Search PubMed⌕ Search

Biomedical subjects

H Yao

Publications and source records attributed to H Yao.

At least 181 records · Page 10Linked to original sources
PubMed1991

Effect of blood glucose level in acute cerebral ischemia in spontaneously hypertensive rats--survival and brain pathology.

The present study was designed to examine the effect of blood glucose level on survival and pathologic changes of the cortical neuronal cells during and after three-hour incomplete cerebral ischemia, which was induced by bilateral carotid artery ligation in spontaneously hypertensive rats (SHRs). Blood glucose levels were varied by intraperitoneal infusion of 50% glucose (hyperglycemia) or insulin with hypertonic saline (hypoglycemia) or hypertonic saline (normoglycemia). None of the hyperglycemic or normoglycemic animals died during three-hour ischemia, whereas 45% of hypoglycemic animals died (p greater than 0.001). The survival rate for twenty-four hours after recirculation was in the following ascending order: hypoglycemia, normoglycemia, and hyperglycemia. Neither hypoglycemia nor hyperglycemia (38-392 mg/dL) in nonischemic animals developed any morphologic changes in the cerebral cortex. However, both the ischemic and recirculated brains showed various degrees of histologic changes such as shrinkage of the neuronal cells with cytoplasmic vacuoles, perineuronal edema, and swelling of neuropils. Such ischemic damage of the brain was more marked in hypoglycemic animals than in hyperglycemic or normoglycemic ones during ischemia, as well as one hour after recirculation. The results suggest that cerebral ischemia and its outcome become more deleterious in hypoglycemic than in normoglycemic and hyperglycemic states. On the other hand, hyperglycemia is not necessarily a disadvantage in acute cerebral ischemia with or without reperfusion in this model.

Animals↗
PubMed1991

[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis].

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.

Acidosis, Lactic↗
PubMed1990

Acute effects of antihypertensive agents on cerebral blood flow in hypertensive rats.

The acute effects of various antihypertensive agents on cerebral blood flow and mean arterial pressure (MAP) were studied in anesthetized (amobarbital 100 mg/kg) spontaneously hypertensive rats. Cerebral blood flow in the cortex and thalamus was measured by the hydrogen clearance method before and during a 60-min i.v. infusion of calcium antagonist (nifedipine), angiotensin converting enzyme inhibitor (captopril) or beta-blocker (propranolol). Nifedipine, 30 or 150 micrograms/kg per h, decreased dose dependently the MAP by 20 or 31%, and concomitantly increased cortical blood flow by 28 or 74%, and thalamic blood flow by 51 or 64%, respectively. Captopril, 10 or 100 mg/kg per h, decreased MAP by 7 or 14%, but changed cerebral blood flow minimally. In contrast, propranolol, 1.0 or 5.0 mg/kg per h, decreased MAP by 13 or 11%, with a concomitant reduction of cortical and thalamic blood flow by 20 or 15 and 33 or 37%, respectively. It is concluded that the changes in cerebral blood flow in response to hypotension are varied by antihypertensive drugs depending on the direct or indirect effect of the drugs (dilatation or constriction) on cerebral vessels. Nifedipine seems to dilate while propranolol constricts cerebral vessels.

Animals↗
PubMed1990

Ischemic flow threshold for striatal dopamine release in rats.

To determine the level of cerebral blood flow reduction which causes striatal dopamine release, extracellular dopamine and cerebral blood flow was simultaneously determined using in vivo brain dialysis and a hydrogen clearance method, respectively, in the striatum of spontaneously hypertensive rats before and during experimental cerebral ischemia. The ischemic flow threshold for neurotransmitter dopamine release was found to be 20% of the resting value or 8-10 ml/100g/min of cerebral blood flow, being similar to those for energy and membrane failures.

Animals↗
PubMed1990

Regional distribution of DNA and RNA in rat brain: a sensitive determination using high-performance liquid chromatography with electrochemical detection.

DNA and RNA contents in 20 brain regions or nuclei of the rat were determined by a highly sensitive method using high-performance liquid chromatography with electrochemical detection. The high DNA and RNA contents were found in the hypothalamic nuclei, especially the median eminence-arcuate nucleus. These results may be available for the preparation of nucleic acids as the regional control.

Amygdala↗
PubMed1990

Cerebral blood flow and oxygen metabolism in patients with vascular dementia of the Binswanger type.

We performed clinical and neuroradiologic studies, including positron emission tomography, in five patients with vascular dementia of the Binswanger type. The clinical features of these cases consisted of slowly progressive dementia, together with vascular risk factors such as hypertension and often a history of minor stroke, and characteristic white matter lesions on brain computed tomograms or magnetic resonance images. Digital subtraction angiography of the cervical and intracranial arteries demonstrated no occlusive lesion in any patient. Both cerebral blood flow and the cerebral metabolic rate for oxygen were markedly reduced in the white matter (54-77% of control values), and both were decreased in the parietal (73% of control), frontal (74-80%), and temporal (74-83%) cortices, where no abnormalities were detected by brain computed tomography or magnetic resonance imaging. We conclude that vascular dementia of the Binswanger type may be caused by disconnection between the cerebral cortex and subcortical structures due to ischemic damage in the white matter.

Aged↗
PubMed1990

Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits.

We used positron emission tomography to examine retrospectively the effects of blood pressure on regional cerebral blood flow and oxygen metabolism in seven normotensive and eight hypertensive patients with a history of transient neurologic deficits. In the hypertensive patients, a decrease in regional cerebral blood flow was closely related to blood pressure; these changes were most pronounced in the supratentorial structures, especially the striatum and thalamus. In contrast, the regional cerebral metabolic rate for oxygen was less related to blood pressure. Consequently, the regional oxygen extraction fraction was increased in the hypertensive patients, while regional cerebral blood volume and the regional cerebral blood flow volume ratio were unchanged. Multivariate regression analysis confirmed that hypertension was an independent factor affecting regional cerebral blood flow. The analysis also disclosed that age, sex, hematocrit, smoking, and PaCO2 affected regional cerebral blood flow. These findings suggest that the hemodynamic reserve in hypertensive individuals is reduced, which may predispose them to cerebral ischemia and perhaps stroke, even during small decreases in cerebral perfusion pressure.

Blood Pressure↗
PubMed1990

Hindbrain ischemia produced by bilateral vertebral artery occlusion and moderate hypotension in spontaneously hypertensive rats.

Hindbrain ischemia was induced by bilateral vertebral artery occlusion and moderate hypotension in spontaneously hypertensive rats (SHRs). Mean arterial blood pressure was lowered to 80 mmHg in SHRs and to 50 mmHg in Wistar-Kyoto rats (WKYs) by a controlled hemorrhage, and then the vertebral artery was bilaterally occluded through alar foramina of the first cervical vertebra. Following vertebral occlusion, blood flow of the cerebellum was significantly decreased to 9.4 +/- 2.0 mL/100g/min (+/- SEM) while flow of the cerebrum remained at 32.1 +/- 5.4 in SHRs. In contrast, cerebellar blood flow in WKYs was preserved at 24.2 +/- 2.9 mL/100g/min. Brain lactate, pyruvate, and adenosine triphosphate (ATP) were determined in SHRs after sixty minutes of hypotension with or without vertebral occlusion. Although infratentorial metabolites were actually unaltered in rats with hypotension alone, infratentorial lactate and lactate/pyruvate ratio significantly increased to 14.38 +/- 3.61 mmol/kg and 67.7 +/- 12.1, respectively, with a concomitant decrease in ATP in SHRs with hypotension and vertebral occlusion. Bilateral vertebral artery occlusion, together with moderate hypotension, was shown to produce a marked reduction of cerebellar blood flow and to induce ischemic metabolic changes in the infratentorial brain in SHRs.

Animals↗
PubMed1990

Striatal glutamic acid and gamma-aminobutyric acid in transient cerebral ischemia in spontaneously hypertensive rats.

A massive striatal dopamine release (241-fold increase) was observed in a previous study during acute cerebral ischemia in rats. In this study, extracellular levels of glutamic acid (GLU), gamma-aminobutyric acid (GABA) and lactic acid were simultaneously determined using in vivo brain dialysis in the striatum of spontaneously hypertensive rats during cerebral ischemia and after recirculation. Extracellular GABA levels increased to 932 +/- 75% (mean +/- SEM) of the resting level and GLU increased to 390 +/- 63% during 20 min ischemia. Although ischemia-induced release of GLU and GABA was demonstrated in this study, the degree of increase was smaller than that of dopamine. These findings may be relevant to the pathophysiology of cerebral ischemia in the striatum.

Animals↗
PubMed1990

[Monoamine contents and norepinephrine turnover in brain stem nuclei of young and adult spontaneously hypertensive and Wistar-Kyoto rats].

To investigate the brain stem monoamine mechanism in the development and maintenance of hypertension of spontaneously hypertensive rats (SHR), we determined monoamine contents and norepinephrine turnover in discrete brain stem nuclei which are known to relate with cardiovascular control. Specific areas and brain stem nuclei were dissected from serial frozen slices of 300 microns thickness according to the atlas of Palkovits and Jacobowitz. The dissected tissues were homogenized, centrifuged and the supernatants were injected into high performance liquid chromatography with electrochemical detection (HPLC-ECD). Norepinephrine (NE), dopamine (DA), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) contents were determined. NE turnover was also determined 2 hour after alpha-methyl-p-tyrosine administration (250 mg/kg, i.p.). In 4-week old SHR, the only significant change observed was decreased NE contents in the nucleus tractus solitarii (NTS). Such decreases in NE contents of the NTS were also found in 8- and 16-week old SHR. However, there were no differences in NE turnover in the NTS between SHR and WKY. Increased NE contents were found in the A1, A5, and nucleus reticularis gigantocellularis (RG) in the later stages (8 and 16 weeks) in SHR. Furthermore, increased NE turnover was seen in the RG of SHR at 16-week old, indicating increased neuronal activity. Dopamine, 5-HT and 5-HIAA showed no consistent changes between SHR and WKY. Increased NE levels were observed in later stages after development of hypertension, suggesting the increased NE in adult SHR may represent a central adaptive change secondary to the established hypertension. Since increased NE levels were consistently found in or around the regions which are known as vasomotor centers, we assume that these increased NE might serve to maintain hypertension or to inhibit a further increase in blood pressure. In contrast, the NE contents were decreased with constant turnover in NTS of SHR aged 4, 8, and 16 weeks. Constant turnover in NE could not compensate for reduced NE in NTS and may lead to a functional reduction or reduced noradrenergic activity. This defect in intrinsic noradrenergic neurons in NTS may trigger the development of genetic hypertension in SHR. In conclusion, the present results demonstrate that NE levels of SHR in the NTS were consistently decreased compared with those of WKY in all age groups. In later stages, increased NE levels were observed in A1, A5 and RG of SHR. These results indicate that brain stem monoamine system, especially noradrenergic neurons, contributes to the development and maintenance of hypertension in SHR.

Aging↗
PubMed1989

Effect of thromboxane synthetase inhibitor on cerebral circulation and metabolism during experimental cerebral ischemia in spontaneously hypertensive rats.

The protective effect of thromboxane synthetase inhibitor, OKY-046, on brain ischemia was studied in spontaneously hypertensive rats. Cerebral ischemia was developed by bilateral carotid artery ligation (BCL) for 1 or 3 h and thereafter, circulation was restored for 15 min. OKY-046, 5 or 30 mg/kg, or saline as control was administered i.v. before BCL. Neither blood pressure nor blood gases were altered by OKY-046 or saline injection. During BCL, cerebral cortical blood flow was reduced to 25 and 15% of the resting value at 30 and 60 min, respectively, and these changes were not different among the groups. In rats with ischemia longer than 1 h, the blood flow was well preserved by OKY-046, 30 mg/kg, to 10-17% of the resting level, thus significantly higher than that (less than 5%) in non-treated rats. After 15 min recirculation, the supratentorial lactate level was lower and adenosine triphosphate (ATP) was higher in OKY-046-treated rats than in the saline-treated ischemic rats. Plasma thromboxane B2 was increased markedly in 1 h ischemic-reperfused rats without treatment and the increase was almost completely inhibited by OKY-046. In contrast, 6-keto-prostaglandin F1 alpha was increased 8.5-fold after ischemia and the increase was not affected by the treatment. OKY-046 seems to have an antiischemic effect on acutely induced cerebral ischemia. Selective inhibition of thromboxane A2 production and an inversely high level of prostaglandin I2 may be an important contribution to protection of the microcirculation during ischemia and preservation of ischemic cerebral metabolism.

Adenosine Triphosphate↗
PubMed1989

Involvement of brain stem noradrenergic neurons in the development of hypertension in spontaneously hypertensive rats.

This study attempted to investigate the possible involvement of the brain stem noradrenergic system in the development of hypertension in spontaneously hypertensive rats. Steady-state norepinephrine, dopamine, serotonin and 5-hydroxyindoleacetic acid concentrations and norepinephrine turnover were determined in the individual brain stem nuclei using high performance liquid chromatography with electrochemical detection. Decreased norepinephrine contents in the nucleus tractus solitarii in spontaneously hypertensive rats compared with Wistar-Kyoto rats at the age of 4, 8, and 16 weeks were demonstrated. In later stages (8 and 16 weeks), increased norepinephrine levels were observed in the nucleus reticularis gigantocellularis, the A1 and A5 areas. Norepinephrine turnover was not different between spontaneously hypertensive rats and Wistar-Kyoto rats in the nucleus tractus solitarii at the age of 4 and 16 weeks and increased in the nucleus reticularis gigantocellularis of spontaneously hypertensive rats at 16 weeks. Our results indicate that altered norepinephrine metabolism in the specific brain stem nuclei, especially the consistently decreased norepinephrine in the nucleus tractus solitarii of spontaneously hypertensive rats, contribute to the development of genetic hypertension.

Adrenergic Fibers↗
PubMed1989

Cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma.

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.

Brain Damage, Chronic↗
PubMed1989

Cerebral ischemia in spontaneously hypertensive rats with type 2 (noninsulin-dependent) diabetes mellitus, cerebral blood flow and tissue metabolism.

The present study was designed to examine the effect of chronic type 2 (noninsulin-dependent) diabetes mellitus on cerebral blood flow and metabolism during cerebral ischemia induced by bilateral carotid artery occlusion in spontaneously hypertensive rats. Diabetes was produced by streptozotocin treatment in 2-day neonates and the experiment was performed at the age of 5 months. The level of mean arterial pressure was not different between diabetic and nondiabetic rats. At 1 h after ischemia, cerebral blood flow was decreased to 1% of the resting value and supratentorial lactate was increased by 8-fold of control, being virtually the same in both groups of rats. In contrast, reduction of cerebral ATP was much less in diabetic rats (1.64 +/- 0.15 mmol/kg) than in nondiabetic rats (0.74 +/- 0.07 mmol/kg) (p less than 0.001); ATP in nonischemic control is 2.80-2.85 mmol/kg. These results could not be explained by the difference in cerebral blood flow between the groups during ischemia. The results suggest that chronic mild hyperglycemia exerts rather a protective effect on the brain against ischemic insult. Effective utilization of metabolites, such as glucose and ketone bodies, may play an important role to minimize metabolic derangements in the ischemic brain in type 2 diabetic-hyperglycemic rats.

Adenosine Triphosphate↗
PubMed1989

[A case of coexisting descending thoracic aortic aneurysm and atypical aortic coarctation treated successfully by surgery using the thromboexclusion method].

The thromboexclusion method was successfully applied to a 43-year-old male with aortitis syndrome. Preoperative aortogram showed a fusiform aneurysm of the descending aorta just below the left subclavian artery and atypical coarctation of the descending aorta distal to this aneurysm. Pressure gradient across the stenosis was about 70 mmHg. The technique of flow reversal and thromboexclusion was performed in this patient because of severe calcification in the aortic arch and the entire descending aorta. A long extra-anatomical bypass between the ascending aorta and the infrarenal abdominal aorta was made, and a permanent aortic clamp was placed across the aorta at the left subclavian artery. Hypertension in the arm disappeared immediately after the operation, and postoperative catheterization revealed no pressure gradient between the ascending and the abdominal aorta. Computed tomogram performed 18 days after the operation and aortogram done 44 days postoperatively disclosed thrombi formation in the aneurysm.

Adult↗
PubMed1989

[A case of 72-year-old female with congenital esophago-bronchial fistula].

A 72-year-old female with congenital esophago-bronchial fistula is reported. She had complained of cough attack during meals and repeated pneumonia since childhood. A chest x-ray film showed chronic bronchitis in the right lower lung field. Esophagogram revealed a fistula between the esophagus and the right lower lobe bronchus. Resection of the right lower lobe and removal of the fistulous tract were successfully performed. Histological examination of the resected fistula with slight inflammatory change showed muscle layer and transitional zone between the stratified squamous epithelium of esophagus and the ciliated columnar epithelium of bronchus. This is the oldest case in the Japanese literature.

Age Factors↗
PubMed1989

[A case of a two-chambered right ventricle associated with aneurysm of the sinus of Valsalva].

A 51-year-old male with a two-chambered right ventricle associated with an aneurysm of sinus of Valsalva, who underwent successful surgical repair without ventriculotomy, is reported. Preoperative right ventriculogram revealed that the right ventricle was divided by the anomalous muscle bundle, and the aneurysm of sinus of Valsalva growing from the right coronary sinus protruded just below the pulmonary valve. The right ventricular pressure was 107/10 mmHg and the pressure gradient between the right ventricle and the pulmonary artery was 88 mmHg. Trans-pulmonary arterial resection of the aneurysm of Valsalva sinus was performed and the anomalous muscle bundle was successfully removed through the pulmonary arteriotomy and the right atrial incision. Post-operative right ventricular pressure dropped to 42 mmHg, and there was no stenosis in the right ventricle.

Aortic Aneurysm↗