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Biomedical subjects

S Imai

Publications and source records attributed to S Imai.

At least 613 records · Page 34Linked to original sources
PubMed1986

[A case of carotid rete mirabile associated with pseudoxanthoma elasticum: a case report].

A case of carotid rete mirabile (CRM) with pseudoxanthoma elasticum (PXE) was reported. A 55-year-old woman was admitted to our hospital with complain of left motor weakness. Plain CT scan showed a lacuna in the right internal capsule. Right retrograde brachial angiography and left carotid angiography demonstrated that internal carotid arteries were hypoplastic and winding, and there were abnormal networks between ICA in the cavernous portion and internal maxillary artery, which was a branch of external carotid artery. Diagnosis of CRM was made. Fundoscopy showed bilateral angioid streaks and histological examination of a eruption in her right neck revealed degeneration of elastic fiber and calcium deposits in the derm, which findings were verified to be PXE. So this case was diagnosed of CRM combined with PXE. She got better by conservative therapy in 3 weeks and discharged on foot. On previous literatures 5 cases of CRM were reported and one of which was associated with PXE. CRM is a normal anatomical structure noted lower mammals like cat, sheep and pig. 10% of PXE, which is systemic disorder of elastic fiber, showed CNS lesions. Our case seems to be CRM combined with PXE by chance. But two of 6 cases of CRM were with PXE, so it is necessary that a case of PXE should be examined angiographically.

Carotid Arteries↗
PubMed1986

[Juvenile spring eruption].

This report deals with two Japanese patients with juvenile spring eruptions, exhibiting characteristic cutaneous lesions. The course of the disease is described.

Child↗
PubMed1985

Effect of phenytoin on intracellular calcium and intracellular protein changes during pentylenetetrazole-induced bursting activity in snail neurons.

Effects of phenytoin (PHT) on the intracellular calcium and intracellular protein changes during pentylenetetrazole (PTZ)-induced bursting activity in the neurons of the Japanese land snail Euhadra peliomphala were examined. In the examination with a computer controlled electron probe X-ray microanalyzer, PHT clearly inhibited the intracellular calcium shift induced by PTZ as well as the calcium binding state change near the cell membrane. PHT also clearly inhibited the intracellular protein changes induced by PTZ. PHT, however, did not show any change in the transmembrane ionic currents such as the sodium current, calcium current and potassium current. These findings suggest that one of the main sites of anticonvulsant action of PHT is pathologically changed intracellular calcium movement and intracellular protein changes during seizure discharge.

Animals↗
PubMed1985

Creutzfeldt-Jakob disease. An autopsy case of the panencephalopathic type and a review of the literature.

This is a case report of a purported panencephalopathic type of Creutzfeldt-Jakob (C-J) disease in a 61-year-old Japanese farmer. He died nine months after the onset of clinical symptoms. This variety of C-J disease was named and reported in 1981 by Mizutani. The characteristic feature is extensive degeneration of cerebral white matter not related to cortical damage in addition to the spongiform changes in the cortical gray matter. The case was diagnosed clinically and at post mortem marked neural loss, astrocytic macrogliosis, and degeneration of subcortical white matter were found. Senile plaques and neurofibrillary tangles were virtually absent. Degeneration of the white matter is uncommon in C-J disease, and when it occurs is usually mild, and limited in distribution.

Brain↗
PubMed1985

Analysis of the left ventricular early diastolic function in old myocardial infarction by gated radionuclide angiography.

In order to determine the validity of the left ventricular (LV) diastolic function for evaluation of ischemic heart disease, gated radionuclide angiography was performed in 37 patients with transmural myocardial infarction (MI) [18: anterior, 19: inferior infarction] and 10 normal control subjects. LV ejection fraction (LVEF) was decreased in patients with anterior MI but not in those with inferior MI. Time to peak filling rate was not significantly prolonged in both anterior MI and inferior MI. Filling fraction was apparently reduced only in anterior MI. However, peak filling rate (PFR) was significantly reduced even in inferior MI as well as in anterior MI. PFR correlated well with LVEF in normal control, anterior MI and inferior MI. In both anterior MI and inferior MI, their coefficients were smaller than in controls. The normal PFR always indicated normal LVEF, while normal LVEF was not necessarily indicative of normal PFR. Results indicated that LV diastolic function estimated by equilibrium radionuclide angiography might reflect more precisely LV dysfunction in old MI than LV systolic function. The reduction of LV diastolic function in old MI was more prominent than that of LV systolic function. Therefore, it may be deduced that evaluation of LV diastolic function is essential to the estimation of the degree of ischemic myocardial cell damage and the efficacy of drugs on ischemia-induced LV dysfunction.

Aged↗
PubMed1985

[Effects of Young's solution (YNG solution) on cardiac function and mitochondrial function during one hour ischemia at 30 degrees C and after reperfusion].

In a previous paper from this laboratory, protective effects of YNG solution on the myocardial mechanical function and metabolism of the heart arrested at 10 degrees C ascribable to the presence of Mg2+ were demonstrated. In order to further clarify the role played by Mg2+ in the protection, the present experiment was conducted using the isolated perfused guinea pig heart arrested at 30 degrees C. While the time to arrest of the contraction was equally short both with YNG (K+ + Mg2+) and K (K+) solutions, the time to resumption of contraction was significantly longer with K solution than with YNG solution, and the regular contraction was not resumed with the former solution. The recovery of the coronary flow, left ventricular pressure and dp/dt after reperfusion was around 100% with YNG solution, while the recovery was significantly poorer with K solution. Although the mitochondrial function was well maintained during the arrest both with YNG and K solution, the recovery of the mitochondrial function after reperfusion was observed only with YNG solution; severe damage was noted in mitochondria of the hearts arrested with K solution. There was a good correlation between the changes in mitochondrial function and those in cardiac function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Displacement by alpha-adrenergic agonists and antagonists of 3H-prazosin bound to the alpha-adrenoceptors of the dog aorta and the rat brain.

To characterize the alpha 1-adrenoceptors in the dog aorta and the rat brain and to assess the antagonistic potencies of various chemicals inclusive of newly synthesized ones, radioligand binding assays were performed, and the potencies thus obtained were compared with those obtained from pharmacological observations. Reproducible binding to and displacement from the dog aorta of 3H-prazosin were observed. The rank orders of the inhibition of 3H-prazosin binding to the membrane preparations of the aorta expressed as IC50 (the concentration of drugs inhibiting 50% of maximal specific binding of 3H-prazosin) were: prazosin greater than YM09538 greater than phentolamine greater than yohimbine greater than phenoxybenzamine greater than labetalol greater than S-596 greater than dibenamine greater than K-351 greater than propranolol greater than hydralazine greater than N-696 for alpha-blockers and I-epinephrine greater than clonidine greater than I-norepinephrine greater than phenylephrine greater than I-isoproterenol for agonists. IC50 values of phenoxybenzamine, labetalol, dibenamine and K-351 obtained in the brain preparations were higher than those obtained in the preparation of the aorta. There was a good correlation (r = 0.90) between the IC50 values obtained in the dog aorta and in the rat brain, suggesting that the alpha 1-adrenergic receptors in the dog aorta and the rat brain resemble each other. Good correlations (aorta, r=0.97 and brain, r=0.94) were also observed between IC50 values derived from the binding assay in the aorta or the brain and the pA2 values obtained as regards to the contractile response of the rat aorta to phenylephrine. Thus, this method could be useful for the assessment of newly synthesized chemicals as alpha-adrenergic antagonists.

Adrenergic alpha-Agonists↗
PubMed1985

Enhanced responsiveness of the coronary blood vessel of the dog heart-lung preparation to PGI2 after chronic chemical sympathectomy.

Chronic chemical denervation of the sympathetic nervous system with 6-OH dopamine resulted in an augmentation of the coronary blood flow (CBF) increase inherent in the canine heart-lung preparation, but not in an augmented accumulation of 6-keto PGF1 alpha in the circulating blood. In denervated HLP, 6-keto PGF1 alpha was lower and the vasodilator response to PGI2 larger at the start of the experiments. It was concluded that exaggerated increase in CBF was due to a potentiation of the vasodilator response to PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effect of l-carnitine chloride and its acetyl derivative on the electrophysiological derangement induced by palmityl-l-carnitine in isolated canine ventricular muscle.

Using the microelectrode technique, the effects of l-carnitine (LC) and acetyl-l-carnitine (ALC) on the changes in the transmembrane action potential of the canine ventricular muscle induced by palmityl-l-carnitine (PLC) were studied in comparison with those of disopyramide (D). LC (5 X 10(-3) M) itself had no effect on the electrophysiological parameters of the ventricular muscle. ALC (5 X 10(-3) M) increased the maximum rate of rise (dV/dt max) slightly and decreased the action potential duration (APD), although these changes were not statistically significant. D (1.5 X 10(-3) M) decreased dV/dt max and prolonged APD and the absolute refractory period (ARP). PLC (3 X 10(-4) M) decreased the resting membrane potential, action potential amplitude and dV/dt max, and it shortened APD and ARP. LC and ALC (5 X 10(-3) M) improved the electrophysiological derangement produced by PLC to the same degree. On the other hand, application of D (1.5 X 10(-5) M) resulted in no improvement of the electrophysiological derangement produced by PLC.

Acetylcarnitine↗
PubMed1985

Inhibition by thiamine tetrahydrofurfuryl disulfide (TTFD) of the arachidonic acid cascade-line activation as evidenced in the heart-lung preparation of the dog.

The effects of thiamine tetrahydrofurfuryl disulfide (TTFD) on the gradual increase in the coronary blood flow (CBF) inherent in the canine heart-lung preparation were studied. TTFD is a disulfide-type derivative of thiamine reported to have an antiinflammatory effect in experimental animals. Since it was found that the substance could reverse the gradual increase in CBF, the possibility that the reversal was brought about through an inhibition of activation of the arachidonic acid cascade-line was tested, examining the effects of this substance on the CBF increase produced by arachidonic acid (AA) and prostacyclin (PGI2). The vasodilator response to AA, which was barely detectable at the start of the experiment at which CBF was at a physiological low level, became potentiated as the gradual increase in CBF occurred, returning to the initial magnitude after TTFD, while the vasodilator response to PGI2 remained essentially unchanged during the entire course of the experiment. It was concluded that TTFD reversed the gradual increase in CBF in the HLP through the inhibition of the arachidonic acid cascade-line activation.

Animals↗
PubMed1985

Alpha-blockade and vasodilatation induced by nipradilol, arotinolol and labetalol in pithed rats.

In pithed rats two recently-introduced beta-blockers, nipradilol and arotinolol, as well as labetalol shifted the pressor dose-response curve for phenylephrine to the right. Labetalol and arotinolol did not modify the pressor dose-response curve for clonidine, while nipradilol induced a definite rightward shift. These results indicate that labetalol and arotinolol are selective alpha 1-blockers, while nipradilol is a non-selective one. In addition, all the three beta-blockers produced complex changes in the blood pressure in pithed rats. A fall of the diastolic blood pressure induced by labetalol and nipradilol was preceded by a slight rise, while arotinolol produced a fall at lower doses and a rise at higher ones. The hypotension by labetalol was abolished after propranolol, while the hypertension was suppressed by prazosin, indicating that labetalol has an intrinsic beta- and alpha 1-sympathomimetic effect. The hypertension and the hypotension produced by nipradilol and arotinolol persisted even in the presence of propranolol and prazosin or propranolol and yohimbine.

Adrenergic alpha-Antagonists↗
PubMed1985

Role of the alpha-adrenergic blocking effect in the acute hypotensive effect of beta-adrenergic blocking drugs with alpha-blocking activities in conscious SHR.

Acute hypotensive effects and the mechanisms of three beta-adrenergic blocking drugs with alpha-blocking activity were studied in comparison with those of prazosin, propranolol and hydralazine in the conscious spontaneously hypertensive rat (SHR). Prazosin lowered the blood pressure dose-dependently and inhibited the pressor response to phenylephrine. Three beta-adrenergic blocking drugs with alpha-blocking activity, labetalol (30 mg/kg), arotinolol (100 mg/kg) and nipradilol (100 mg/kg) also lowered the blood pressure to the same extent as prazosin (0.3 mg/kg), but the inhibition of the pressor response to phenylephrine produced by them was disproportionately slight. Propranolol (100 mg/kg) did not lower the blood pressure. These results suggest that the acute hypotensive effects of three beta-adrenergic blocking drugs with alpha-blocking activity were attributable only partially to the alpha-adrenergic blocking effect; a mechanism or mechanisms other than the alpha-adrenergic blocking effect must be invoked to explain the acute hypotensive effect produced by lower doses of these drugs in the conscious SHR.

Adrenergic alpha-Antagonists↗
PubMed1985

Beneficial effects of diltiazem on the ischemic derangements of the myocardial metabolism assessed by 31P-NMR in the isolated perfused rat heart.

Using the isolated perfused heart preparations of the rat, effects of diltiazem, a calcium antagonist, on the ischemic derangements of the mechanical function and the energy metabolism of the ventricular myocardium were studied. The myocardial tissue levels of creatine phosphate (CP), ATP, inorganic phosphate (Pi) and pH were determined with 31P-NMR. Global ischemia was induced by cross-clamping of the aortic inflow line for 15 min, which resulted in a fall of CP, ATP and pH and a rise of Pi. The test hearts were perfused with diltiazem-containing solution (10(-7), 10(-6) and 10(-5) M) for 12 min prior to the induction of the global ischemia. A significant dose-related decline of the myocardial mechanical function expressed as (left ventricular pressure) X (heart rate) was observed in diltiazem-treated hearts. In doses above 10(-6) M, diltiazem delayed the onset of the fall of the myocardial CP and pH levels and the rise of Pi induced by ischemia, and there was an excellent correlation between the suppression of the myocardial mechanical function observed before induction of ischemia and the level of the myocardial CP and pH at the initial phase of ischemia, indicating that the improvement of the myocardial energy metabolism was due to the cardiodepressant effects of the compound.

Animals↗