Proximal gastrectomy reconstructed by interposition of a jejunal pouch. Surgical technique.
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Biomedical subjects
Publications and source records attributed to M Tsukamoto.
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We investigated the prevalence of various autoantibodies [anti-cardiolipin antibody (aCL), lupus anticoagulant (LA), immune complexes (ICs), anti-nuclear antibody (ANA), and anti-deoxyribonucleic acid antibody (aDNA)] in hemophiliac individuals with (n = 50) and without (n = 42) infection by human immunodeficiency virus type 1 (HIV-1). The positivity rate for ANA was similar in both groups, and none of the patients was positive for LA and aDNA. aCL was positive in 35 of 50 (70%) HIV-1-positive hemophiliac individuals and 33 of 42 (79%) HIV-1-negative hemophiliac individuals. However, the majority of the aCL was revealed to be beta 2-glycoprotein I independent, thus corresponding to a syphilis type aCL that does not cause the so-called antiphospholipid syndrome. A total of 39 of the 45 HIV-1 positive hemophiliac individuals (87%) and 34 of 41 HIV-1-negative hemophiliac individuals (83%) had at least one type of IC [C1q-, C3d-, and/or murine monoclonal rheumatoid factor (mRF)- IgG]. The mechanism producing various autoantibodies in hemophiliac persons irrespective of their HIV-1 status is still unclear, but pathogens (e.g., HIV-1, hepatitis B, and hepatitis C) and alloantigens in the blood products that these patients require may be possible candidates. The clinical significance of the presence of these autoantibodies and the underlying mechanisms involved both need to be clarified further.
The effect of thrombospondin (TSP) on attachment, spreading, cell toxicity and proliferation of cultured rat mesangial cells (M cell) were investigated. The results are as follows: 1. Attachment and spreading of M cell on the culture plates coated with TSP were inhibited in a dose dependent manner, 2. 50 micrograms/ml TSP in the medium brought about the significant detachment of the adhered M cell. 3. TSP had no demonstrable effects on 51Cr-release from M cell, 4. 3H-thymidine uptake into M cell was inhibited by TSP in a dose dependent manner. These results indicate that TSP modulates attachment, spreading and proliferation of M cell. Therefore, it is suggested that overproduction of TSP in M cell under some pathophysiologic conditions such as diabetic nephropathy may influence the M cell functions in a self-suppression.
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The effects of bile acids and bilirubin, which increase in blood in obstructive jaundice, on bicarbonate secretion were studied experimentally using isolated antral mucosa of the guinea pig. Antral mucosal preparations were mounted between Ussing chambers. Basal and bethanechol-stimulated secretion were measured by a pH stat device using 5 mM HCl. After 10(-4), 10(-3), and 5 x 10(-3) M taurocholic acid, 10(-4) and 10(-3) M cholic acid, and 1.2 x 10(-4) and 2.4 x 10(-4) M bilirubin conjugate were added to the serosal solution, basal and bethanechol-stimulated secretion were also measured. Taurocholic acid, at any dose, did not affect basal secretion, but bethanechol-stimulated secretion was inhibited dose dependently. Cholic acid and bilirubin conjugate did not affect basal secretion, but bethanechol-stimulated secretion was significantly inhibited. Although the addition of bile acid or bilirubin into the serosal solution under experimental conditions is not the same as obstructive jaundice, these studies suggest that the inhibition of bicarbonate secretion in the gastric mucosa may have an important role in the formation of acute gastric mucosal lesions in obstructive jaundice.
We investigated the clinical significance of the venous occlusion (VO) test on patients with systemic lupus erythematosus (SLE) with or without circulating lupus anticoagulant (LA) concerning whether changes in the blood coagulation and fibrinolysis system in vivo subsequent to VO reflect mechanical stimulation of the endothelium or presence/development of endothelial damage. The tissue plasminogen activator antigen (tPA:Ag) before VO was much lower in the LA-positive patients than in the LA-negative ones (p < 0.01) and the von Willebrand factor antigen (VWF:Ag) pre-VO was significantly higher in the patient group, regardless of LA status, than in the control group (p < 0.01). But the mean increment in tPA:Ag and VWF:Ag post-VO, when expressed as the percentage of the baseline level, showed no appreciable difference between LA-positive and -negative groups. Thrombomodulin (TM) basically, on the other hand, was higher in the patients of either LA status than in the controls (p < 0.01) with a significant post-VO increase in the SLE group, which was more marked in the LA-positive patients, against no substantial change in the controls (p < 0.01). It is known that tPA and VWF:Ag are released simply as a result of endothelial stimulation and that the release of TM is preceded by endothelial damage. Based on the present results, we may well conclude that (1) the endothelium is functionally intact in SLE patients, (2) an injury of the endothelium, possibly as a consequence of vasculitis, preexists in LA-positive patients, and thus to measure the TM response to VO would offer a helpful tool in diagnosing the preexisting endothelial damage in these clinical settings.
The effect of total-body cold exposure on plasma concentrations of von Willebrand factor (vWF), endothelin-1 (ET) and thrombomodulin (TM), all of which are considered to be generated from the endothelium, was studied in systemic lupus erythematosus (SLE) patients with and without Raynaud's phenomenon. The plasma levels of vWF, ET and TM in SLE patients, irrespective of the presence of Raynaud's phenomenon, were significantly higher than in normal controls even before the cold provocation test. After the cold provocation test, plasma levels of vWF and ET were significantly higher in SLE patients with Raynaud's phenomenon than in those without and in normal controls. No significant increase in TM was observed in either the SLE patients or the controls. These results suggest that SLE patients, regardless of the presence of Raynaud's phenomenon, are in a hypercoagulable state and that this state may be further intensified by cold exposure. Hence, it is concluded that we should consider antithrombotic therapy for SLE patients, especially those with Raynaud's phenomenon, to prevent unwanted activation of the coagulation system and possible endothelial damage.
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It is reported that nitroglycerin (NTG) induces the elevation of intracranial pressure (ICP). Because of it, the use of NTG in patients exhibiting the increased ICP especially in the neurosurgical field is thought to be avoided. However, these reported cases dealt with normal patients. Few cases under the condition of exactly increased intracranial pressure were studied. Our 31 patients of the hemorrhagic intracranial lesion (subarachnoid hemorrhage and hypertensive intracranial hemorrhage) at the acute stage were treated by NTG infusion as an antihypertensive drug, and the ICP was measured using the epidural pressure transducer. The 31 patients were divided into three groups. Group 1 consists of the 14 patients exhibiting normal ICP (< 15mmHg). Group 2 consists of 9 patients showing elevated ICP (15mmHg < or =). Group 3 consists of 8 patients treated with glycerol before the NTG infusion. Group 1 demonstrates a statistically significant elevation of ICP corresponding with the blood pressure depression. Group 2 showed no significant elevation of it. Group 3 disclosed no remarkable elevation of it both in the elevated ICP cases and the normal ICP cases. As mentioned above, the intravenous NTG caused a remarkable increase of ICP in the normal compliance of the intracranial contents and no elevation of ICP in the poor compliance. We conclude that NTG can be used for blood pressure control at an acute stage even in hemorrhagic intracranial lesion as anti-depressor.
Effects of TPE on prevention of hepatic failure after massive hepatectomy were studied experimentally using dogs. A 70% or 85% hepatectomy (Hx) was performed two weeks after TPE. All of the 70%Hx groups with(+)/without(-) TPE were alive for over two weeks after hepatectomy. While all of the 85%Hx group without TPE died, eight of ten in the 85%Hx group with TPE survived. Without TPE, total bilirubin levels in sera were elevated markedly in the 85%Hx group and moderately in the 70%Hx group after hepatectomy. The levels of escaped enzymes in sera, such as GOT or GPT, were also elevated remarkably in the TPE(-) groups. Although the levels of these enzymes were also high in the 85%Hx.TPE(+) group, these values were as same as those of 70%Hx.TPE(-) group. In the 85%Hx.TPE(-) group, critical diminution of functional hepatic cell mass and severe portal hypertension occurred after hepatectomy and coagulopathy and death followed to these phenomena. TPE might prevent the onset of these critical phenomena, and diminish the damage caused by massive hepatectomy. These results suggest that TPE is useful for prevention of postoperative hepatic failure so that we could perform massive hepatectomy safely, and extend the operative indication.
The immunohistochemical distribution of 15 blood coagulation factors in the germinal centers (GCs) of human Peyer's patches (PPs) was studied. Although factor VIII, active alpha-thrombin, and fibrinogen were hardly evident in the GCs, the majority of coagulation factors, such as kallikrein, high-molecular-weight kininogen, factors XII, X, IX, VII, V, XIIIa and XIIIb, prothrombin, anti-thrombin III and inactive alpha-thrombin were found, showing a lace-like staining pattern similar to that obtained with a monoclonal antibody, R4/23, specific for follicular dendritic cells (FDCs) in the GCs. By immunoelectron microscopy, positive reactions for factor X and XIIIa were found on the surfaces of FDCs, GC cells, and/or in the intercellular spaces of GCs, being especially marked on the surface of the labyrinth-like structure of FDCs. It is concluded that a majority of coagulation factors are localized in the GCs of human PPs. Furthermore, it is suggested that some of these coagulation factors have a close topographical relationship with FDCs.
This report is concerned with results of surgical treatment for Marfan's syndrome combined with annulo-aortic ectasia (AAE) and mitral regurgitation (MR). Of the 23 patients with Marfan's syndrome who received Bentall's procedure during 14 year period, seven (30%) of these patients had both AAE and MR. The MR grade of seven patients by cardiac Doppler or left ventriculographic studies were grade 1 in 2, 2 in 1, 3 in 1, and 4 in 3. Atrial fibrillation was present in 4 patients. New York Heart Association Functional Class on admission in these 7 patients were II in 1, III in 4, and IV in 2. The mitral valve was replaced with mechanical valve in 4 patients by left atrial approach whose MR grade were over 3. In the 4 patients the mitral annuli were extremely dilated, both valve leaflets were massively redundant, and all chordae were elongated and turned chordae and vegetation were detected due to infective endocarditis. Only Bentall's procedure was performed in 3 patients whose MR were minimal. There were no early death, but two late deaths. One of them died of cardiac failure 2.3 years after Bentall's procedure because grade 2 MR was increased. Another one died from ventricular arrhythmia 1.6 years after MVR and Bentall's procedure. The remaining 5 patients are doing well for 3 months to 11.5 years after operation. For Marfan's syndrome combined with AAE and MR, early operation is recommended before left ventricular impairment. Mitral valve repair was not performed, both to save time and because anticoagulant therapy was need for aortic valve replacement. Concomitant MVR was to be done for moderate to severe MR.
The hemodynamics during hemodilution occurred after hepatectomy for hepatocellular carcinoma with liver cirrhosis and its influences on the liver functions were studied. The hematocrit value gradually decreased about 10% until the 4th postoperative day owing to hemodilution after hepatectomy. While anemia progressed, cardiac index inversely increased. Under such a condition, oxygen consumption was maintained so that acidosis did not develop. Arterial blood ketone body ratio was also kept within a normal range except for a case whose hematocrit value decreased to 17.1%. Although the escaped hepatic enzymes such as GOT and GPT increased in the serum after hepatectomy, hemodilution was not responsible for their increase. While total bilirubin increased in the severe hemodiluted group, the increase was not due to hemodilution but caused by blood transfusion. The protein synthesis of the liver measured by rapid turnover protein levels in plasma was depressed after surgery, and this depression prolonged to the 14th postoperative day in the group whose hematocrit value decreased below 20%. These results suggest that it is better to keep hemodynamics without blood transfusion unless the hematocrit value decrease below 20%, and also better to maintain the hematocrit above 20% for liver regeneration after hepatectomy.
The surgical results of 38 patients who underwent reoperation for primary tissue failure of bioprosthesis in the mitral position between May 1982 and June 1990 were analyzed to determine the risk factors affecting the hospital mortality. The type of bioprostheses requiring reoperation were Hancock valve in 21 patients, Liotta valve in 15 patients and Mitroflow valve in 2 patients. Twenty-five preoperative and perioperative variables were collected and analyzed by univariate statistics using chi 2 test or Student's test. Four of thirty eight patients died postoperatively in the hospital, yielding an overall mortality of 10.5%. The causes of hospital mortality were low output syndrome in 2 patients and multiple organ failure in 2 patients. By univariate analysis, male, NYHA IV class, prosthetic stenosis, hepatic failure, renal failure, and pulmonary failure were risk factors predictive of high hospital mortality. In spite of recent improvement of surgical technique and myocardial protection, the hospital mortality of patients with NYHA IV class and advanced organ failure still remains unacceptable. Therefore, it is essential to perform reoperation for primary tissue failure of bioprosthesis before severe myocardial decompensation occurs. To accomplish this goal, patients with bioprosthesis who survived beyond the certain time should be followed periodically using echocardiogram.
Diffuse atelectasis often occurs in the dorsal region of the lung of critically ill patients under long term mechanical ventilation. Conventional physical therapies (ex. PEEP, Sigh) have little effect on diffuse dorsal atelectasis. We provided respiratory care with prone position for 7 patients with severe respiratory distress (Two patients were treated twice). Improvement of their Respiratory Indexes (RI, mean 2.97) was obtained in the prone position for 6-163 (mean 35.8) hours. Ventilation efficiency also improved. Static lung compliance didn't change. It was assumed that the prone position was the factor responsible for the improvement of pulmonary V/Q ratio, the change of movement pattern of the diaphragm, and the ease of postural drainage of sputum. There were no complications. We conclude that prone position respiratory care has high utility for critically ill patients with diffuse dorsal atelectasis.
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Experiments were made in which Aedes aegypti mosquitoes fed on a dog infected with Dirofilaria immitis, in order to determine the distribution pattern of microfilariae (Mf) in the dog's periphery blood and the number of Mf taken by the mosquitoes. Mosquitoes fed on an anesthetized dog at some 50 shaved skin spots and they were weighed immediately before and after feeding. This enabled us to examine not only the Mf number taken by each mosquito but also the Mf intake density in terms of Mf number per mg of blood. The Mf intake density showed a wide variation at the different parts of the dog's body, and the frequencies of Mf showed uneven distributions which were fitted best by the negative binomial. Significant differences were detected in the Mf intake density at different parts of the skin, but these differences were concluded as a non-consistent result because a similar result was not reproduced in the next experiment. It was presumed that not only the Mf number per mosquito but also the Mf intake density increased as the blood intake by the mosquitoes increased. This increase of both the Mf number per mosquito and the Mf intake density was also supported by another experiment in which mosquitoes were fed at the same skin spots consecutively one after another.
HCO3- secretion was investigated in isolated guinea pig antral mucosa mounted in Ussing chambers. The rate of HCO3- secretion was measured by a pH-stat system. The antral mucosa spontaneously secreted HCO3- at a rate of about 0.5 microEq cm-2 h-1. Bethanechol (100 microM) or 8-bromoadenosine 3':5'-cyclic monophosphate (8-Br-cAMP, 1 mM) induced a significant increase in HCO3- secretion. Prostaglandin E2 (1 microM) also produced an increase in HCO3- secretion, although it was less effective than either bethanechol or 8-Br-cAMP. Histamine (100 microM) did not affect HCO3- secretion. This preparation may be suited to the study of the precise mechanisms by which neurohumoral factors regulate gastric HCO3- secretion.