Biomedical subjects
Publications and source records attributed to S Sumita.
The enhanced toxicity of acid instilled directly into the rectum, without benefit of dilution and neutralization in the upper intestine, is evident in a case of acetic acid intoxication by accidental rectal administration of 50 mL of 9% acetic acid to a 5-year-old boy. The complications included necrosis of the colon, acute renal failure, acute liver dysfunction, disseminated intravascular coagulopathy (DIC) and sepsis.
OBJECTIVE: We investigated the correlation between the endogenous hormonal changes of pituitary-adrenal and pituitary-thyroid hormones and the prognosis of patients in multiple organ failure, and elucidated the mechanism of blunted thyrotropin (TSH) secretion by histological and immunocytochemical studies of anterior pituitary glands. PATIENTS: Forty-three patients were studied who had been admitted to the intensive care unit of Sapporo Medical University Hospital and had been diagnosed as having multiple organ failure. MEASUREMENTS: Pituitary adrenal hormones [corticotropin (ACTH), cortisol] and pituitary thyroid hormones [TSH, triiodothyronin (T3), free-T3, thyroxine (T4), free-T4, thyroxine-binding globulin (TBG)] were measured, and TSH and prolactin (PRL) responses thyrotropin-releasing hormone (TRH) were examined within 24 hours of admission to the ICU. Individual variables were compared between survivors (n = 19) and nonsurvivors (n = 24). Thirteen patients (five survivors, eight nonsurvivors) were investigated again before discharge from the ICU or death. Morphology was examined by hematoxilin-eosin staining, and avidin-biotin-peroxidase complex immunostaining was used to demonstrate the spectrum of TSH in 14 nonsurvivors. RESULTS: (1) ACTH levels remained within the normal range, while cortisol levels increased to above normal levels. Neither hormone showed significant differences between survivors and nonsurvivors. In nonsurvivors, cortisol levels decreased before death despite the increased ACTH levels. (2) T3 and free-T3 levels decreased markedly to below normal values, and reverse-T3 levels increased markedly to above normal values. Nonsurvivors showed significant differences in TSH, T4 and reverse-T3 levels compared with survivors. (3) TSH response to TRH was blunted in both groups but PRL response to TRH was normal. Nonsurvivors showed severely depressed TSH response. Nonsurvivors continued to show blunted TSH response to TRH, while this improved in survivors. (4) The histological study did not show very serious damages to anterior pituitary glands as TSH secretion was depressed. Many TSH immunoreactive cells were also observed by immunocytochemical study. CONCLUSION: Decreased cortisol, low T4 levels and blunted TSH response to TRH correlated with mortality in MOF patients. Histological and immunocytological studies suggest that blunted TSH secretion is not caused by pituitary damages or TSH exhaustion but by disturbances in TSH secretion. This blunted TSH secretion is reversible and its improvement is an indicator of survival.
The effects of an angiotensin II receptor (AT1) antagonist on sympathetic nervous responses to a mental arithmetic task and a cold pressor test were investigated using a placebo-controlled, single-blind design in 8 patients with essential hypertension (53 +/- 3 years). All patients received a placebo for 2 weeks (placebo run-in period), after which the control group (P; n = 4) continued to receive the placebo, while the experimental group (TCV; n = 4) received TCV-116 at 4 mg/day for 4 weeks (treatment period). After basal measurements were carried out, an arithmetic task and a cold pressor test were conducted on the last day of each period. Blood pressure (BP), heart rate (HR) and electrocardiogram (ECG) were continuously monitored. Muscle sympathetic nerve activity (MSNA) was assessed by determining the burst rate of the mean voltage neurogram obtained from the tibial nerve. Sympathovagal balance was also assessed, by determining the area ratio of the low frequency (LF: 0.05-0.15 Hz) to high frequency bands (HF: 0.16-0.5 Hz) of a power spectral analysis of HR variability (maximum entropy method). During the placebo run-in period, there were no significant differences in basal BP, HR, LF/HF or MSNA between the two groups. During the treatment period, basal mean BP in the TCV group was significantly lower (p < 0.05) than that in the P group, but there were no significant differences in basal HR, LF/HF or MSNA between the two groups. Although the arithmetic stress significantly increased BP, HR and LF/HF in both groups, MSNA was not significantly altered in either group.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To study whether the suppression of the thyrotropin (thyroid-stimulating hormone, TSH) response to thyrotropin-releasing hormone (TRH) correlates with severity of illness and death in patients with nonthyroidal critical illness. DESIGN: Prospective study. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Forty-one critically ill patients without thyroid disease with multiple organ failure who were admitted to the ICU. MEASUREMENTS AND MAIN RESULTS: The TSH response to TRH was tested within 24 hrs of ICU admission. Blood samples were obtained just before, and at 15, 30, 60, 90, and 120 mins after 500-micrograms injection of synthetic TRH. Triiodothyronine, free-triiodothyronine, thyroxine, free-thyroxine and TSH concentrations were measured in the samples obtained just before TRH injection. Acute Physiology and Chronic Health Evaluation (APACHE II) scores and Sepsis scores were calculated based on the data obtained within 24 hrs of ICU admission. Individual variables were compared between survivors and nonsurvivors. The APACHE II scores and Sepsis scores of nonsurvivors were significantly higher than those scores of survivors. The overall occurrence of suppressed TSH response to TRH was 88%. Peak TSH concentration of the TSH response was significantly lower in nonsurvivors than in survivors. Serial measurement of the TSH response showed that nonsurvivors experienced a decrease in peak TSH concentration from 1.55 +/- 0.78 to 0.55 +/- 0.30 microIU/mL; in survivors, it increased from 2.10 +/- 0.26 to 7.38 +/- 1.83 microIU/mL. Conversely, the basal TSH concentration did not change in either survivors or nonsurvivors. The "severity" of illness of nonsurvivors remained high; their mean APACHE II score varied from 20.0 +/- 1.9 to 22.1 +/- 1.3 and the mean Sepsis score varied from 20.0 +/- 4.3 to 25.4 +/- 4.0, while the same scores for survivors decreased significantly (p < .05): their APACHE II score decreased from 16.2 +/- 0.7 to 7.6 +/- 2.0 and the Sepsis score went from 14.0 +/- 1.9 to 6.0 +/- 1.6. CONCLUSIONS: In critically ill patients with multiple organ failure, suppression of the TSH response to TRH frequently occurs and correlates with severity of illness and outcome. Our data indicate that measurement of the TSH response is helpful in evaluating the severity of illness and prognosis for critically ill patients.
A 67-year-old man was scheduled for left upper lobectomy under epidural and general anesthesia. About 1 hour after the beginning of operation, he developed cardiac arrest due to sudden massive bleeding from the pulmonary artery. In spite of open chest cardiac massage and intravenous administration of epinephrine, we could not resuscitate him successfully. More than 30 minutes after the cardiac arrest, cardiopulmonary bypass (CPB) was started and mean arterial blood pressure was maintained at 50-60 mmHg. His pulmonary artery was repaired under CPB. One hour after CPB, the weaning from artificial circulation was attempted and the spontaneous beating was observed. However, he developed low cardiac output syndrome due to long time ischemia resulting in hemorrhagic infarction. Therefore, the intra-aortic balloon pumping was started and his hemodynamics was immediately restored. We presume that CPB is useful for intraoperative resuscitation and this gives us new application of advanced life support for the patient in whom the conventional technique is ineffective.
Pulmonary dysfunction often follows cardiopulmonary bypass (CPB). In the present study, we examined (1) the effects of the human urinary tripsin inhibitor ulinastatin on the extravascular lung water volume (EVLW), and (2) A-aDO2 as an indicator of pulmonary function, in 30 adult patients undergoing CPB. We administered 600,000 U of ulinastatin intravenously immediately before start of CPB in 15 patients (U group). In the control group without ulinastatin, remarkable transient increases in EVLW and A-aDO2 occurred after CPB. In contrast, in the U group extravascular lung water volume level was maintained within the normal range and an inhibited transient increase in A-aDO2 after CPB was observed. We conclude that the administration of ulinastatin in patients undergoing CPB may be useful to prevent pulmonary dysfunction following CPB.
Glycosylations of 3-O-(2,3,4-tri-O-acetyl-alpha-L-rhamnopyranosyl(1-->2)- 3,4-di-O-acetyl-alpha-L-arabinopyranosyl)-23-O-acetylhederageni n (15) with mono- (16), di- (17) and trisaccharide bromide (18) gave the bisdesmoside peracetates 19, 20 and 22, respectively, which were treated with 5% KOH in MeOH to give the bisdesmosides 25-27. Hydrolysis of the glycosides 6 and 9 having beta-D-glucopyranose as a terminal sugar component with beta-glucosidase in acetate buffer (pH 4.7) gave compounds 28 and 29, respectively. Cytoprotective effects of the synthesized triterpenoidal saponins against CCl4-induced hepatic injury were compared with those of saponins isolated from the leaves of Aralia elata Seem. (Araliaceae) using isolated hepatocytes from rat liver. Although the monodesmosides 1-4 having neutral sugar components only at the O-3 position on the aglycones showed no cytoprotective effect, bisdesmosides having sugar components at both the O-3 and O-28 positions on the aglycones had potent effects, even when the species of the sugar components were different. The bisdesmosides 10, 11, and 27 having five monosaccharides in the molecules exhibited the most potent cytoprotective effects.
Stepwise glycosidation was adopted for the construction of glycyrrhetic acid beta-glycosides (27-30) having beta (1-->2)-linked disaccharides such as 2-O-beta-D-glucuronopyranosyl-beta-D-glucopyranose, 2-O-beta-D-glucuronopyranosyl-beta-D-galactopyranose, 2-O-beta-D-glucopyranosyl-beta-D-glucuronopyranose and 2-O-beta-D-galactopyranosyl-beta-D-glucuronopyranose. In the first glycosidation, 2-O-trichloroacetyl-beta-D-payranosyl chlorides (9-11) were utilized as starting sugar derivatives to react with methyl glycyrrhetinate (5): Glycosidation of 5 with 9 and 10 gave beta- and alpha-monoglycosides (12) and (13), and (15) and (16), respectively. Treatment of the beta-glycosides 12 and 15 with ammonia-saturated ether gave products (14) and (17), respectively. The glycosidation of 5 with 11 followed by treatment with ammonia-saturated ether gave compounds (18) and (19), respectively. The second step glycosidations of 14 and 17 with methyl 2,3,4-tri-O-acetyl-alpha-D-glucuronatopyranosyl bromide (20) gave diglycoside derivatives (23) and (24), respectively, and that of 18 with 2,3,4,6-tetra-O-acetyl-alpha-D-glucopyranosyl bromide (21) and -alpha-D-galactopyranosyl bromide (22) gave diglycoside derivatives (25) and (26), respectively. The removal of the protecting groups of 23-26 gave diglycosides 27-30, respectively, having a beta-D-glucuronopyranose (beta-D-glcUA) as one of two sugar components in the molecules. The cytoprotective effects of the synthesized glycosides 27-30 on carbon tetrachloride (CCl4)-induced hepatotoxicity in vivo were compared with diglycosides 31-33 having only neutral sugar components and naturally occurring glycyrrhizin (34) having two acidic sugar components (beta-D-glcUA).(ABSTRACT TRUNCATED AT 250 WORDS)
We reported a case of type II cryoglobulinemia involving glomerulopathy associated with HCV-induced liver cirrhosis. The patient was a 57-year-old woman. Her past history included chronic hepatitis at 51 years and rheumatoid arthritis at 53 years of age. At 46 years, an erythematous lesion appeared on her legs, which was diagnosed as allergic vasculitis by skin biopsy. At 50 years, proteinuria, hematuria and hypertension were recognized. The next year, the first renal biopsy was performed and showed membranoproliferative glomerulonephritis (MPGN). Recently, the edema of her legs has progressed, and the laboratory data showed proteinuria, hematuria, hypocomplementemia, rheumatoid factor positivity, and increase of monoclonal IgG kappa chain. The second renal biopsy revealed an endocapillary proliferative glomerulonephritis-like lesion with marked infiltration of monocytes and macrophages. The subendothelial deposit showed a fine fibril-like pattern. She was treated with steroids and double filtration plasmapheresis (DFPP) therapy, but the treatment was not very effective. She died of liver cirrhosis, which was probably induced by hepatitis C virus (HCV), and sepsis. Generally, the patients of type II cryoglobulinemia often showed HCV antibody positivity, pointing to HCV as an etiological factor. In this case, renal biopsy was performed twice in the same patient, and the histologic findings suggest the clinicopathological course of cryoglobulinemia.
Continuous thoracic epidural anesthesia (T4/5) using 4-5 ml.h-1 of 1.5% lidocaine with 1:200,000 epinephrine and inhaled anesthesia using nitrous oxide, oxygen and sevoflurane were performed in two patients, (40 and 22 yr-old females) with myasthenia gravis. This combined anesthetic technique provided muscle relaxation for endotracheal intubation and optimal operating conditions, including muscle relaxation and stability of hemodynamics during transsternal thymectomy. Further, continuous epidural anesthesia using 4 ml.h-1 of 0.25% bupivacaine provided postoperative pain relief without other analgesics and stable postoperative respiratory conditions. In conclusion, we confirm the benefits of this technique which provides not only safe and stable conditions during the surgery, but also an improved comfort for patients in the postoperative period following transsternal thymectomy for myasthenia gravis.
Opioid receptors solubilized from rat brain membranes with digitonin were partially purified with a newly prepared affinity resin, AF-Amino Toyopearl, coupled with a mu-antagonist Tyr-Pro-Tyr-Tyr at the C-terminus of the peptide. The purified materials were reconstituted with an inhibitory GTP-binding protein (Gi) in liposome. From displacement analyses, two binding states, with a high and a low affinities for the mu-agonist [D-Ala2,Me-Phe4,Gly-ol5]enkephalin, were observed in the reconstituted system with Gi, only a low-affinity state was observed in the reconstituted system without Gi. The results suggested that the purified materials contained the mu-opioid receptors and could functionally couple with Gi as observed in the cell membranes.
The reactions of beta- and alpha-pyranose peracetates with PCl5 gave products regioselectively chlorinated. The reactions of 1,2,3,4,6-penta-O-acetyl-beta-D-glucopyranose (5) and -beta-D-galactopyranose (6) with PCl5 in CCl4 and that of methyl 2,3,4-tri-O-acetyl-beta-D-glucuronatopyranose (7) with PCl5 in toluene gave 2-O-trichloroacetyl-beta-D-pyranosyl chlorides 4, 12 and 14, respectively, as major products, and alpha-D-pyranosyl chlorides 11, 13 and 15, respectively, as minor products. On the other hand, the reactions of compounds 8 and 9 which were alpha-anomers of 5 and 6, respectively, with PCl5 gave as major products transformed acetyl groups at C-6 to -C(Cl) = CCl2 or -C(Cl)2-CCl3 group (16 and 17 from 8 and 18 from 9). The same reaction of 10, which was alpha-anomer of 7, gave alpha-chloride 15 as a major product. The glycosidation of sugar derivative 4 with sarsasapogenin 23 gave beta-glycoside 24 (29.1%) and alpha-glycoside 25 (46.9%), and that of 12 with 23 gave beta-glycoside 26 (24.0%) and alpha-glycoside 27 (40.8%). The improvement of the yields of beta-glycosides 24 and 26 (66.9 and 62.1% for 24 and 26, respectively) in the glycosidations were accomplished by the employment of alpha-bromides 28 and 29 obtained from 4 and 6, respectively. The glycosidations of monoglycosides 30 and 31 obtained by the treatment 24 and 26, respectively, with ammonia-saturated ether with sugar acetate bromides 32 and 34 gave diglycoside derivatives 35 and 33, respectively.
Pain relief following thoracotomy and arterial concentration profiles after interpleural administration of lidocaine were studied in 23 adult patients. They were allocated to three groups and given interpleural injection of 20 ml each of 1.0% (group 1, N = 9, non-pneumonectomy patients), 1.5% (group 2, N = 10, non-pneumonectomy patients), and 1.5% (group 3, N = 4, pneumonectomy patients) lidocaine with epinephrine (5 micrograms.ml-1). Complete pain relief was obtained within 20 min after injection in all patients. The mean duration of analgesia was 2.8 hr, 3.1 hr, and 5.1 hr in group 1, 2, and 3, respectively. The maximum plasma concentrations of lidocaine (Cmax) were 1.7 +/- 1.0 (mean +/- SD) microgram.ml-1, 2.2 +/- 0.6 micrograms.ml-1, and 0.7 +/- 0.2 micrograms.ml-1 in group 1, 2, and 3, respectively. The mean duration of analgesia was significantly longer in group 3 than in group 2 (P less than 0.01). Cmax was significantly lower in group 3 than in group 2 (P less than 0.01). In conclusion, we consider interpleural injection of lidocaine with epinephrine to be an effective method of providing postoperative analgesia after thoracotomy. Our data also suggest that the duration of analgesia may increase and the plasma levels of lidocaine may remain quite low in total pneumonectomy patients, because local anesthetic solution is not absorbed through the visceral pleura but absorbed only through the parietal pleura alone in these patients.
A case of pulmonary embolism associated with diabetes insipidus is reported in an 18-year-old male. The patient, who had been treated with DDAVP for diabetes insipidus and hydrocortisone for hypocorticism for two years after first operation for the removal of craniopharyngioma, was admitted with recurrence of that tumor. Diabetes insipidus immediately after second operation was controlled with intermittent drip infusion of a small amount of aqueous pitressin under monitorings of body weight hourly using a patient weighing system to keep the weight changes within +/- one kilogram. Serum and urine electrolytes levels, osmolarity, and free water clearance were also monitored every three hours to maintain water-electrolytes balances appropriately. Postoperative course had been uneventful except that CSF rhinorrhea occurred 7 days after operation. The patient was, then, kept in bed with horizontal plane to avoid further leakage of CSF. Two days later, he developed chest pain suddenly with tachypnea, tachycardia, and general cyanosis. The arterial-BGA showed PaO2 of 53.5mmHg and PaCO2 of 35.3mmHg in room air. The definite diagnosis of pulmonary embolism was made by technetium microaggregate lung perfusion scans and by pulmonary angiograms. The patient was treated with heparin, 15000IU/day, and urokinase, 720000IU/day. The symptoms due to pulmonary embolism had improved gradually within a couple of weeks. Recent articles have shown an unexpected high incidence of deep vein thrombosis and pulmonary embolism in neurosurgical patients associated with the elevation of blood coagulability. Brain tumors, especially suprasellar mass with hypothalamic dysfunction have been suggested to cause thromboembolic disorders frequently. The clinical course was described and factors causing pulmonary embolism on this patient was discussed.
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In the present report we described two cases of malignant hyperthermia under halothane anesthesia. Case 1; A 54-year-old, 58 kg-male was scheduled for the operation of giant arterio-venous malformation. Anesthesia was induced with thiamylal, fentanyl and pancuronium, and maintained with oxygen, nitrous oxide and halothane. The patient was subjected to halothane inhalation for 26 hours prior to the development of the malignant hyperthermia. Although body temperature rose to 41 degrees C, it returned to normal with the administration of 280 mg of dantrolene and systemic cooling. Case 2; A 31-year-old, 68 kg-female was scheduled for tonsillectomy. Anesthesia was induced with thiamylal, oxygen, nitrous oxide and halothane. After the administration of 70 mg of SCC, marked muscular rigidity occurred and endotracheal intubation was impossible. The operation was postponed. Two months after the first anesthesia, operation was successfully performed under NLA with droperidol and fentanyl. Caffeine contracture test was performed in each case by skinned fiber method and the result showed that the sensitivity to caffeine increased in the isolated skeletal muscle fiber bundles from these patients. Thresholds of caffeine contracture of these skinned fiber bundles were all lower than 5mM caffeine.
The authors present a rare case of a 58-year-old female who had cardiac arrest due to massive abdominal hemorrhage because of the rupture of pancreatic pseudocyst during an emergency operation. We succeeded in resuscitation by performing emergency thoracotomy and internal cardiac compression. Thoracic aortic cross clamping was employed to control bleeding, and we could perform the operation. She recovered without any neurological deficits. Thoracic descending aortic cross clamping should be always considered both before and during operation for the control of massive abdominal hemorrhage to avoid circulatory collapse.
Five hundred and thirty-three patients have been treated after thoracic and cardiovascular surgery in our ICU during the last four years. Cardiac failure was shown in 150 cases, respiratory failure in 132 cases, renal failure in 76 cases, and hepatic failure in 84 cases. The appropriate mechanical organ-supports (MOS) were applied in the following cases: intra-aortic balloon pumping (IABP) in 48 cases, veno-arterial bypass (VAB) in 18 cases, left ventricular assist device (LVAD) in 1 case, respirator in 132 cases, continuous hemofiltration (CHF) in 44 cases, hemodialysis (HD) in 13 cases, peritoneal dialysis (PD) in 21 cases, Continuous intensive peritoneal dialysis (CIPD) in 7 cases, and plasma exchange (PEx) in 22 cases. The results of MOS6 which required exocorporeal circulation were not satisfactory, especially CHF (mortality rate 75.0%), HD (76.9%), and VAB (100%). Though, the results of IABP (35.4%) and CIPD (14.3%) were significantly better. The main cause of early death (within 6 post-operative days) was low output syndrome (LOS) (63.6%). However, that of late death (beyond 14 post-operative days) was sepsis (66.7%). Therefore, it is important for the survival of these patients to control LOS during the early post operative period and then to concentrate on the prevention of infection.