular formation (MRF) on behavior and electroencephalogram were examined in rats (n=18) during a 15 min period (Exp. 1), and subsequent effects of sound stimulation with key jingling applied at 15, 30, and 45 min after the injections were observed (Exp. 2). The microinjections of 2 nmol dose of NMDA (n=10) induced hyperactivity (9 of 10 rats) and running/circling (8 of 10 rats) in Exp. 1, and hyperactivity (3 of 10 rats) in Exp. 2. Moreover, the microinjections of 10 nmol dose of NMDA (n=8) induced not only hyperactivity (8 of 8 rats) and running/circling (7 of 8 rats) but also generalized tonic-clonic seizures (GTCS) (5 of 8 rats) in Exp. 1; these seizure patterns were also elicited by sound stimulation in Exp. 2. The seizure patterns were accompanied by electroencephalographic seizure discharges in the MRF and the motor cortex. In contrast, the control group rats (n=10) which received a single dose of saline microinjection into the unilateral MRF showed no behavioral or electroencephalographic changes in both Exp. 1 and 2. These findings suggest that the MRF has an important role in the development of GTCS, which follows hyperactivity and running/circling, and that potentiation of excitatory neurotransmission in the MRF participates in the development of audiogenic seizures as well as GTCS.

[Stress pulsed Doppler echocardiography in the evaluation of diastolic left ventricular function].

The effect of sublingual nifedipine on left ventricular (LV) function was assessed by analyzing LV inflow velocity patterns using pulsed Doppler echocardiography (PDE) and radioisotope (RI) angiography in 23 patients with hypertrophic cardiomyopathy (HCM), 13 with hypertensive heart disease (HHD) and 24 with ischemic heart disease (IHD). The results were as follows: LV inflow velocity pattern and M-mode echocardiography after the administration of nifedipine (Study-I). The deceleration time (DT) of the diastolic rapid filling wave was shortened after nifedipine in HCM and HHD, but not in IHD. The acceleration time (AT) of the diastolic rapid filling wave and the A/D ratio (amplitude of an atrial contraction wave/amplitude of a diastolic rapid filling wave) were not significantly changed in all groups. Peak negative Vcf was significantly improved after nifedipine in HCM, but unchanged in the other groups. Fractional shortening and peak Vcf did not change in all groups. LV inflow velocity pattern and RI angiography after nifedipine (Study-II). The mean LV rapid filling rate (V1) based on the LV volume curve by multi-gated blood pool scans increased during nifedipine in HCM and HHD, but other diastolic indices, such as the peak filling rate and 1/3 filling fraction, were unchanged. The DT-V1 relationship during nifedipine shifted toward the right and downward in HCM and HHD. In IHD, however, this relationship shifted toward the left and downward in cases with reduced LV function (V1 less than 1.0 EDC/sec), but toward the right and downward in patients whose LV function was maintained (V1 greater than or equal to 1.0 EDC/sec). Nifedipine therapy was associated with an improved LV filling in nearly all cases of HCM and HHD, and in some cases of IHD. PDE and RI angiography are useful for evaluating LV diastolic function during sublingual nifedipine in various heart diseases.