[Acid-base equilibrium of the blood during extracorporeal circulation of high flow perfusion].
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Biomedical subjects
Publications and source records attributed to M Hashimoto.
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The feasibility of determining the time interval from left atrial appendage (LAA) flow was examined using transesophageal Doppler echocardiography. Time intervals were compared between LAA flow and mitral flow patterns during late diastole in 8 patients with mitral stenosis and in 12 controls. The start of ejection flow from the LAA was later than the initiation of mitral flow, but the termination was same in both flows, indicating the contribution of LAA ejection to the latter half of the left atrial booster pump function. The pre-ejection time and the time interval from P-wave to end-ejection correlated significantly with left atrial dimensions (r = 0.55, and r = 0.70, respectively). The pre-ejection time, duration of the ejection flow from the LAA, and duration of mitral flow in the atrial contraction phase were significantly longer in patients with mitral stenosis (126 +/- 14 msec, 131 +/- 36 msec, and 167 +/- 28 msec, respectively) than in the controls (109 +/- 13 msec, 108 +/- 15 msec, and 141 +/- 17 msec, respectively). These results indicate that electrical conduction time from the right atrium to LAA can be estimated from the LAA ejection flow, and the time is related to the left atrial size. In patients with mitral stenosis, LAA contraction may contribute to left ventricular filling in the latter half of the atrial contraction phase.
Leiomyomas or benign tumors of smooth muscle origin are extremely rare in the larynx. A review of the literature revealed only 15 confirmed cases of leiomyoma, eight leiomyosarcomas, and no cases of leiomyoblastoma. An unusual case of "bizarre" laryngeal leiomyoma arising from the vocal cord, which is believed to be the first reported case in the literature is presented herein.
Duodenal gastrinomas do not seem to behave as malignantly as sporadic pancreatic gastrinomas. Statistical analysis of 49 patients with sporadic pancreatic gastrinoma and 21 patients with sporadic duodenal gastrinoma reported since 1980 in Japan revealed that the incidence of hepatic metastasis was 57% in patients with sporadic pancreatic gastrinoma and only 9% in patients with sporadic duodenal gastrinoma (p less than 0.01). These findings suggest that there is an essential biological differences between duodenal and pancreatic gastrinoma. Five patients with sporadic duodenal microgastrinoma (tumor diameter less than 5mm) in our hospital had no hepatic metastases; however, 4 patients had lymph node metastases. Immunohistochemical study of 5 sporadic duodenal microgastrinomas and 6 sporadic pancreatic gastrinomas revealed that the sporadic duodenal gastrinomas contained significantly fewer insulin-producing or glucagon-producing cells than sporadic pancreatic gastrinomas. The cellular composition of the metastatic lymph nodes from duodenal microgastrinomas was similar to that of the primary tumor. This difference in cellular composition between the duodenal microgastrinomas and the pancreatic gastrinomas suggests that the process of development and differentiation of gastrinoma cells is different.
Whole body autoradiography revealed that the distribution pattern of [14C]dehydrocorydaline in the mouse and rat liver was heterogeneous (or reticular) regardless of time after intravenous administration of the labeled agent. Microautoradiography by dry-mounting method revealed that the macroscopic heterogeneous pattern was due to the periportal localization of the radioactive compound in the hepatic lobule. By comparison with [14C]salicylid acid, [14C]diphenylhydantoin and [14C]p-chlorophenoxyacetic acid whose distribution pattern are homogeneous in the liver, the present studies indicated that the existence and persistence of heterogeneous distribution of [14C]dehydrocorydaline in the liver had the following causes: 1. Shortly after intravenous administration, the amount of [14C]dehydrocorydaline circulated to the liver was greatly restricted by its significant distribution in non-hepatic tissues. This was shown by the whole body autoradiography, radiometry of tissues and quantitative comparison of volumes of distribution in non-hepatic tissues. Therefore, 2. perilobular hepatocytes alone could take up [14C]dehydrocorydaline and consequently, centrilobular cells were unavailable to it: heterogeneous distribution pattern is formed. This was shown by microautoradiography as described above, and by the rapid and significant uptake of [14C]dehydrocorydaline by isolated hepatocytes in vitro and by the liver to which the labeled agents were continuously administered in situ. It was also substantiated by the more homogeneous distribution pattern in the liver of the rat to which greater amount of [14C]dehydrocorydaline was gradually given into the portal vein and of the mouse with allyl formate-induced perilobular damage. 3. Redistribution of [14C]dehydrocorydaline scarcely occurred in the whole body and therefore radioactive substance was not significantly supplied to the liver: the distribution pattern remained unchanged. This was shown by the whole body autoradiography and radiometry of tissues.
Whole body autoradiography revealed that the distribution pattern of [35S]chlorpromazine and [14C]imipramine in the mouse and rat liver was heterogeneous (or reticular) shortly after intravenous administration of the labeled agents and then became homogeneous. Microautoradiography by dry-mounting method revealed that the macroscopic heterogeneous pattern of [35S]chlorpromazine was due to its periportal localization in the hepatic lobule. The present studies indicated that the heterogeneous distribution was re-arranged to a homogeneous one in the following way: 1. The amount of [35S]chlorpromazine and [14C]imipramine circulated to the liver was greatly restricted by their significant distribution in non-hepatic tissues shortly after administration. This was shown by whole body autoradiography, radiometry of tissues and volumes of distribution in non-hepatic tissues. Therefore, 2. perilobular hepatocytes alone could take up the agents and consequently, centrilobular cells were unavailable to them: heterogeneous distribution pattern is formed. This was shown by microautoradiography described above, and by the rapid and significant uptake of the agents by isolated hepatocytes in vitro and of [35S]chlorpromazine by the liver to which the agent was continuously administered in situ. However, 3. re-distribution of [35S]chlorpromazine and [14C]imipramine occurred thereafter. Therefore, the radioactive compounds were significantly supplied to the liver late after administration: the pattern became homogeneous. This was shown by the whole body autoradiography and radiometry.
Whole body autoradiography revealed that the distribution pattern of [14C]aminotriazole in the mouse liver was homogeneous after intravenous administration of the labeled agent and then became heterogeneous (or reticular). Microautoradiography by dry-mounting method revealed that the macroscopic heterogeneous pattern was due to the central localization of the radioactive compound in the hepatic lobule. The present studies indicated that the heterogeneous distribution could be explained as follows. The amount of [14C]aminotriazole circulated to the liver was large since the compound was not so significantly distributed in non-hepatic tissues: distribution pattern was homogeneous in the liver. This was shown by whole body autoradiography and radiometry of tissues. A part of [14C]aminotriazole radioactivity present in the liver was gradually bound covalently to hepatic macromolecules. This was shown by whole body autoradiography after whole body sections of the mouse were extracted by acid, and by the biochemical fractionation of the liver. The covalently bound radioactivity alone became apparent in centrilobular hepatocytes: the distribution was heterogeneous. This was shown by microautoradiography and by the finding that the elimination rate of the bound radioactivity was slower than that of unbound radioactivity.
When [14C]haloperidol decanoate, an ester of haloperidol and decanoic acid, was given intramuscularly to rats, levels of total radioactivity and haloperidol decanoate in medial iliac and hypogastric sacral lymph nodes nearest to injection sites were the highest in examined lymph nodes and plasma. These lymph node levels became maximum 16 days after administration and declined gradually with half-life (around 14 days) similar to those of plasma total radioactivity, haloperidol decanoate and haloperidol. However, when the labelled ester was given intravenously, plasma total radioactivity disappeared far more rapidly. Much more radioactivity was found in hind limbs whose femoral muscles had been injected than in other body parts, even at late stages after administration. Haloperidol alone was found in the brain after [14C]haloperidol decanoate was given either intramuscularly or intravenously. It was concluded that haloperidol decanoate injected in rat femoral muscle was rate-limitedly distributed in lymph circulation and that the absorbed ester did not penetrate the brain through the blood-brain barrier but formed haloperidol did.
[14C]Haloperidol decanoate was hydrolysed by partially purified carboxylesterase but not in plasma, blood, lymph and lymphatic liquid. These fluids inhibited the enzyme-mediated hydrolysis of the ester. Within the same incubation period as above, the ester was found hydrolysed to various extents in cell cultures of isolated rat liver cells, of human and rat lymphocytes and of established cell lines (BGM cells, WI-38 cells and L6 cells). Thus, the hydrolysis of the ester was demonstrated in vitro with use of viable cell cultures instead of enzyme preparation. From the time course study on the metabolism of haloperidol decanoate in cell cultures, it was concluded that haloperidol decanoate was first concentrated in the cells and hydrolysed to haloperidol. Based on these results, the metabolic sequences in vivo leading to the formation of active principle haloperidol after intramuscular administration of its decanoate were discussed.
We describe a technique for computed tomographic (CT) fluoroscopy-guided celiac artery or superior mesenteric artery (SMA) catheterization for use with CT hepatic arteriography or CT arterial portography, respectively. Patients underwent conventional hepatic angiography to define the anatomy and to place a catheter within the celiac artery or the SMA. Subsequently, the catheter was repositioned in the target vessels under CT fluoroscopy. Our success rate was 94%.