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Biomedical subjects

A Iguchi

Publications and source records attributed to A Iguchi.

At least 235 records · Page 13Linked to original sources
PubMed1990

[In vivo insulin sensitivity in adrenodemedullated rats].

Insulin sensitivity and responsiveness were determined in adrenal demedullated rats (ADMX) with euglycemic insulin clamp technique. Adrenal medulla was extirpated bilaterally a week before the study. Catheters were placed at right atrium via right jugular vein for sampling blood and at inferior vena cava via femoral vein for the infusion of insulin and glucose solution. Insulin was infused at rates of 4.4, 8.8, 14.7, 29.3, 88.0, 293.0 mU/kg/min. Blood was collected every five min. during the clamp and glucose infusion rate was modulated to control the blood glucose concentrations at fasting levels. Glucose metabolism was calculated from the amount of glucose infused from 60th to 120th min. during the euglycemic clamp. The results obtained were as follows: 1. Glucose metabolisms of ADMX in each infusion rate of insulin, 4.4, 8.8, 14.7, 29.3, 88.0, 293.0 mU/kg/min were 5.2 +/- 0.5, 12.5 +/- 0.5, 17.6 +/- 1.2, 19.8 +/- 2.3, 29.0 +/- 1.5, and 25.2 +/- 1.9 mg/kg/min, respectively. 2. Glucose metabolisms of control group in each dose were 6.6 +/- 0.4, 9.0 +/- 0.9, 18.5 +/- 1.2, 23.4 +/- 2.4, 24.6 +/- 1.1, and 27.0 +/- 1.3 mg/kg/min, respectively. 3. Significant difference (p less than 0.01) in glucose metabolism between ADMX and control was observed at the insulin infusion rate of 8.8 mU/kg/min which might be equivalent to physiological hyperinsulinemia. 4. There were not any differences in insulin responsiveness between both groups. These results suggest that epinephrine regulates insulin sensitivity under physiological hyperinsulinemic condition via defects of insulin receptors.

Adrenal Medulla↗
PubMed1990

Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats.

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.

Adrenergic Fibers↗
PubMed1990

[Peritoneal dialysis in neonates and infants after open heart surgery].

Peritoneal dialysis was required in 20 (12.8%) of 156 neonates and infants for acute renal failure following open heart surgery using cardiopulmonary bypass. Cardiac diagnosis was TAPVD (7 cases), PA with IVS (2), ECD (2), coarctation of the aorta with VSD (2) and other cardiac malformations (7). The indication for dialysis was oliguria of less than 1.0 ml/kg over 4 hours resistant to volume repletion, inotropic agent and diuretics. Peritoneal dialysis was performed using dialysis catheter and glucose containing dialysis solutions. The mean predialysis BUN and serum creatinine were 30.4 mg/dl and 2.7 mg/dl respectively. The highest serum creatinine during dialysis was 4.5 mg/dl, and all but one patient had BUN level of under 100 mg/dl. Dialysis with glucose containing solution could allow sufficient fluid removal as a result, fluid overload was restored. Plasma protein and electrolytes balance were corrected within 48 hours. Two neonates and 4 infants survived. Thirteen patients died on dialysis: nine of those deaths were related to low cardiac output, 2 death were attributable to respiratory insufficiency, and 2 cases died due to sepsis. One infant died of an unexplained cardiac arrhythmia after renal failure had been improved. It is concluded that peritoneal dialysis is beneficial in neonates and infants who become oliguria following open heart surgery.

Acute Kidney Injury↗
PubMed1990

[A case of right ventricular failure after CABG successfully supported by right heart bypass with a centrifugal pump].

A 67-year-old woman underwent CABG because of severe triple vessel disease. She could not wean from CPB in spite of full inotropic drugs and IABP support due to right ventricular failure probably caused by the perioperative right ventricular infarction. Right heart bypass (RHB) with a centrifugal pump was used. Finally she could wean from CPB and took an uneventful postoperative course except mediastinitis. During 5 days of RHB operation ACT was maintained between 180s and 200s by systemic heparinization. RHB with a centrifugal pump is a reliable method to assist a failing right ventricle.

Aged↗
PubMed1990

[A case of massive hemoglobinuria due to patch dehiscence--following patch closure of ventricular septal defect].

A three-month-old baby with persistent intravascular hemolytic anemia following patch closure of subpulmonic ventricular septal defect was reported. Mechanical hemolysis was diagnosed by the presence of blood cell fragments and schistocytes in peripheral blood smear. It was thought that destruction of red cells developed by turbulent flows and direct contact of red blood cells with bared rough surfaces of the teflon patch at the site of dehiscence. When the cause of severe hemolysis was attributed to inadequate intracardiac repairs, immediate second surgical intervention should be performed.

Female↗
PubMed1989

Vagally mediated insulin secretion by stimulation of brain cholinergic neurons with neostigmine in bilateral adrenalectomized rats.

This study investigated the relationship between central cholinergic neurons and insulin secretion in bilateral adrenalectomized fed rats. Neostigmine (a cholinesterase inhibitor, 5 x 10(-8) mol) administered into the third cerebral ventricle produced significant increases in hepatic venous plasma insulin and glucose concentrations, whereas i.v. injection of the same dose of neostigmine did not. Prior acute subdiaphragmatic vagotomy or i.p. pre-injection with methylatropine (10(-8) mol) completely prevented the neostigmine-induced rise in plasma insulin concentration. Intraperitoneal pretreatment with hexamethonium (5 x 10(-8) mol) also significantly reduced the plasma insulin response. These peripheral pretreatments did not change the plasma glucose response to neostigmine. Intraventricular co-administration of 10(-9) mol methylatropine, a dose that was ineffective when pre-injected i.p., eliminated the plasma insulin and glucose responses to neostigmine, whereas hexamethonium (5 x 10(-8) mol) had no influence on either response to neostigmine. These observations suggest that stimulation of central cholinergic-muscarinic neurons with third cerebral ventricular injection of neostigmine results in vagally mediated insulin secretion in bilateral adrenalectomized fed rats.

Adrenalectomy↗
PubMed1989

A rare case of recurrent vasodepressive attacks of 2-hours duration: analysis of the mechanism by muscle sympathetic nerve activity recording.

Muscle sympathetic nerve activity was recorded in a 57-year-old male patient suffering from severe hypotensive attacks with bradycardia for 10 years. Continuous blood pressure recording demonstrated frequent drastic falls in pressure. Disappearance and reappearance of muscle sympathetic nerve activity coincided with the onset and termination of attacks. Awakening from sleep or emotional and/or cardiovascular stress seems to trigger hypotension. Cardiac pacemaker was not useful in limiting the attack, because right ventricular pacing caused abrupt falls in both blood pressure and heart rate.

Bradycardia↗
PubMed1989

Central nervous system control of glycogenolysis and gluconeogenesis in fed and fasted rat liver.

The influence of brain cholinergic activation on hepatic glycogenolysis and gluconeogenesis was studied in fed and 48-hour fasted rats. Neostigmine was injected into the third cerebral ventricle and hepatic venous plasma glucose, glucagon, insulin, and epinephrine were measured. The activity of hepatic phosphorylase-a and phosphoenolpyruvate-carboxykinase (PEP-CK) was also measured. Experimental groups: 1, intact rats; 2, rats infused with somatostatin through the femoral vein; 3, bilateral adrenodemedullated (ADMX) rats; 4, somatostatin infused ADMX rats; 5, 5-methoxyindole-2-carboxylic acid (MICA) was injected intraperitoneally 30 minutes before injection of neostigmine into the third cerebral ventricle of intact rats. MICA treatment completely suppressed the increase in hepatic glucose in fasted rats, but had no effect in fed rats. Phosphorylase-a activity was not changed in fasted rats, but increased in fed rats, intact rats, somatostatin-infused rats, somatostatin-infused ADMX rats, and ADMX rats in that order. PEP-CK was not changed in fed rats, but increased at 60 and 120 minutes after neostigmine injection into the third cerebral ventricle in fasted rats. We conclude that, in fed states, brain cholinergic activation causes glycogenolysis by epinephrine, glucagon, and direct neural innervation. In fasted states, on the other hand, gluconeogenesis is dependent on epinephrine alone to increase hepatic glucose output.

Adrenal Medulla↗
PubMed1989

The relative importance of nervous system and hormones to the 2-deoxy-D-glucose-induced hyperglycemia in fed rats.

We examined the relative contributions of hormones and nervous system to the total 2-deoxy-D-glucose (2-DG)-induced central nervous system-mediated hyperglycemia. 2-DG was injected into the third cerebral ventricle in the following four groups of rats, and hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were measured: 1) intact rats; 2) intact rats receiving somatostatin with insulin infusion through the femoral vein to inhibit glucagon secretion and maintain the basal insulin level; 3) bilateral adrenalectomized (ADX) rats to prevent epinephrine secretion; and 4) ADX rats receiving somatostatin with insulin infusion. Comparing areas under glucose curves among the intact rats, those receiving somatostatin with insulin infusion, ADX rats, and ADX rats receiving somatostatin with insulin infusion, the area under the glucose curve was intact rats greater than intact rats receiving somatostatin with insulin infusion greater than ADX rats receiving somatostatin with insulin infusion greater than ADX rats. These results suggest that there are three distinct sympathetic nervous system responses to 2-DG-induced central nervous system-mediated hyperglycemia. 2-DG-induced hyperglycemia is not dependent on only one of those three systems, it is dependent on all of them. The relative potency of the factors to 2-DG-induced hyperglycemia increases in the following order: direct neural innervation of liver (including suppressive epinephrine action on insulin secretion), glucagon, and direct epinephrine action on liver.

Adrenalectomy↗
PubMed1989

Involvement of the hippocampus in central nervous system-mediated glucoregulation in rats.

To find out whether the hippocampus is involved in central nervous system-mediated glucoregulation, we injected saline, neostigmine, dopamine, norepinephrine, bombesin, beta-endorphin, somatostatin, and prostaglandin F2 alpha into the dorsal hippocampus in anesthetized fed rats. After injection of dopamine, norepinephrine, bombesin, beta-endorphin, somatostatin, or prostaglandin F2 alpha, the level of hepatic venous plasma glucose did not differ from that in saline-treated control rats. However, neostigmine, an inhibitor of acetylcholine esterase, caused a dose-dependent increase in the hepatic venous plasma glucose concentration. This neostigmine-induced hyperglycemia was dose-dependently suppressed by coadministration of atropine, but not by hexamethonium. Injection of neostigmine (5 X 10(-8) mol) resulted in an increase not only in glucose but also in glucagon, epinephrine, and norepinephrine in hepatic venous plasma. In bilateral adrenalectomized rats, neostigmine-induced hyperglycemia was suppressed, but the hepatic venous plasma glucose concentration still increased significantly. These results indicate that the hippocampus is involved in central nervous system-mediated glucoregulation through cholinergic muscarinic activation, partly via epinephrine secretion.

Adrenalectomy↗
PubMed1989

Central nervous system-mediated glucagon secretion is enhanced by alpha 2-adrenoreceptor activation.

We assessed the response of the adrenergic receptor in pancreatic glucagon secretion to central nervous system stimulation. Injection of neostigmine (5 x 10(-8) mol) into the third cerebral ventricle in intact rats resulted in increased epinephrine and norepinephrine secretion associated with glucagon secretion. This glucagon secretion was still observed in bilateral adrenalectomized (ADX) rats, although its concentration was significantly lower than that in the intact rats. This glucagon rise was significantly inhibited by ip treatment of ganglionic blocker with hexamethonium. Intraperitoneal injection of alpha-adrenergic receptor antagonist phentolamine (5 x 10(-7) mol), but not of beta-adrenergic receptor antagonist propranolol (1 x 10(-6) mol), reduced the hyperglucagonemic effect of a subsequent neostigmine injection in intact and ADX rats, although these antagonists did not influence epinephrine or norepinephrine secretion in intact rats. In addition, ip injection of the selective alpha 2-receptor antagonist yohimbine (5 x 10(-7) mol), but not of the selective alpha 1-receptor antagonist prazosin (1 x 10(-6) mol), inhibited the neostigmine-induced glucagon secretion in intact and ADX rats. From this evidence it is suggested that central nervous system-mediated glucagon release is enhanced by alpha 2-adrenoreceptor stimulation by either catecholamines or the autonomic nervous system.

Adrenalectomy↗
PubMed1989

[Pseudolymphoma of the bladder: a case report].

We report a 63 year-old female with solid, nonpapillary, and smooth-surfaced bladder tumescence of approximately 30 and 7 mm in diameter. Biopsy of the tumor and other apparently normal epithelium revealed dense lymphocytic infiltrations with formation of many lymph follicles. Because of the relatively large nodular form of the lesion we regarded this to be pseudolymphoma of the bladder rather than follicular cystitis. Pseudolymphoma in the bladder has not yet been reported in English literatures to our knowledge. The tumorous changes have disappeared by 6 months after the initial 3 week chemotherapy.

Biopsy↗
PubMed1989

[Experimental study of materials used for intra-atrial baffle for the Mustard operation].

An experimental model was developed to study the fate of prosthetic materials used for the construction of an intra-atrial baffle for the Mustard operation. Total atrial septa were replaced in sixteen puppies with autologous pericardium (n = 3), glutaraldehyde-preserved canine pericardium (n = 4), glutaraldehyde-preserved porcine pericardium (n = 3), EPTFE reinforced sheet (Gore-Tex sheet, n = 3) and EPTFE reinforced cardiovascular patch (Gore-Tex patch, n = 3). Septal replacement was performed under total circulatory arrest and surface induced deep hypothermia. All animals were sacrificed six months after the septal replacement. Pathological examination revealed that all septal grafts were well healed, completely covered by neoendothelium and had contracted to approximately 60% of their original size. There were no significant difference between groups. Histologic examination showed the good tissue adaptation of autologous pericardium and Gore-Tex patch materials. The thinnest layers of neoendothelium covered autologous pericardial baffle. Glutaraldehyde-preserved pericardium and Gore-Tex sheet did not adapt well to host atrial tissue. These materials were easily detached from their neoendothelial substrates. It was concluded that the autologous pericardium as well as a Gore-Tex patch may be superior to other prosthetic materials used for the construction of an intra-atrial baffle for the correction of transposition of the great arteries.

Animals↗
PubMed1989

[Surgical treatment of tricuspid regurgitation].

The purpose of this study is to compare early and late results of tricuspid valve replacement (TVR), tricuspid annuloplasty (TAP) and non operative management for patients with tricuspid regurgitation (TR). 5 patients underwent TVR and 70 patients received TAP (Kay-Boyd's annuloplasty in 16, Bex reducer method in 40, Carpentier's ring method in 14). 21 patients were managed non-operatively. The following results were obtained. TR should be repaired aggressively, if the regurgitation was more than second degree and tricuspid annulus was above three finger breadth. Judging from the pattern of residual TR after Kay-Boyd's annuloplasty and Bex reducer method, Bex reducer and Carpentier's ring should be placed over the three commissures except the conduction tract.

Heart Valve Prosthesis↗
PubMed1988

Relative contributions of the nervous system and hormones to CNS-mediated hyperglycemia.

We quantitatively determined the relative contributions of hormonal factors and the nervous system to the total glucose response after stimulation of the cholinergic neurons in the central nervous system of fed rats. Hepatic venous plasma glucose, glucagon, insulin, epinephrine, and norepinephrine were measured during 120 min after injection of neostigmine (5 X 10(-8) mol) into the third cerebral ventricle in rats subjected to bilateral adrenodemedullation (ADMX) to prevent epinephrine secretion (observed insulin secretion), with and without intravenous infusion of somatostatin to prevent glucagon and insulin secretion. Injection of neostigmine in intact rats resulted in increases in glucose, glucagon, epinephrine, and norepinephrine. Comparison of glucose areas suggests that 22% of the hyperglycemic response is due to the glucagon effect, that 29% is due to the epinephrine effect, and that an unknown factor other than epinephrine or glucagon, which may include activation through direct neural innervation of the liver via alpha-adrenergic receptor, contributes 49%. The suppressive effect of epinephrine on insulin secretion, which is potentially stimulated by direct neural activation of the pancreas, contributes 18% of the net hyperglycemia.

Adrenal Medulla↗
PubMed1988

The roles of glucagon and adrenal epinephrine in mediating hyperglycemia induced by third cerebroventricular injection of bombesin.

The roles of glucagon and adrenal epinephrine in mediating bombesin-induced central hyperglycemia were further studied in anesthetized rats. Bombesin (10(-9) mol) injected into the third cerebral ventricle produced an increase in plasma concentrations of glucose, glucagon, and epinephrine. Prior bilateral adrenalectomy completely prevented the hyperglucagonemic and hyperglycemic responses to third cerebral ventricle injection of bombesin. These results support the view that bombesin-induced increases in plasma glucose and glucagon are fully dependent on adrenal epinephrine secretion. Furthermore, during constant intravenous infusion of somatostatin, the hyperglycemic response to third cerebral ventricle injection of bombesin was not significantly influenced despite complete inhibition of the increase in plasma glucagon. Therefore, it is suggested that bombesin-induced central hyperglycemia is mainly mediated by epinephrine itself rather than via epinephrine-stimulated glucagon secretion.

Animals↗
PubMed1988

Central versus peripheral effect of clonidine on hepatic venous plasma glucose concentrations in fasted rats.

To evaluate whether clonidine exerts its action within the central nervous system or outside the central nervous system to induce hyperglycemia, we compared the effects of clonidine injected into the third cerebral ventricle or intravenously on hepatic venous plasma glucose concentrations in fasted rats. Clonidine administration produced a dose-dependent hyperglycemia in each case. At all tested doses (5, 50, and 100 nmol) the hyperglycemic responses to clonidine injected intravenously were not significantly different from those to clonidine injected into the third cerebral ventricle. Intraperitoneal pretreatment with yohimbine (50 nmol) or phentolamine (50 nmol), both alpha-adrenergic antagonists, reduced the hyperglycemic response to clonidine (100 nmol) given intravenously, but these antagonists preinjected into the third cerebral ventricle did not reduce the response. Moreover, no significant differences in venous plasma clonidine concentrations were observed when intravenous and third cerebral ventricle injections of clonidine (100 nmol) were compared. These results suggest that clonidine-induced hyperglycemia is mainly mediated by the peripheral mechanism rather than through the central mechanism. To gain an insight into the peripheral mechanism for the hyperglycemic action of clonidine, we measured the plasma immunoreactive glucagon and insulin concentrations after intravenous clonidine (100 nmol). We found that plasma immunoreactive glucagon concentrations significantly increased, whereas plasma immunoreactive insulin concentrations did not change significantly despite hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗