The purpose of the present study was to examine the effect of Acetylcholinesterase inhibitor (AChEI) on r-CBF (group A) and its protecting effect on focal ischaemic cell damage (group B). The pial arterial diameter and the r-CBF were measured with a width analyzer and with a laser Doppler flowmeter through a cat cranial window on the ectosylvian gyrus. The ischaemic area was measured histologically. We used intravenous injection of AChEI([-])(S)-N-ethyl-3-[(1-dimethyl- amino)ethyl]-N-methyl-phenylcarbamate, SDZENA 713, Sands Pharmacy) to block AChE. Twenty minutes after injection AChEI (0.6 mg/kg) the pial arteriole dilated 108.5 +/- 1.8% and the r-CBF increased 115.4 +/- 2.6%. The pial arteriole dilated maximally to 137.6 +/- 6.5% at 120 minutes after injection and the r-CBF increased maximally to 137.1 +/- 19.5% at 60 minutes after injection. The protecting effect was evaluated using cats and 1 hour of occlusion of the middle cerebral artery (MCA). Twenty minutes after injection of AChEI, the pial arteriole dilated to 116.7 +/- 2.4% and the r-CBF increased to 111.9 +/- 2.6% significantly. During MCA occlusion the r-CBF decreased to 24.7-41.4% in group B and 25.1-32.6% in sham group (group C). The pial arteriole dilated 145.0-184.0% in group C and 150.7-171.6% in group B during MCA occlusion and 30 minutes after reperfusion the pial arteriole returned to 120.0 +/- 3.3% in group C and 123.4 +/- 11.3% in group B. There were no significant changes in the r-CBF and the vessel diameter between group B and C during the 2 hours after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

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To assess the differential stimulus to central and intravascular osmoreceptors during recovery from thermal dehydration, we measured Na concentrations in cerebrospinal fluid ([Na]CSF) and plasma ([Na]p) continuously and compared these during simulated drinking by gastric water infusion (INF) in euhydrated and thermally dehydrated rats under anesthesia. Continuous measurement of [Na]CSF was obtained with a double-barreled Na electrode placed in the lateral ventricle. Continuous measurement of [Na]p was obtained from a flow cell Na electrode in an extracorporeal shunt. Measurements were made during 10 min of INF (2.5 ml/100 g body wt) into the stomach and during 20 min of recovery. Changes in [Na]CSF always lagged behind those in [Na]p and were quantitatively smaller after INF. The decrease in [Na]CSF occurred sooner in dehydrated than in euhydrated rats in response to the decrease in [Na]p (P < 0.01). These results suggest that water and/or Na movement between blood and CSF is accelerated during restitution from thermal dehydration, acting to prevent overhydration during the early phase of rehydration.

The relationship between portal hemodynamics and the energy metabolism of the liver with acute hepatic venous occlusion (HVO) was investigated by assessing the changes in the hepatic blood flow, arterial blood ketone body ratio (AKBR) and adenylate energy charge potential (ECP) of the liver tissue in canine model. Acute HVO was induced by the ligation of both the supra- and infrahepatic inferior vena cava (IVC) over the protruding ends of a heparin-coated polyethylene cannula inserted into the IVC. All dogs with only HVO (n = 5) died within 30 min. HVO dogs with additional mesocaval (MC) shunt (n = 10) survived longer than 7 days, during which time their AKBR were maintained in the normal range (over 1.0). ECP was also maintained above the normal level (over 0.850) during the 28-day period. Along with increasing portal pressure caused by the narrowing of the shunt anastomosis, the hepatic blood flow decrease gradually, resulting in a sudden decrease in AKBR and ECP when the portal pressure increased over 11 mm Hg. It is suggested that the normalization of portal pressure is one of the most important factors for maintaining the hepatic energy metabolism and that MC shunt is an effective therapy for maintaining the function of the liver with HVO, as long as portal pressure can be kept within normal range.

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