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Biomedical subjects

A Nonaka

Publications and source records attributed to A Nonaka.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Premixing of 5% dextrose in Ringer's acetate solution with propofol reduces incidence and severity of pain on propofol injection].

The purpose of this study was to compare the effect of premixed 5% dextrose in Ringer's acetate solution and premixed lidocaine with propofpl on the reduction of pain during injection of propofol in adult patients. We conducted a prospective, randomized, double-blinded trial. Ninety-six patients were randomly allocated to one of three groups according to the agents added to 1% propofol 20 ml; Group C, normal saline 2 ml, Group L, 2% lidocaine 2 ml, and Group A, 5% dextrose in Ringer's acetate solution 2 ml. The pain on injection was rated as none, mild, moderate, or severe. Seventy percent of patients in the C group experienced pain, while 33% and 25% of patients experienced pain in the A group and the L group, respectively. Forty-two percent of patients in the C group complained moderate to severe pain but only one patient in both A group and L group. In conclusion, 5% dextrose in Ringer's acetate solution premixed with 200 mg propofol significantly reduces incidence and severity of pain associated with propofol injection and is easier to use than premixed lidocaine.

Adult↗
PubMed1999

In vivo evaluation of platelet-endothelial interactions in retinal microcirculation of rats.

PURPOSE: This study was designed to develop a new method to evaluate the dynamics of platelets in the retinal microcirculation in vivo and to investigate quantitatively the platelet-endothelial interactions in rat retina with the use of this system. METHODS: Isolated platelet samples were labeled with carboxyfluorescein diacetate succinimidyl ester. After intravenous administration, platelet behavior in the retinal microcirculation was evaluated with a scanning laser ophthalmoscope. The images were recorded on S-VHS videotape and analyzed with a computer-assisted image analysis system. The platelet- endothelial interactions in the retinal microcirculation were also investigated with the use of lipopolysaccharide-stimulated endothelium or platelets activated with thrombin. RESULTS: Fluorescent platelets were recognized as distinct dots in the retinal microcirculation and could be traced frame by frame. The velocity of platelets in the retinal arteries, capillaries, and veins was 26.1+/-6.4, 1.6+/-0.4, and 19.9+/-8.2 mm/sec, respectively. In control rats, even the activated platelets showed minimal interaction with retinal endothelial cells. In contrast, stimulated retinal endothelium showed active platelet- endothelial interactions; many platelets were observed rolling and adhering along the major retinal veins. The interactions between platelets and stimulated endothelial cells were substantially inhibited with the injection of P-selectin monoclonal antibody. CONCLUSIONS: The present study demonstrated a new method to visualize platelet behavior in the retinal microcirculation in vivo. This method will allow quantitative evaluation of platelet dynamics and platelet- endothelial interactions in retinal pathologic conditions.

Animals↗
PubMed1998

Effects of overexpression of the Na+-Ca2+ exchanger on [Ca2+]i transients in murine ventricular myocytes.

We measured [Ca2+]i and [Na+]i in isolated transgenic (TG) mouse myocytes overexpressing the Na+-Ca2+ exchanger and in wild-type (WT) myocytes. In TG myocytes, the peak systolic level and amplitude of electrically stimulated (ES) [Ca2+]i transients (0.25 Hz) were not significantly different from those in WT myocytes, but the time to peak [Ca2+]i was significantly prolonged. The decline of ES [Ca2+]i transients was significantly accelerated in TG myocytes. The decline of a long-duration (4-s) caffeine-induced [Ca2+]i transient was markedly faster in TG myocytes, and [Na+]i was identical in TG and WT myocytes, indicating that the overexpressed Na+-Ca2+ exchanger is functionally active. The decline of a short-duration (100-ms) caffeine-induced [Ca2+]i transient in 0 Na+/0 Ca2+ solution did not differ between the two groups, suggesting that the sarcoplasmic reticulum (SR) Ca2+-ATPase function is not altered by overexpression of the Na+-Ca2+ exchanger. There was no difference in L-type Ca2+ current density in WT and TG myocytes. However, the sensitivity of ES [Ca2+]i transients to nifedipine was reduced in TG myocytes. This maintenance of [Ca2+]i transients in nifedipine was inhibited by Ni2+ and required SR Ca2+ content, consistent with enhanced Ca2+ influx by reverse Na+-Ca2+ exchange, and the resulting Ca2+-induced Ca2+ release from SR. The rate of rise of [Ca2+]i transients in nifedipine in TG myocytes was much slower than when both the L-type Ca2+ current and the Na+-Ca2+ exchange current function together. In TG myocytes, action potential amplitude and action potential duration at 50% repolarization were reduced, and action potential duration at 90% repolarization was increased, relative to WT myocytes. These data suggest that under these conditions, overexpression of the Na+-Ca2+ exchanger in TG myocytes accelerates the decline of [Ca2+]i during relaxation, indicating enhanced forward Na+-Ca2+ exchanger function. Increased Ca2+ influx also appears to occur, consistent with enhanced reverse function. These findings provide support for the physiological importance of both these modes of Na+-Ca2+ exchange.

Action Potentials↗
PubMed1998

Abnormal myocyte Ca2+ homeostasis in rabbits with pacing-induced heart failure.

To determine whether there are abnormalities in myocyte excitation-contraction coupling and intracellular Ca2+ concentration ([Ca2+]i) homeostasis in pacing-induced heart failure (PF), we measured L-type Ca2+ current (ICa,L) and Na+/Ca2+ exchanger current (INa/Ca) with voltage clamp and measured intracellular Na+ concentration ([Na+]i) and [Ca2+]i with the use of sodium-binding benzofuran isophthalate (SBFI) and fluo 3 in ventricular myocytes isolated from control and paced rabbits. The peak systolic and diastolic levels and the amplitude of electrically stimulated [Ca2+]i transients (0.25 Hz, extracellular Ca2+ concentration = 1.08 mM) were significantly less in PF myocytes. Also, there was prolongation of the times to peak and decline of [Ca2+]i transients. ICa,L density was markedly decreased in PF myocytes. INa/Ca at -40 mV elicited by rapid exposure to 0 Na+ solution with a rapid solution switcher was significantly reduced in PF myocytes, suggesting that the function of the Na+/Ca2+ exchanger is impaired in these myocytes. In PF myocytes the decline of the [Ca2+]i transient when the Na+/Ca2+ exchanger was abruptly disabled was markedly prolonged compared with the decline in control myocytes, consistent with depressed sarcoplasmic reticulum (SR) Ca2+-ATPase function. RNase protection assay showed decreased levels of Na+/Ca2+ exchanger and SR Ca2+-ATPase mRNA in PF hearts, consistent with the function studies. We conclude that the functions of L-type Ca2+ channels, Na+/Ca2+ exchanger, and SR Ca2+-ATPase are impaired in myocytes from rabbit hearts with failure induced by rapid pacing. These abnormalities result in reduced [Ca2+]i transients and systolic and diastolic dysfunction and appear to account for the abnormal ventricular function observed.

Animals↗
PubMed1998

Influence of prior Na+ pump activity on pump and Na+/Ca2+ exchange currents in mouse ventricular myocytes.

We examined the dependence of peak Na+ pump and Na+/Ca2+ exchanger currents on prior Na+ pump inhibition induced by exposure to zero extracellular K+ in voltage-clamped adult murine ventricular myocytes. Abrupt activation of the Na+ pump by reexposure of myocytes to extracellular K+ with a rapid solution switcher resulted in the development of a transient peak current at approximately 500 ms, followed by a decline over 1-2 min to a steady-state level. The magnitudes of both the peak Na+ pump current (Ip) and the peak outward Na+/Ca2+ exchange current, activated by rapidly reducing extracellular Na+ to zero with the solution switcher, were dependent on previous Na+ pump activity. [Na+] gradients (Na+-binding benzofuran isophthalate fluorescence) between the patch pipette and the bulk cytosol were relatively small and could not account for the large differences between peak and steady-state Ip and reverse Na+/Ca2+ exchanger currents. Our results are consistent with the presence of a subsarcolemmal Na+ concentration gradient, which is similar for the Na+ pump and the Na+/Ca2+ exchanger. These findings also support the hypothesis that the Na+ pump and the Na+/Ca2+ exchanger are colocalized in the sarcolemma.

Animals↗
PubMed1998

Effect of clarithromycin on alpha1-acid glycoprotein levels in normal and diabetic rats.

The elevation of alpha1-acid glycoprotein (AGP) serum level, a member of the acute phase proteins (APP) synthesized by the liver, is induced during inflammation. In this study, we show that clarithromycin (CAM), a 14-membered macrolide antibiotic, causes an increase in the serum levels of AGP in a dose-dependent manner. AGP levels peak at 48h after a single administration with CAM In order to elucidate the mechanism of AGP induction by CAM, the effects of CAM, phenobarbital (PB), ethynylestradiol (EE2) and dexamethasone (DEX) treatments on APP fluctuation patterns were examined. In addition, modulation of the AGP induction by CAM, PB, EE2 and DEX in the diabetic state was examined. In contrast to treatment by PB, CAM treatment increased alpha2-macroglobulin levels to a much lesser extent than that observed during inflammation. On the other hand, albumin levels were unaffected by CAM treatment but decreased during inflammation. In addition, AGP induction by CAM, EE2 and DEX were attenuated in streptozotocin-induced diabetic rats, whereas the PB-induced increase in AGP levels was potentiated in diabetic rats. Thus, CAM and DEX treatments appear to induce similar fluctuations in APP levels. These results suggest that CAM increases AGP levels via a mechanism which may be different from PB and typical inflammatory pathways.

Animals↗
PubMed1997

The minimum alveolar concentration of sevoflurane in rats.

There are only limited data on sevoflurane minimum alveolar concentration (MAC) in rats. This study was designed to determine the minimum alveolar concentration value for sevoflurane in younger and older rats. Minimum alveolar concentration determination was performed in spontaneously breathing animals, 9-week-old rats (younger, n = 8) and more than 13-month-old rats (older, n = 8). Rats were instrumented with a silastic catheter in the abdominal aorta via the femoral artery to allow for arterial blood gas sampling. Subsequently, minimum alveolar concentration for sevoflurane was determined in 40 younger and 38 older rats. Minimum alveolar concentration for sevoflurane in younger rats was significantly higher than in the older rats (2.68 +/- 0.19 vs. 2.29 +/- 0.19, P < 0.001). Subgroup analysis indicated that minimum alveolar concentration for sevoflurane was not affected by the presence of an arterial catheter in the abdominal aorta (younger, 2.75 +/- 0.08 vs. 2.67 +/- 0.21; older, 2.23 +/- 0.19 vs. 2.30 +/- 0.18). Minimum alveolar concentration is profoundly affected by the age of the animal, but not by limited instrumentation.

Aging↗
PubMed1997

Mechanism of the negative inotropic effect of midazolam and diazepam in cultured foetal mouse cardiac myocytes.

We have investigated the effects of midazolam and diazepam on intracellular calcium (Ca2+) handling in foetal mouse ventricular myocytes using the Ca(2+)-sensitive fluorescent indicator, indo-1. We also investigated separately whether flumazenil or the L-type Ca2+ channel agonist, Bay K8644, antagonized these myocardial depressive effects. Midazolam and diazepam decreased the Ca2+ transient and beating rate in a concentration-dependent manner, and these decreases were prevented by Bay K8644. Flumazenil did not antagonize the myocardial depressive effects. In myocytes whose sarcoplasmic reticulum was inhibited by ryanodine, midazolam and diazepam had the same potent cardiodepressive effects. Midazolam and diazepam are direct cardiac depressants, which decrease the Ca2+ transient and beating rate, and the L-type Ca2+ channel is important in the negative inotropism and chronotropism caused by these drugs.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

A case of coronary artery spasm during spinal anesthesia.

We present a rare case of coronary artery spasm during spinal anesthesia in a patient who had neither complications nor prior history of coronary artery disease. Some factors are involved in the occurrence of perioperative coronary artery spasm. Many cases of coronary artery spasm during general anesthesia, or general plus epidural anesthesia, have been reported. Although spinal anesthesia by itself has not been reported to be a cause of coronary artery spasm, it is likely, in the current case, that the combination of the activated parasympathetic nerve system by the retraction of the peritoneum and spinal anesthesia might have caused the coronary artery spasm. Anesthesiologists need to be aware that coronary artery spasm may occur during spinal anesthesia, especially when the peritoneum is retracted.

Adult↗
PubMed1996

A rare case of severe acute pancreatitis complicated with pancreatic pseudocysts, obstructive jaundice and intraperitoneal hemorrhage.

A 58-year-old man visited our hospital because of back pain. Blood examinations revealed the presence of acute inflammation and an increase of pancreatic enzymes. Abdominal computed tomography indicated pseudocysts in the pancreas. The patient was diagnosed as having acute pancreatitis with pseudocysts formation. During the course of the disease, a newly formed pseudocyst in the pancreatic head compressed the common bile duct, leading to the obstructive jaundice. In addition, the rupture of a pseudocyst in the pancreatic tail caused intraperitoneal hemorrhage. This is an interesting case of acute pancreatitis with pseudocysts in which two rare complications developed.

Acute Disease↗
PubMed1996

[Effects of amrinon and prostaglandin E1 on intraoperative central and peripheral temperatures during peripheral arterial surgery].

Effects of amrinon (AM) and prostaglandin E1 (PG) on body temperatures during surgery under general anesthesia were studied. Thirty-nine elective peripheral arterial surgery patients were assigned to one of three groups. All groups received dopamine (DOA) 3 micrograms.kg-1.min-1 after intubation and ten patients receiving only DOA served as a control group. Fifteen patients who received AM 1 microgram.kg-1 followed by AM 5 micrograms.kg-1.min-1 were assigned as an AM group. Fourteen patients who received PG 0.02 micrograms.kg-1.min-1 were defined as a PG group. Rectal and fingertip temperatures were monitored continuously during surgery. Fingertip temperatures in both AM and PG groups were significantly higher than those in the control group 120 minutes after the administration of drugs. On the other hand, rectal temperatures in all groups did not differ significantly throughout the study. The rectum-fingertip temperature gradient was lower in both AM and PG group than in the control group. These results suggest that bolus injection of AM 1 microgram.kg-1 followed by AM 5 micrograms.kg-1.min-1 and PG 0.02 micrograms.kg-1.min-1 may be effective for maintaining central and peripheral temperatures during surgery under general anesthesia.

Aged↗
PubMed1995

Cardiac effects of methylmethacrylate in the rat heart-lung preparation with or without volatile anesthetics.

We have assessed the deleterious effects of methylmethacrylate (MMA) on cardiac function and metabolism in the isolated heart-lung preparation with or without volatile anesthetics. Wistar rats were prepared for the heart-lung model. They were randomly divided into 5 groups as follows. (1) Control (C) group. (2) Cement (M) group; they received MMA. (3) Halothane (H) group; they received MMA and 1% halothane. (4) Isoflurane (I) group; they received MMA and 1.5% isoflurane. (5) Sevoflurane (S) group; they received MMA and 2.5% sevoflurane. MMA 1000 micrograms/ml was administered 7 min after the start of perfusion except in the C group. At the end of the experimental period, the hearts were freeze-clamped and then myocardial high energy phosphates, lactate and glycogen were measured. Cardiac output in all groups but C group decreased significantly. PO2 of the perfusion blood in the M, H, I and S groups was significantly lower than that in the C group. Myocardial ATP in the M, H, I and S groups was significantly lower than that in the C group. ADP and AMP in the M, H, I and S groups were higher than those in the C group. There were no significant differences in lactate and glycogen levels between the 5 groups. MMA 1000 micrograms/ml is much higher than the blood level (0.05-31.89 micrograms/ml) which was reported in clinical patients who had femoral prosthesis. Therefore, the direct contribution of MMA itself to cardiac depression may be less than the other factors such as embolism in clinical situations. Volatile anesthetics did not influence the deleterious effects of MMA on cardiac function and metabolism.

Anesthetics↗
PubMed1995

[Anesthetic management of a neonate with primary cardiac rhabdomyoma].

We have experienced anesthetic management for cardiac rhabdomyoma in a 21-day-old male, whose pulmonary trunk was obstructed by the tumor. He was anesthetized with fentanyl 70 micrograms.kg-1 and oxygen. The operative and post-operative courses were uneventful. Cardiac tumor, especially cardiac rhabdomyoma, in infant is rare. Anesthesia for the resection of the cardiac tumor must be carried out carefully, because sudden death due to arrhythmias as well as cardiac or respiratory failure is the most dangerous complication.

Anesthesia↗
PubMed1994

Effects of artificial blood (FC-43 emulsion) on myocardial energy metabolism in the rat heart-lung preparation.

We have assessed the effects of artificial blood (FC-43 emulsion) on myocardial energy metabolism in the rat heart-lung preparation. Animals were allocated to four groups (n = 8 each group) according to the ratio of perfusion blood and FC-43 as follows: group 1 = control, perfusion blood only; group 2 = 50% FC-43; group 3 = 75% FC-43; and group 4 = 100% FC-43. Hearts were perfused initially to a cardiac output of 30 ml min-1 and mean arterial pressure of 50 mm Hg. Thirty minutes after perfusion, the hearts were freeze-dried for 6 days. Myocardial high energy phosphates (ATP, ADP and AMP) were measured by high pressure liquid chromatography. Myocardial lactate and glycogen concentrations were measured by enzymatic methods. There were almost no significant differences in cardiac output, systolic pressure, right atrial pressure and heart rate among the groups. Oxygen contents of the perfusate in all FC-43 groups were significantly lower than those in the control group. Myocardial ATP concentrations in rats receiving 50%, 75% and 100% FC-43 were significantly lower than those in the control group. In addition, myocardial ADP and AMP concentrations in rats receiving 75% and 100% FC-43 were significantly higher than those in the control group. Although there is adequate oxygen-carrying capacity in FC-43 to maintain cardiac function during perfusion, the energy levels in the hearts perfused with FC-43 were lower than those in normal hearts.

Adenosine Diphosphate↗
PubMed1994

Effects of inhalation anesthetics on myocardial and hepatic energy metabolism in normotensive and spontaneously hypertensive rats subjected to hemorrhage.

Forty spontaneously hypertensive rats (SHRs) and forty normotensive Wistar-ST rats (NRs) were used to assess the influence of anesthetics on myocardial and hepatic energy metabolism after hemorrhage. They were divided into five pairs of groups: a control group (pentobarbital 6 mg.100 g BW-1 ip), and four others which received 1.2% halothane, 2.2% enflurane, 1.4% isoflurane, and 3.3% sevoflurane, respectively. Following a 10 min stabilization period, blood (2 ml.100 g BW-1) was gradually withdrawn over a 5 min period from a femoral artery. Thirty min after the induction of hemorrhage, the heart and liver were removed and myocardial and hepatic metabolites (ATP, lactate, pyruvate and glycogen) were measured by enzymatic methods. There were no significant differences in myocardial metabolites among either the anesthetic groups or between SHRs and NRs. However, hepatic ATP levels in all SHR groups were significantly lower than those in NR groups. Moreover, ATP levels in the inhalation anesthetic groups of SHRs were significantly higher than that in the control group of SHRs. All inhalation anesthetics, especially isoflurane, may reduce metabolic deterioration of the liver during hemorrhage when compared to barbiturate anesthesia.

Adenosine Triphosphate↗
PubMed1994

Effects of intravenous anaesthetics on function and metabolism in the isolated rat heart-lung preparation.

The influence of several intravenous anaesthetics on the heart was assessed using the isolated rat heart-lung preparation. Each group received 10(-3)mol litre-1 and 10(-4)mol liter-1 of ketamine, 6 micrograms ml-1 and 60 micrograms ml-1 of midazolam, 6 micrograms ml-1 and 60 micrograms ml-1 of diazepam or 0.6 micrograms ml-1 and 6 micrograms ml-1 of flunitrazepam. Systolic blood pressure in rats receiving high doses of midazolam, diazepam and ketamine were higher than that in the control group. Heart rate in rats receiving high doses of ketamine and diazepam were lower than that in the control group. However, there were no significant changes in cardiac output among the groups. Maximum rate of left ventricular tension development in rats receiving high doses of midazolam and diazepam increased significantly in comparison with that in the control group. There were no significant changes in myocardial high energy phosphates among the groups. None of the intravenous anaesthetics, even in doses which were 100 times greater than therapeutic doses, showed any depressant effects in this preparation. Moreover, it is surprising that midazolam and diazepam produced direct increases in myocardial contractility. These results suggest that the cardiodepressant effects of intravenous anaesthetics may be due to their effects on the central nervous system.

Adenosine Diphosphate↗
PubMed1992

Evidence for a role of free radicals by synthesized scavenger, 2-octadecylascorbic acid, in cerulein-induced mouse acute pancreatitis.

To define the role of free radicals and of lipid peroxide involvement during the progress of cerulein-induced acute pancreatitis in mice, we evaluated the effect of a novel free radical scavenger, 2-octadecylascorbic acid (CV-3611), on pancreatic edema formation, and the levels of serum enzymes (amylase, lipase) and of lipid peroxide in pancreatic tissue. Mice were divided into three groups: control group, intraperitoneal injection of saline only; pancreatitis group, cerulein 50 micrograms/kg injected intraperitoneally six times at 1-hr intervals; treatment groups, CV-3611 10 mg/kg subcutaneously just after intraperitoneal cerulein injection. After the cerulein injection, the degree of pancreatic edema formation, serum amylase and lipase levels, and the amount of lipid peroxide in pancreatic tissue increased significantly during the observation period of 12 hr. Treatment with CV-3611 resulted in significant reduction in pancreatic edema formation at 3.5 hr (P less than 0.05) and 9 hr (P less than 0.05), serum amylase and lipase levels at 3.5 hr (P less than 0.05) and 12 hr (P less than 0.05), and lipid peroxide levels at 3.5 hr (P less than 0.05), 6 hr (P less than 0.05) and 12 hr (P less than 0.05). These results indicate that a novel free radical scavenger, CV-3611, has a strong therapeutic effect during the development of acute pancreatitis and suggest that oxygen-derived free radicals play an important role in the pathogenesis of acute pancreatitis.

Acute Disease↗