Inhibitory effects of D2 agonists by striatal injection on excessive release of dopamine and hyperactivity induced by Bay K 8644 in rats.

We investigated by means of behavioral and neurochemical studies the effects of either D(1) or D(2) agonist on excessive dopamine release and hyperactivity induced by the microinjection of Bay K 8644, and an L-type Ca(2+) channel stimulant, into the rat caudate putamen under a novel environmental condition. Hyperactivity (locomotor activity and rearing counts) and significant increases in extracellular dopamine levels induced by Bay K 8644 were concomitantly observed. D(1) agonist, SKF81297, administered into the caudate putamen did not block Bay K 8644-induced hyperactivity measured by monitoring both animal activity and increases in extracellular dopamine levels detected by microdialysis. Pretreatment with the D(2) agonists, bromocriptine, talipexole and pramipexole, into the caudate putamen significantly blocked Bay K 8644-induced hyperactivity for 45 min after Bay K 8644 administration, although the single administration of these agonists significantly potentiated locomotor activity and rearing behavior. Furthermore, these agonists significantly suppressed Bay K 8644-induced extracellular dopamine levels. Our results indicate that these D(2) agonists (1) act on postsynaptic neuronal D(2) receptors under conditions of normal or low dopamine release in the caudate putamen, and (2) act on presynaptic D(2) receptors (autoreceptors) when excessive levels of dopamine are released or hyperdopamine neuronal activity is induced. Consequently, the effect of D(2) agonists in the clinical treatment of Parkinson's disease may be due to stimulation of postsynaptic D(2) receptors rather than presynaptic autoreceptors.

Can PET data differentiate Alzheimer's disease from vascular dementia?

The present study endeavored to differentiate Alzheimer's disease (AD) from vascular dementia (VaD) by comparing the metabolic and hemodynamic parameters. Positron emission tomographic (PET) studies were carried out in 13 patients with probable AD and 20 patients with VaD. PET findings were not included in the diagnostic criteria of AD or VaD. Using oxygen-15 labeled compounds, cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), cerebral blood volume, and vascular transit time (VTT) were measured quantitatively during the resting state. To evaluate vascular reactivity (VR), CBF was also measured during 7% CO2 inhalation. Regional CBF from the parietal cortex positively correlated with the neuropsychological scores in both AD and VaD groups. The typical parietotemporal pattern of hypoperfusion and hypometabolism was observed in the AD group, whereas the frontal lobe including the cingulate and superior frontal gyri were predominantly affected in the VaD group. The occipital cortex was preserved in both groups. A significant increase of the OEF was found in the parietotemporal areas in the AD group. No significant prolongation was seen with VTT. There was a marked difference in VR between the two groups: VR was depleted in the VaD group, whereas VR was normal in the AD group. The increased OEF with preserved vascular reserve seen in AD may implicate participation of a vascular factor in the pathogenesis of AD, possibly at the capillary level. Thus, PET provides important functional information in discriminating AD from VaD by comparing the patterns of hypoperfusion and/or hypometabolism, and in the understanding of the underlying hemodynamic pathophysiology.

[Vascular and metabolic reserve in a case of hypoplasia of bilateral internal carotid arteries].

We report a 64-year-old right-handed man who presented with a hypoplasia of bilateral internal carotid arteries (ICAs). The patient complained of a vertigo and was diagnosed as having a benign paroxysmal positional vertigo. Upon neurological examination, he was completely free from neurological deficits. MR angiogram revealed an occlusion of both ICAs. On conventional angiogram, the right ICA was occluded about 3 cm distal from its origin, and the left ICA was occluded at the precavernous portion. There was an abundant collateral blood flow to the frontal, temporal and parietal lobes through the posterior communicating arteries. Both carotid canals were hypoplastic on 3D-CT. The patient was then diagnosed as having a hypoplasia of both ICAs. Using a positron emission tomography (PET), cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and vascular transit time (VTT) were measured during resting state, and the vascular reactivities to carbon dioxide inhalation (VRCO2), and to the intravenous administration of Acetazolamide (VRACZ) were also evaluated. There was no global or focal reduction in CBF and VTT was within normal limit, whereas a global reduction of CMRO2 caused mild decrease in OEF. Moreover, VRACZ was significantly decreased and an intracerebral steal phenomenon was observed in the parietal cortical areas, whereas VRCO2 was preserved. The discrepancy between VRACZ and VRCO2 observed could be related to the differences in the mechanisms underlying the vasodilating effects of carbon dioxide and ACZ.

[Perioperative myocardial infarction due to graft atheroembolism during coronary artery bypass surgery].

We presented a female patient who had complicated perioperative myocardial infarction resulting from intraoperative embolization with atheromatous debris during coronary artery bypass surgery. On separation from cardiopulmonary bypass, ventricular function was poor and she suffered from severe low cardiac output syndrome postoperatively. The intraoperative electrocardiographic monitoring showed conduction abnormalities, elevation of the ST-T segments and new Q waves. Though it is difficult to diagnosis the onset of perioperative myocardial infarction early, adequate treatment is necessary to preserve ischemic myocardium and to reduce the size of myocardial necrosis.

[Anoxic spell in an adult case for intracardiac repair].

We report a 51-year-old male patient with tetralogy of Fallot who had an anoxic spell during pre-bypass period before intracardiac repair. Immediately after starting sternotomy, SpO2 decreased suddenly from 83% to 30% with PaO2 of 26 mmHg. Heart rate showed an increase to 120-140 bpm with little change in blood pressure. We considered that the causes of this spell were 1) light level of anesthesia, 2) hypoxemia and 3) lack of intravascular blood volume. This case warns us that we should take care to avoid an anoxic spell in an adult case for intracardiac repair.

[Perioperative management for type A acute aortic dissection].

Twenty nine cases of type A acute aortic dissection were subjected to a retrospective study concerning perioperative management. Two keys pointed out for the management were as follow; (1) An optimal control of blood pressure is the most important measure to avoid advance of aortic dissection or rupture of dissecting aneurysm. Both pericardiac tamponade and aortic valve insufficiency should be taken care of from their onset, since they are often complicated after aortic dissections and their onset is fatal. (2) Separated brain perfusion and profound hypothermia with total circulatory arrest might involve a high risk of inducing postoperative brain damage and mortality, especially for old patients.

Intraoperative changes in blood coagulation and the effectiveness of ulinastatin during liver resection.

The blood coagulation status of 16 patients undergoing liver resection was monitored by thrombelastograph (TEG). Coagulation test by TEG was performed at three different times: before and one hour after induction of anesthesia and after liver resection. The four variables such as r (reaction time), k (coagulation velocity), ma (maximum amplitude) and me (maximum elasticity) were measured. In 8 patients, Ulinastatin was not administered during the operation and FFP was transfused after the second measurement of TEG (group I). The other 8 patients were administered totally 300,000 units of Ulinastatin after induction until the second measurement of TEG, thereafter FFP was transfused (group II). The TEG showed poor preoperative coagulation state in both groups. In group I, TEG variables showed coagulopathy was exacerbated significantly during liver resection. In group II TEG variables showed no significant changes during operation. Between the two groups there were statistical differences in the TEG variables during the operation. The TEG was useful for monitoring coagulation function during liver resection. It was impossible to improve TEG data by only replacement of FFP. Ulinastatin was useful in normalizing the coagulation function and in preventing the changes in TEG measurements during liver resection.