Evaluation of cardiac function during hemopurification was performed in 26 patients with chronic renal failure. Cardiac function was measured with a Swan-Ganz thermodilution catheter prior to and every hour after starting the procedure.
The effects of hemodialysis (HD) and hemofiltration (HF) on cardiac function were compared by crossover study. The variation in the left ventricular stroke work index (SWI) associated with the reduction in the pulmonary capillary wedge pressure (PCWP) was smaller (p<0.05) during HF than during HD. The reduction in PCWP and the variation in SWI associated with the increase in the rate of water elimination were smaller (p<0.05) during HF than during HD. These findings suggested that in terms of left ventricular contractility, HF had less effect on cardiac function than did HD.
In the second part of the study, 12 diabetic patients (DN group) were compared with 14 non-diabetic (non-DN group) in terms of cardiac function during HD. The rise in the variation in SWI associated with the increase in the variation in the double product tended to be smaller in the DN group than in the non-DN group. The regression coefficient of the variation in the systemic vascular resistance index (SVRI) to the variation in SWI for the DN group was positive, and different (p<0.05) from the negative coefficient obtained for the non-DN group. These results suggested that during HD the DN group had less effective utilization of oxygen in cardiac muscle and an impaired compensatory mechanism for decreases in cardiac function associated with increased water elimination than did the non-DN group.

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Cerebral metabolism was investigated in cerebral ischemia in fasted Mongolian gerbils by in vivo magnetic resonance spectroscopy (MRS). Ischemia was induced by bilateral carotid artery occlusion and continued for 30 min. Recovery was achieved by releasing the occlusion. High energy adenilates, free phosphates as well as intracellular pH were measured by ³¹P-MRS. Cerebral lactate levels were determined by ¹H-MRS. Furthermore, extracellular sodium levels were monitored by ²³Na-MRS.
The results showed that intracelluler pH decreased to pH=6.601 at 7.5-15 min after carotid legation and was regulated back to pH=6.670 during ischemia. pH returned to preischemic levels 45 min after ischemia and there was an overshoot (pH=7.241) in pH levels at 67.5-75 min after recirculation. The accumulation of lactate was slower and the accumulation continued after intracelluler pH started to regulate back to normal levels. Lactate decreased following recirculation, but was still higher than the preischemic level at 90 min after recirculation. The results show that changes in intracelluler pH is not parallel those in lactate levels, suggesting a different mechanism for regulating intracelluler pH.
The signal intensity of sodium was dropped before ATP disappeared, and rapidly normalized at 14-26 min after recirculation, at which time ATP had also normalized. This result suggests that the loss of signal intensity of ²³Na shows deporalization induced by ischemia and Na-K ATP pump failure.

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The arrhythmogenic role of increased dispersion of repolarization (Dispersion) in monophasic action potentials (MAPs) was studied in 12 open-chest dogs. Following exposure of the heart by pericardial cradle, four MAPS were recorded simultaneously from the right and left ventricular surfaces using the suction electrode technique. Maximum dispersion (maxDIS) was defined as the greatest Dispersion between any two of the four MAPS in atrial pacing and ventricular premature stimulation (VPS). Dispersion was increased by warming the heart with a heat lamp and regional cooling with a cold saline (2-4°C) drip. In control experiments maxDIS in atrial pacing (PCL: 500 ms) was 21±10 ms. MaxDIS was increased when the VPS was applied at the right ventricular apex (RVa) (maxDIS: 73±17 ms), at the left ventricular base (LVb) (maxDIS: 78±34 ms), and at the left ventricular apex (LVa) (maxDIS: 89±20 ms). Ventricular fibrillation, however was not induced by any VPSs. Warming the heart and regional cooling increased Dispersion from the control value to 180±58 ms (p<0.001), mainly because of the increased MAP duration difference (ΔMAPD) in atrial pacing, but no ventricular fibrillation occurred spontaneously. VPS applied at the LVa induced ventricular fibrillation following marked increase of maxDIS, which was due to added contributions of AMAPD and the maximal difference between activation times (ΔAT). With RVb cooling ventricular fibrillation was induced in 16/20 cases (80%) (maxDIS: 286±124 ms), with RVa cooling in 6/9 cases (67%) (maxDIS: 263±109 ms), and with LVb cooling in 11/23 cases (48%) (maxDIS: 172±67 ms). There was significant linear correlation between maxDIS and ΔAT (r=0.88, p<0.01), and also AMAPD (r=0.80, p<0.01).
We conclude that the increased Dispersion plays an important role in the induction of ventricular fibrillation. This temperature gradient model is a favorable tool to study the role of Dispersion as one of the important factors which induce ventricular fibrillation.

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Prolyl hydroxylase (EC 1.14.11.2) synthesis was examined in the cultured corneas of 17-day-old chick embryos which were cultured in F-12 medium supplemented with fetal calf serum. The amount of prolyl hydroxylase in cells was measured by immunoelectrophoresis using antibodies directed against this enzyme. The results indicated that the amounts of prolyl hydroxylase depended on cell density. The cells were harvested at the early-log phase and plated at high cell density to mimic the culture condition of cells at the stationary phase (crowding). The amount of ³⁵S-prolyl hydroxylase indicated a two-fold increase in the rate of prolyl hydroxylase synthesis after crowding. By use of ³²P-labeled cDNA for the β-subunit of prolyl hydroxylase a proportionate increase of the mRNA was noted in accordance with the increase in the rate of prolyl hydroxylase synthesis, suggesting that this enzyme synthesis is regulated at the transcriptional level.

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Pancreatic arteries were studied in 20 Japanese fetuses (7-8 months). The results were as follows:
1) Pancreatic arteries were originated from the common hepatic artery, the gastroduodenal artery, the splenic artery, and from the superior mesenteric artery.
2) The posterior pancreaticoduodenal arcade was seen in all cases, while the anterior pancreatic-oduodenal arcade was not recognized in one case. The inferior pancreatic artery, the great pancreatic artery and the caudal pancreatic artery were found in 17 cases (85%), 14 cases (70%), and in all cases, respectively.
3) The origins of the dorsal pancreatic artery varied. It arose from the splenic artery in 8 cases (40%), the common hepatic artery in 1 case (5%), the superior mesenteric or jejunal artery in 3 cases (15%), and from a bifurcation point of the splenic and common hepatic arteries in 2 cases (10%). In 3 cases (15%), the dorsal pancreatic artery was formed as a communicating branch between the splenic artery and the superior mesenteric artery.
4) The main arterial supply for the pancreatic body and tail was from the celiac artery in 8 cases (40%), and from both the celiac and the superior mesenteric arteries in the other 12 cases (60%).

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The author took interest in the existence of effector cells which had natural killer (NK) activity on the lung, in other words organ-associated NK cells, compared the augmentated effect of pulmonary NK activity by poly I : C with that of spleen NK activity, and also investigated the effect of activated pulmonary NK cells on established pulmonary metastasis.
It was shown that pulmonary NK cells in C57BL/6 mice had significant cytotoxicity against YAC-1 target cells in a 4 h-⁵¹Cr release assay, although their cytotoxicity was remarkably low as compared with that of spleen cells. However, by treatment with poly I : C, pulmonary NK activity was significantly augmented compared with spleen NK activity. This cytotoxicity was abrogated by treatment with anti-asialo GM₁ antibody. From these results, it was considered that the effector cell was a NK cell.
When poly I : C was administrated intraperitoneally from 3 days after intravenous inoculation of B16-F10 melanoma cells, the number of the pulmonary metastatic nodules was significantly decreased. The number of pulmonary metastatic nodules was not suppressed by a combination treatment of poly I : C and anti-asialo GM₁ antibody to the same degree as in treatment by anti-asialo GM₁ antibody alone.
The experimental group which underwent a combination treatment of poly I : C and carrageenan showed a suppression of the number of pulmonary metastatic nodules to the same degree as the group treated with poly I : C alone. Therefore it was shown that the effect of pulmonary metastatic suppression with poly I : C was caused not by macrophages but by pulmonary NK cells.
In this study, the NK activity of the pulmonary cells in C57BL/6 mice was found to be lower than that of spleen, but the pulmonary NK activity was remarkably augmented by poly I : C. Also the activated pulmonary NK cells suppressed the established pulmonary metastasis.

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We know that the mast cell or basophil degranulation and the release of chemical mediators such as histamine may play an important role in inducing immediate type allergic reactions.
In this experiment, employing purified rat peritoneal mast cells (RPMC) the degranulation pattern of RPMC and percent release of histamine from RPMC by pharmacologic (compound 48/80, kallikrein or peptidoglycan) or allergic (IgE-anti IgE complex) stimuli were examined. The inhibitory effects of cate-colamine (isoproterenol), an adenylate cyclase stimulator, methylxanthine (IBMX: 3-isobutyl-l-methyl-xanthine), a phosphodiesterase inhibitor and chemical mediators (histamine, serotonin, bradykinin) on compound 48/80-induced RPMC degranulation and also those of catecolamine, methylxanthine and chemical mediators on IgE-anti IgE complex-induced histamine release from RPMC were tested.
Compound 48/80-induced RPMC degranulation was remarkably inhibited not only by treatment with isoproterenol and IBMX, but also by treatment with histamine. It was not, however, inhibited by serotonin or bradykinin. The inhibitory effect of histamine on compound 48/80-induced RPMC degranulation was blocked by pretreatment with H₂-antagonist (cimetidine), but not by Hl-antagonist (diphenhydramine). The cyclic adenosine 3', 5'-monophosphate (cAMP) content of RPMC was significantly increased by pretreatment with histamine as well as isoproterenol and IBMX.
These facts suggest that cAMP acts as a regulator or modulator of the RPMC degranulation and the histamine release from mast cells and that the inhibitory effect induced by histamine may be related to the H₂-receptor existing on the surface of mast cells.

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A long latency EMG (C-response) which was produced by stimulation of the median nerve and recorded from the m. abductor pollicis brevis was studied in order to know if it was of use in diagnosis of cervical myelopathy. Inasmuch as the latency II (peak latency) of the C-response was correlated with the height of a given subject, the ratio of the latency against the height (C/h value) was employed to study the C-response. The C/h value was measured in 19 patients with myelopathy, before and after surgery, as well as in 20 healthy subjects (controls). The patients were classified into 3 types. I, II and III, according to the severity of the clinical manifestations. The CA value was significantly higher in the patients that in the controls, but the value did not change after surgery even in cases in which clinical signs were markedly improved.
These results indicate that the CA value is useful in determining the existence of cervical cord dysfunction, but not in evaluating the effects of surgical treatment.

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Using grafts from brain-dead donors for liver transplantation is a very controversial subject in Japan and those candidates for transplantation who have received livers outside of Japan have been harshly criticized.
Under these circumstances, a partial liver transplantation is an attractive method in terms of preserving the donor's life, freshness of the graft and easier donor availability. In other words, for adults with noncancerous incurable liver disease the donor's left lobe can be transplanted after the recipient has had a left lobectomy, and for children with biliary atresia the whole liver and vena cava can be replaced with a parent's left lobe and iliac vein.
Our report concerns the procedures of orthotopic partial liver transplantation for canines and humans.

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