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Biomedical subjects

S Naruse

Publications and source records attributed to S Naruse.

At least 217 records · Page 12Linked to original sources
PubMed1985

Observations of energy metabolism in neuroectodermal tumors using in vivo 31P-NMR.

The energy metabolism of living tumors in rats and hamsters were investigated by obtaining in vivo 31P-NMR spectra, and the effects of chemotherapy on tumors were evaluated by observing the changes of these spectra. Tumor cells of rat glioma, human glioblastoma and human neuroblastoma were inoculated subcutaneously in the lumbar region of the animals. After the tumor grew to over 1.5 cm in diameter, in vivo 31P-NMR spectrum data was obtained selectively from the tumor with a TMR-32 spectrometer (Oxford Research Systems, U.K.). Several peaks (ATP, inorganic phosphate (Pi), phosphodiesters and phosphomonoesters (PME) were observed in the tumors. The heights of these peaks varied widely corresponding to the tumor growth. However, the spectrum pattern of each tumor in an active stage was found to be essentially the same regardless of histological type or tumor origin. The phosphocreatine (PCr) peak was small, ATP and PME peaks were large and tissue pH calculated from the chemical shift of Pi was low in each tumor group. After intravenous injection of a large dose of a chemotherapeutic agent, ATP peaks decreased and the Pi peak increased gradually, resulting in a dominant Pi peak pattern after several hours in all groups. With lower drug doses, spectrum changes were temporarily seen in the tumors. These findings indicated that drugs with a high dose have a selective and a direct action on the energy metabolism of tumor tissues. In vivo 31P-NMR spectra measurement is very valuable not only to investigate the energy metabolism in tumor tissue but also to evaluate the effects of chemotherapy on the tumor.

Animals↗
PubMed1985

In vivo studies of energy metabolism in experimental cerebral ischemia using topical magnetic resonance. Changes in 31P-nuclear magnetic resonance spectra compared with electroencephalograms and regional cerebral blood flow.

The energy state of the brain during and after transient cerebral ischemia was examined in rats by in vivo measurement of 31P-nuclear magnetic resonance (NMR) spectra using a topical magnetic resonance spectrometer. EEGs and regional CBF (rCBF) were monitored on the same ischemic models. Immediately after the induction of ischemia, the height of the ATP and phosphocreatine peaks in the spectrum began to decrease with a concurrent increase of the inorganic phosphate (Pi) peak. The calculated pH from the chemical shift of Pi decreased during ischemia. The EEG pattern became flat immediately after ischemic induction. The rCBF decreased below the sensitivity level of the measuring instrument. With 30-min ischemia, the 31P-NMR spectrum returned to a normal pattern rapidly after recirculation. However, recovery of the EEG was delayed. The rCBF after recirculation showed postischemic hyperemia followed by hypoperfusion. In cases of 120-min ischemia, none of the spectra showed recovery. Thus, we could investigate the dynamic process of pathophysiological changes occurring in the ischemic brain in vivo.

Animals↗
PubMed1985

Comparison of the action of cholinomimetics and pentagastrin on gastric secretion in dogs.

Stimulation of acid secretion by muscarinic cholinomimetic agents depended on the periodic interdigestive activity of the stomach. This explains the peak and following fade. Pentagastrin stimulated gastric secretion after a fixed interval and did not depend on the interdigestive activity. Neither gastrin nor methacholine directly contracted the gallbladder in the doses used. A sustained secretion of gastric acid and pepsin, such as follows a meal, required both hormonal stimulation and gastric distension. The magnitude of the acid response from Heidenhain pouches following meals suggested that pentagastrin doses commonly used experimentally greatly exceed the physiological.

Animals↗
PubMed1985

Measurements of in vivo 31P nuclear magnetic resonance spectra in neuroectodermal tumors for the evaluation of the effects of chemotherapy.

The effects of chemotherapy on living tumor tissue in hamsters and rats were investigated by measuring the 31P nuclear magnetic resonance spectra using topical magnetic resonance. Human neuroblastoma, human glioblastoma, and rat glioma tumor cells were inoculated s.c. in the lumbar region of the animals. After the diameter of the tumors increased to 1.5 cm, in vivo 31P nuclear magnetic resonance spectra were measured selectively in the tumors with a TMR-32 spectrometer. Adenosine triphosphate, inorganic phosphate (Pi), phosphodiester, and phosphomonoester peaks were observed. The phosphocreatine peak was hardly detectable, adenosine triphosphate and phosphomonoester peaks were high, and tissue pH, calculated from the chemical shift of Pi, declined. Regardless of the tumor origin or the histological type, the spectral pattern of each neuroectodermal tumor was found to be essentially the same. After i.v. injection of a large dose of a chemotherapeutic agent, adenosine triphosphate peaks decreased and Pi increased gradually, resulting in a dominant Pi peak pattern after 6 to 12 hours. However, during the same period, there were no observable changes in the spectra of normal organs. These findings indicated that the drugs have a selective and direct action on the energy metabolism of tumor cells. With lower drug doses, no remarkable changes were seen in the spectrum. Measurement of in vivo 31P nuclear magnetic resonance spectra is valuable not only to investigate the energy metabolism in tumor tissue but also to evaluate the effects of chemotherapy.

Adenosine Triphosphate↗
PubMed1984

In vivo measurement of energy metabolism and the concomitant monitoring of electroencephalogram in experimental cerebral ischemia.

The energy metabolites in rat brain in vivo were measured by using topical magnetic resonance (TMR) during the whole course of ischemia, in combination with the concomitant monitoring of electroencephalogram (EEG). Immediate loss of high energy phosphorus compounds, phosphocreatine (PCr) and ATP, resulted in the flattening of EEG after the induction of ischemia. PCr and ATP returned to almost normal level 30 min after recirculation of the ischemic brain, but EEG showed no recovery and the abnormality lasted for 12 h. The measurement of in vivo 31P-NMR is essential for the decision of the convalescence of cellular function in the brain.

Adenosine Diphosphate↗
PubMed1984

Measurements of in vivo energy metabolism in experimental cerebral ischaemia using 31P-NMR for the evaluation of protective effects of perfluorochemicals and glycerol.

Effects of perfluorochemical (PFC) and glycerol on energy metabolism in cerebral ischaemia were examined by the sequential measurements of in vivo 31P-NMR spectrum using topical magnetic resonance (TMR). Experimental cerebral ischaemia was induced in forty-five Wistar rats by a four-vessel occlusion method. The 31P-NMR spectrum and the EEG were monitored during preischaemic and ischaemic periods and after circulation was restored for various periods up to 240 min. There were several peaks in the 31P-NMR spectrum of the preischaemic rat brain; beta-ATP, alpha-ATP, gamma-ATP, phosphocreatine (PCr), phosphodiesters, inorganic phosphate (Pi) and sugar phosphate. As soon as the ischaemia was induced, PCr and ATP decreased and Pi increased. The chemical shift of the increased Pi peak decreased, showing acidosis of the brain tissue. After circulation was restored following the 30 min ischaemia, recovery of the 31P-NMR spectrum occurred within 30 min in all sixteen untreated rats. Recovery of the 31P-NMR spectrum was induced by recirculation only in half of the six rats in the untreated 60 min ischaemia group. None of the six rats in the untreated group showed recovery of the spectrum after 120 min ischaemia. When 20% Fluosol-DA was administered at a dose of 20 ml/kg before the induction of ischaemia, all eight rats showed recovery of the spectrum after 120 min ischaemia. Moreover, four of six rats treated with both PFC and glycerol showed temporary recovery even after 240 min ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1984

Vagal control of gall-bladder contraction.

The role of the vagi in gall-bladder contraction was studied in conscious dogs with chronic biliary fistulae. The interdigestive periodic contraction of this organ was abolished by bilateral cervical vagal blockade, atropine or pentolinium, but neither methacholine nor carbachol initiated contraction when the duodenum was kept alkaline. The orthodox view that gall-bladder evacuation is primarily controlled by humoral mechanisms needs re-evaluation. Vagal blockade prevented the usual gall-bladder contraction in response to duodenal acidification.

Animals↗
PubMed1984

The role of motilin in periodic interdigestive pancreatic secretion in dogs.

The role of motilin in the periodic interdigestive secretion of the pancreas was studied in conscious dogs, each with a chronic gastric fistula, a Heidenhain pouch and a Thomas duodenal fistula. Motilin increased pancreatic water, bicarbonate and protein secretion and the motility of the stomach, duodenum and Heidenhain pouch in a manner which closely resembles the spontaneous changes which occur during interdigestive activity. Endogenous motilin released by duodenal alkalinization had the same effect as exogenous hormone. Continuous infusion of motilin did not cause continuous pancreatic secretion and gut motility but merely shortened the interval of the periodic interdigestive activity. Exogenous and endogenous motilin were ineffective following atropine. Hexamethonium abolished the pancreatic and duodenal peaks but not the changes in gastric and pouch motility induced by motilin or duodenal alkalinization.

Animals↗
PubMed1984

Characteristics of secretin-stimulated pancreatic secretion in dogs.

The effect of the periodic interdigestive activity of the gut on secretin-stimulated pancreatic secretion was studied in eight conscious dogs each with a Thomas duodenal fistula, a gastric fistula and a Heidenhain pouch. Pancreatic water and bicarbonate responses to a small dose of secretin were greatly augmented in phase with the spontaneous periodic activity of the gut. This augmentation was closely related to pancreatic protein secretion. As the dose of secretin was increased the interval between peaks was prolonged, the peaks became less sharp, the nadirs were raised, and finally the periodic activity was no longer seen. Bilateral cervical vagal blockade with local anaesthetics reduced the secretin-stimulated bicarbonate secretion by 50% but the augmentation at the peak was not abolished. Atropine abolished the periodic augmentation completely and reduced the bicarbonate response by 80%. The peak response of volume and bicarbonate to secretin obeyed Michaelis-Menten kinetics. The nadir secretin dose response, however, was a sigmoid curve with a Hill coefficient larger than one. The action of atropine or hexamethonium was to shift the peak response kinetics to the nadir kinetics. It is concluded that the pancreatic response to secretin is greatly modulated by the spontaneous periodic activity of nerves.

Animals↗
PubMed1984

In vivo 31P-NMR studies on aerobic recovery of frog muscle following tetanus.

Aerobic recovery after a 60-sec tetanus of skeletal muscle of frog was studied using the in vivo 31P-NMR method with a topical magnetic resonance spectrometer (TMR) at 17 degrees C. Creatine phosphate recovered with a time constant of about 25 min-1. Sugar phosphates increased by the Pasteur effect, and saturated at about 4.5 mmol/kg muscle. The high level of the sugar phosphates was sustained during the following 60 min.

Adenosine Triphosphate↗
PubMed1984

[Formalin-induced minor tremor response as an indicator of pain].

Formalin which was said to produce prolonged pain and inflammation was injected subcutaneously into the back of guinea pigs, and minor tremor pain response (MTP-response) was measured using the MT-pick up, integrator and digital volt meter. The MTP-response curve showed a biphasic pattern. Immediately after injection, the MTP-response curve showed a significant peak which lasted for about 2 min (the first phase) and subsequently dipped rapidly, and after 5 min, it began to rise slowly again and had a peak at 30 min (the second phase). Morphine (6 mg/kg, s.c.) inhibited completely the first and second phases. Levallorphan (1.2 mg/kg), however, reversed the inhibitory effect of morphine at the first phase, but not at the second phase. Aspirin (200 mg/kg, i.p.), aminopyrine (100 mg/kg, s.c.) and pentazocine (5 mg-10 mg/kg, s.c.) inhibited significantly the formalin-induced MTP-response at both phases. Pyridinol carbamate (200 mg/kg, i.p.) and hydrocortisone (25 mg/kg, i.p.) had no effect on the MTP-response at the first phase, but inhibited it at the second phase. There was a parallelism between the time course of the vascular permeability induced by formalin and that of the second phase of MTP-response. From these results, it is suggested that the first phase of MTP-response is derived from the direct effect of formalin on free nerve endings, while the second phase is derived from the inflammation. Since two kinds of pain features were differentiated in this method, the relationships with so-called "immediate pain" and "delayed pain" were discussed. Furthermore, this method can be utilized to assess pain and the action of analgesics objectively and quantitatively.

Aminopyrine↗
PubMed1983

Cyclic changes of plasma pancreatic polypeptide and pancreatic secretion in fasting dogs.

Fasting conscious dogs, each with a gastric fistula, Heidenhain pouch and Thomas duodenal fistula, were used. Basal pancreatic secretion showed periodic increases in phase with the periodic contraction of the stomach and duodenum. Periodic increases of plasma pancreatic polypeptide (PP), but not of gastrin, were observed in phase with the periodic contraction and secretion of the gut. Ganglion blockade abolished the cyclical activity, both secretory and motor, of the gut and of plasma PP. Intraduodenal infusion of lidocaine suppressed the spontaneous increase of pancreatic secretion and plasma PP. It is concluded both that the cyclical release of PP and the increase in pancreatic secretion are under the control of the intrinsic nerves of the duodenum.

Animals↗
PubMed1983

Neural control of periodic secretion of the pancreas and the stomach in fasting dogs.

The role of nerves in periodic secretion of the pancreas and the stomach in relation to the motility of the upper gastrointestinal tract was studied in conscious fasting dogs which had previously been provided with chronic gastric and pancreatic fistulae and a Heidenhain pouch. Both atropine and pentolinium abolished the periodic increase in gastric and pancreatic secretion and motility of the gut. Bilateral cervical vagal blockade with lidocaine reduced the motility of the stomach, the duodenum and the pouch preceding their peaks, but the motility at the peaks remained unchanged except in the case of the stomach. Pancreatic secretion preceding its peak was also decreased by vagal blockade but that at the peak was not significantly different from the control peak. Periodic pepsin secretion, from both the fistula and pouch, was decreased by vagal blockade. It is concluded that the secretion and motility of the upper gut in fasting dogs is controlled by periodic activity of the vagus and intrinsic nerves.

Animals↗
PubMed1983

In vivo 31P NMR studies on experimental cerebral infarction.

Sequential metabolic changes in rat brain were monitored by in vivo measurements of 31P NMR spectra using a topical magnetic resonance (TMR) spectrometer, during the course of experimentally induced cerebral infarction and also during recovery produced by restoration of circulation. The experimental cerebral infarction was rendered by a slightly modified version of the method of Pulsinelli and Brierley (1979). The bilateral coagulation of the vertebral arteries at the level of alar foramina of the first cervical vertebra (preinfarction) did not show any change in NMR spectrum, but the subsequent bilateral ligation of internal carotid arteries produced a decrease in the peaks of ATP and phosphocreatine and a concomitant increase in the peak of inorganic phosphate within a few minutes. Intracellular pH, calculated from the chemical shift of inorganic phosphate, declined. These changes became maximal at approximately 30 min after the infarction. Reinstatement of blood flow to the cerebrum, produced by untying the ligature of internal carotid arteries, resulted in an immediate restoration of the peaks of ATP and phosphocreatine, which was followed by a reduction in the peak of inorganic phosphate within a few minutes. The spectrum recovered to its preinfarction pattern about 30 min after the restoration of the circulation. These experiments demonstrate that phosphorus compounds change very rapidly during infarction, and that these changes were reversible at least during a 30 min period.

Adenosine Triphosphate↗
PubMed1982

Effect of pancreatic juice on basal pancreatic and gastric secretion in dogs.

1. The effect of duodenal infusion of pancreatic juice on basal pancreatic and gastric secretion was studied in five conscious dogs provided with pancreatic fistulae, gastric fistulae and Heidenhain fundic pouches. 2. Pancreatic juice and trypsin stimulated a pancreatic secretion rich in protein. 3. Autodigested juice without proteolytic activities also stimulated the secretion. Boiling the juice or addition of trypsin inhibitor to the juice diminished the augmented secretion. 4. It seems, therefore, that trypsin is necessary even in proteolytically inactive autodigested juice for pancreatic stimulation. 5. In dogs, unlike rats and pigs, basal pancreatic secretion is not under negative feed-back control by duodenal tryptic activity. 6. Basal gastric secretion was not significantly changed by duodenal infusion of pancreatic juice.

Animals↗
PubMed1982

Proton nuclear magnetic resonance studies on brain edema.

The water in normal and edematous brain tissues of rats was studied by the pulse nuclear magnetic resonance (NMR) technique, measuring the longitudinal relaxation time (T1) and the transverse relaxation time (T2). In the normal brain, T1 and T2 were single components, both shorter than in pure water. Prolongation and separation of T2 into two components, one fast and one slow, were the characteristic findings in brain edema induced by both cold injury and triethyl tin (TET), although some differences between the two types of edema existed in the content of the lesion and in the degree of changes in T1 and T2 values. Quantitative analysis of T1 and T2 values in their time course relating to water content demonstrated that prolongation of T1 referred to the volume of increased water in tissues examined, and that two phases of T2 reflected the distribution and the content of the edema fluid. From the analysis of the slow component of T2 versus water content during edema formation, it was demonstrated that the increase in edema fluid was steady, and its content was constant during formation of TET-induced edema. On the contrary, during the formation of cold-injury edema, water-rich edema fluid increased during the initial few hours, and protein-rich edema fluid increased thereafter. It was concluded that proton NMR relaxation time measurements may provide new understanding in the field of brain edema research.

Animals↗
PubMed1982

[Nuclear magnetic resonance studies of effects of glycerol on brain edema].

Effects of glycerol on the state of water in edematous brain tissues were studied by the pulse FT NMR technique. Brain edemas were induced experimentally by cold injury and triethyl tin (TET) intoxication in Wistar rats. Ten percent w/v glycerol (1 g/kg body weight) were injected intravenously at 30 minutes before decapitation for the NMR measurements. Transverse relaxation times (T2) in the cerebral gray and white matter were measured by Meiboom-Gill pulse sequence at the resonant frequency of 100 MHz. Water content was calculated from the difference between wet and dry weight after heating in an oven at 95-100 degrees C for 72 hours after the NMR measurements. In the normal brain T2 value was 76.4 msec and 75.4 msec in the gray and white matter respectively. In the edematous brain, T2 separated into two components, one slow and one fast, corresponding with the increase of water content. Values of the slow component (slow T2) were characteristic of both types of brain edema. In the cold injury edema, slow T2 values became 105 msec in the gray matter and 96 msec in the white matter, while in the TET induced edema, it became 450 msec in the white matter. After glycerol infusion, slow T2 became faster in these regions in both types of brain edema, showing 92.1 msec in the gray matter and 88.1 msec in the white matter of the cold injury edema, and 388 msec in the white matter of TET induced edema. The degree of the changes of slow T2 values per unit change of water content was greater in the cold injury edema than in the TET induced edema. Serum osmolality elevated 23.8 mOsmol greater than the control value after glycerol infusion in this experiment. It is concluded from these findings that glycerol retracts free mobile water molecules from the edema fluid by osmotic pressure gradient.

Animals↗