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S Kashimoto

Publications and source records attributed to S Kashimoto.

At least 91 records · Page 5Linked to original sources
PubMed1988

Effects of isoflurane on myocardial metabolism during postischaemic reperfusion in the rat.

In experiments on isolated rat heart lung preparation, the effects of isoflurane on myocardial metabolism during postischaemic reperfusion were evaluated with intramyocardial high energy phosphates, lactate and glycogen. Hearts were perfused for 10 min initially and made globally ischaemic for 8 min in ischaemic groups. Afterwards, they were reperfused for 12 min. Isoflurane was administered from 5 min after the start of perfusion to the end of reperfusion. There was no significant difference in myocardial lactate levels between ischaemic isoflurane and control groups. However, the ATP level in the hearts in the ischaemic isoflurane group was significantly higher than that in the ischaemic control group (17.96 +/- 1.31 vs 15.50 +/- 0.87; P less than 0.005). The administration of isoflurane to the isolated rat heart during pre- and post-ischaemia enhanced metabolic recovery in the postischaemic state.

Adenosine Diphosphate↗
PubMed1987

Fifty percent nitrous oxide depresses recovery from anoxic heart failure induced by 100% nitrous oxide.

In experiments on an isolated rate heart lung preparation, the effects of 100% oxygen, 50% nitrous oxide or air on myocardial metabolism during recovery from anoxic heart failure were evaluated with intramyocardial high energy phosphates, lactate and glycogen. A hundred percent nitrous oxide was administered until the cardiac output decreased from 30 to 20 ml/min, and then 50% nitrous oxide, air or 100% oxygen was administered. Fifty percent nitrous oxide reduced the cardiac output and caused heart failure again. The ATP level and energy charge in hearts with 50% nitrous oxide were significantly lower than those in the others. These data indicate that 50% nitrous oxide during recovery from anoxic heart failure had deleterious effects on myocardial function and metabolism.

Journal Article↗
PubMed1987

Effects of thiopental on cardiac energy metabolisms in postischemic reperfusion in rat.

In experiments on isolated rat heart lung preparation, the effects of thiopental on myocardial metabolisms in postischemic reperfusion were evaluated with intramyocardial high energy phosphates, lactate, pyruvate and glycogen. The release of CPK in the perfusate blood was also measured at the end of reperfusion. After 10 min perfusion, hearts were made globally ischemic for 8 min and reperfused for 12 min. Large dose of thiopental (100 microg/ml) reduced the energy charge and glycogen content. Reperfusion with an anesthetic dose of thiopental (10 microg/ml) resulted in an exacerbation of the CPK release. Protection by thiopental during ischemia was not observed and its high dose may be harmful.

Journal Article↗
PubMed1987

Effects of halothane and enflurane on myocardial metabolism during postischaemic reperfusion in the rat.

In experiments on isolated rat heart-lung preparation, the effects of halothane and enflurane on myocardial metabolism during postischaemic reperfusion were evaluated with intramyocardial high energy phosphates, lactate and glycogen. Hearts were perfused for 10 min initially and made globally ischaemic for 8 min. Afterwards, they were reperfused for 12 min. Halothane or enflurane was administered from 5 min after the start of perfusion to the end of reperfusion. There were no significant differences in contents of high energy phosphates between control (C), halothane (H) and enflurane (E) groups (ATP: 15.50 +/- 0.87, 16.05 +/- 1.99 and 15.16 +/- 2.03 mumol/g dry wt, respectively). However, lactate levels in the hearts in Groups H and E were significantly higher than those in Group C (44.04 +/- 10.54, 40.63 +/- 10.34 vs 28.63 +/- 5.98). Slight deterioration in the myocardial oxidation-reduction state may be caused by inhalational anaesthetics when they are administered during the postischaemic reperfusion period.

Anesthesia, General↗
PubMed1987

Protective effects of superoxide dismutase against oxygen toxicity in rat's heart lung preparation.

Oxygen toxicity in the non-ischemic and non-hypoxic heart has not been reported. In an experiment on isolated rat heart lung preparation, the effects of superoxide dismutase (SOD) on oxygen toxicity during hyperoxic perfusion were evaluated with intramyocardial high energy phosphates and the release of creatine phosphokinase (CPK) in the perfusate blood. Although there were no significant differences in high energy phosphates between SOD-treated and untreated hearts, the CPK release from the SOD-treated hearts was significantly less than from the untreated hearts. SOD increased the oxygen pressure of perfusate blood, too. These results indicate that hyperoxia induced cardiac and lung cell damage which was protected by SOD.

Adenosine Diphosphate↗
PubMed1986

Recombinant human tumor necrosis factor--II. Antitumor effect on murine and human tumors transplanted in mice.

Recombinant human tumor necrosis factor (rHu-TNF) was found to exhibit potent antitumor activities not only against murine tumors, i.e. Meth A sarcoma, B 16 melanoma, colon 26 adenocarcinoma, Lewis lung carcinoma and MH134 hepatoma, transplanted in syngeneic mice but also against human tumors, i.e. HMV-2 melanoma, PC-10 lung carcinoma and GOTO neuroblastoma, heterotransplanted in nude mice. rHu-TNF caused necrosis of all tumors tested and inhibited their growth in a dose dependent manner. Complete regression of tumors was observed in mice bearing Meth A, B16, colon 26, MH134, HMV-2 and PC-10 but not in mice bearing Lewis lung carcinoma and GOTO neuroblastoma. The prolongation of survival time was also observed in syngeneic mice transplanted with murine tumors except Lewis lung carcinoma. The antitumor effect of rHu-TNF was more evident when it was given intratumorally than when given intravenously. The feasibility of rHu-TNF as a drug for cancer therapy is discussed.

Adenocarcinoma↗
PubMed1986

Effects of urinastatin on cardiac energy metabolism in acute hemorrhage in rats.

Urinastatin, one of the trypsin inhibitors extracted from the human urine, has been reported to be useful in treating hypovolemic shock. We studied the effects of urinastatin on cardiac energy metabolism in acute hemorrhage in rats. The hemorrhage was produced by withdrawing blood (60 ml) from the abdominal aorta, and an equivalent volume of saline and 25,000 units/kg of urinastatin were injected over 5 min. The heart was then frozen quickly with liquid nitrogen, and high energy phosphates, lactate, pyruvate and glycogen contents were measured enzymatically. There was no significant difference in either ATP, lactate or pyruvate contents of the heart between the urinastatin-treated and the control groups. However, energy charge ([ATP + 0.5 X ADP]/[ATP + ADP + AMP]) and glycogen levels in the urinastatin-treated group were significantly higher than those in the control group. These findings suggest that urinastatin might produce a metabolic improvement in mitochondrial function and suppress the anaerobic glycogenolysis induced by circulatory deficiency in an acute hemorrhagic state.

Adenine Nucleotides↗
PubMed1986

Effects of naloxone on cardiac energy metabolism in acute hemorrhage in rats.

It has been reported that naloxone may be useful in the treatment of hypovolemic shock. However, the effects of naloxone on cardiac energy metabolism in acute hemorrhage have not been investigated. The effects of naloxone on myocardial metabolism were evaluated in the rat during acute hemorrhage with crystalloid resuscitation. Intramyocardial high energy phosphates, pyruvate, lactate and glycogen were measured. There was no significant difference in high energy phosphates, energy charge, lactate and glycogen contents between control, 1 mg naloxone and 10 mg naloxone groups. However, pyruvate level in hearts in the 10 mg naloxone group was significantly higher than that in control group. Therefore, naloxone reduced the lactate/pyruvate (L/P) ratio. Although naloxone did not improve the mitochondrial function, it improved the oxidation-reduction state in cardiac energy metabolism.

Animals↗
PubMed1986

Antitumor effect of recombinant human interleukin 1 alpha against murine syngeneic tumors.

Interleukin 1 (IL1) has been suggested to have antitumor activity but there is no clear-cut evidence of an in vivo antitumor effect of pure IL1. In this work, the antitumor effect of purified recombinant human IL1 alpha (rHu-IL1 alpha) was assessed on murine tumors transplanted intradermally in syngeneic female mice. rHu-IL1 alpha inhibited the growth of Meth A sarcoma in BALB/c mice, B16 melanoma in C57BL/6 mice and colon 26 adenocarcinoma in CDF1 mice, as well as the spontaneous pulmonary metastasis of Lewis lung carcinoma in BDF1 mice, at intratumoral (itu), intramuscular (im), and/or intravenous (iv) doses ranging from 1 to 30 micrograms/mouse. The antitumor effect of rHu-IL1 alpha was generally dose- and route-dependent, being highest by the itu route, followed by the im and iv routes in that order. Palpable 7-day-old Meth A sarcoma was completely regressed in some mice given rHu-IL1 alpha itu once at doses of 10-30 micrograms/mouse (cured ratio; 71-100%), once a day for 3 days at doses of 3-30 micrograms/mouse (57-86%) or once a day for 7 days at doses of 1-10 micrograms/mouse (14-100%). Palpable 7-day-old B16 melanoma was also regressed completely in some mice given seven itu doses of 10-30 micrograms/mouse (14-86%). One-day-old Meth A sarcoma was more sensitive to rHu-IL1 alpha than 7-day-old Meth A sarcoma. There was no macroscopic sign of inflammation at the site of injection of rHu-IL1 alpha. These results show that rHu-IL1 alpha has antitumor activity in vivo and is worthy of further study as a potential antitumor agent.

Adenocarcinoma↗
PubMed1986

[Combined effect of PT-050 (recombinant human TNF) and antitumor drugs on syngeneic murine tumors].

The combined effect of PT-050 (recombinant human TNF) and various antitumor drugs was investigated using murine colon 26 adenocarcinoma, Meth A sarcoma and B16 melanoma transplanted into syngeneic mice. When colon 26- or Meth A- bearing mice were intravenously given PT-050 in combination with mitomycin C (MMC), doxorubicin (DXR), cis-platinum (CDDP), 5-fluorouracil (5-FU) or cyclophosphamide (CPA), a significant synergistic effect was observed, that is, both the inhibition rate of tumor growth and the cured ratio were increased significantly when compared with those given each drug alone. Similarly, an augmentation of the antitumor effect was also observed in B16-bearing mice by a combined treatment with PT-050 and these antitumor drugs. These results suggest that the combination chemotherapy of PT-050 with various antitumor drugs may be useful for cancer therapy.

Adenocarcinoma↗
PubMed1985

Succinylcholine-induced ventricular arrhythmia during halothane anesthesia.

A case of ventricular tachycardia in a healthy child subsequent to onset of a succinylcholine infusion is described. A 9-year-old male patient was scheduled for an adenoidectomy and bilateral tonsillectomies. There was no history of cardiac arrhythmia. Anesthesia was induced by mask with nitrous oxide and halothane. Immediately after the infusion of 20 mg of succinylcholine, the heart rate was 150 beats/min and then the electrocardiograph (ECG) revealed a short run of ventricular tachycardia. The patient was given 1 mg of propranolol, and enflurane and 100% oxygen were administered. Soon after the propranolol was given, normal sinus rhythm returned. Ventricular tachycardia may occur after a single dose of succinylcholine in a healthy anesthetized child without predisposing disease.

Adenoidectomy↗