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Biomedical subjects

H Abe

Publications and source records attributed to H Abe.

At least 721 records · Page 40Linked to original sources
PubMed1994

Negative regulation of hypothalamic growth hormone-releasing factor messenger ribonucleic acid by growth hormone and insulin-like growth factor I.

Increased growth hormone-releasing factor messenger ribonucleic acid (GRF mRNA) and decreased somatostatin (SRIF) mRNA levels have been reported in the hypothalamus of hypophysectomized rats as well as of dwarf mice. In order to elucidate the effect of the growth hormone-insulin-like growth factor I (GH-IGF-I) axis on hypothalamic GRF and SRIF synthesis, we measured levels of mRNA coding for GRF and SRIF and for pituitary GH in pubertal male rats treated for 3 weeks with antirat GRF gamma-globulin (GRF-ab), anti-SRIF gamma-globulin (SRIF-ab) or both. Immunoneutralization of circulating endogenous GRF resulted in a marked decrease in serum IGF-I and pituitary GH mRNA levels in Northern blot analysis, whereas it caused a significant increase in GRF mRNA levels in the arcuate nucleus as assessed by both Northern blot and in situ hybridization analysis. SRIF mRNA levels in the periventricular nucleus were slightly decreased by GRF-ab treatment when analyzed by in situ hybridization, but not significantly after Northern blot analysis. Immunoneutralization of circulating endogenous SRIF failed to affect mRNA levels of hypothalamic GRF and SRIF but caused a slight reduction in pituitary GH mRNA levels. Levels of mRNA coding for hypothalamic GRF and pituitary GH were also measured by Northern blot analysis in young male rats treated with rat GRF-ab for 2 weeks and replaced with rat GH or IGF-I for the second 1 week. Replacement with either rat GH or IGF-I suppressed the increased hypothalamic GRF mRNA levels. These data indicate that endogenous GRF is essential for normal synthesis of pituitary GH and that both GH and IGF-I negatively regulate the synthesis of hypothalamic GRF.

Animals↗
PubMed1994

Molecular genetics of growth hormone-releasing factors.

To elucidate the effects of GRF on GH synthesis and of the GH-IGF-I axis on hypothalamic GRF synthesis, we measured the mRNA levels of hypothalamic GRF and pituitary GH in pubertal male rats treated for 3 weeks with antirat GRF gamma-globulin (GRF-ab), antisomatostatin gamma-globulin (SRIF-ab) or both. Immunoneutralization of circulating endogenous GRF resulted in a marked decrease in serum IGF-I and pituitary GH mRNA levels in Northern blot analysis, whereas it significantly increased GRF mRNA levels in the arcuate nucleus in both Northern blot and in situ hybridization analysis. Immunoneutralization of circulating endogenous SRIF failed to affect GRF mRNA levels but caused a slight reduction in pituitary GH mRNA. Then, we examined the effect of systemic replacement with rat GH or IGF-I for 1 week on GRF mRNA levels in the hypothalamus of rats treated with GRF-ab for 2 weeks. Replacement with either rat GH or IGF-I significantly suppressed the increased hypothalamic GRF mRNA levels. These data indicate that endogenous GRF is essential in normal synthesis of pituitary GH and that both GH and IGF-I negatively regulate the synthesis of hypothalamic GRF.

Amino Acid Sequence↗
PubMed1994

Biphasic effects of repeated alcohol intake on 24-hour blood pressure in hypertensive patients.

BACKGROUND: The association between alcohol and blood pressure (BP) may be related to the temporal sequencing of alcohol use and BP measurement. We investigated the effects of single and repeated intakes of alcohol on 24-hour BP. METHODS AND RESULTS: Fourteen male habitual drinkers with essential hypertension were placed sequentially on a 4-day control phase: a nonalcoholic drink with the same calories as alcohol was given at dinner (5 PM to 6 PM) and a 7-day drinking phase: alcohol (ethanol, 1 mL/kg) was given at dinner under standardized conditions. Ambulatory BP measurements were performed on day 3 of the control phase and on days 1 and 7 of the alcohol phase. The average 24-hour systolic and diastolic BPs on day 1 were significantly lower than those in the control phase and on day 7. Between 6 PM and midnight, both systolic and diastolic BPs on days 1 and 7 (121 +/- 2/73 +/- 1 and 126 +/- 4/75 +/- 2 mm Hg, respectively) were significantly lower than those in the control phase (139 +/- 4/83 +/- 2 mm Hg). Between midnight and 8 AM (6 to 14 hours after the last drink), both systolic and diastolic BPs on day 7 (138 +/- 4/83 +/- 2 mm Hg) were significantly higher than those in the control phase (131 +/- 4/79 +/- 2 mm Hg) and day 1 (129 +/- 3/77 +/- 1 mm Hg). Between 8 AM and 3 PM, BPs showed no difference among the three phases. CONCLUSIONS: A single intake of alcohol has a depressor effect on BP that lasts for several hours after drinking, while repeated intakes for 7 days have both depressor and pressor effects according to the differences in time intervals after the last drink. This study suggests that the chronic effects of alcohol on BP might be overestimated when based on casual BP measurements alone.

Blood Pressure↗
PubMed1994

Characterization of the excitable gap in a functionally determined reentrant circuit. Studies in the sterile pericarditis model of atrial flutter.

BACKGROUND: Single premature beats were introduced in the reentrant circuit during stable atrial flutter in the canine sterile pericarditis model to test the hypotheses that (1) despite the fact that the reentrant circuit is functionally determined, there is a fully excitable gap; (2) the excitable gap in the reentrant circuit is not uniform; and (3) inhomogeneities of conduction in the reentrant circuit explain the effects of premature beats. METHODS AND RESULTS: A multiplexing system was used to record 190 unipolar electrograms from the right atrial free wall during 18 atrial flutter episodes in 9 dogs. In all 18 episodes, premature stimuli captured the atrial flutter reentrant circuit. At the longest coupling intervals, the return cycle at the site closest to the pacing site did not prolong. As the coupling interval of the premature stimulus decreased, the return cycle then progressively increased, associated with changes in conduction in the reentrant circuit that were not uniform. The result was that coupling intervals associated with introduction of the premature beat also were not constant. The mean duration of the total (ie, fully plus partially) excitable gap was 12 +/- 4 ms in areas of slow conduction, and it was always shorter than the total excitable gap in other areas (22 +/- 6 ms, P < .001). The mean duration of the fully excitable gap based on analysis of the return cycle was 4 +/- 1 ms in the reentrant circuit. In 13 of 18 atrial flutter episodes, a premature stimulus terminated atrial flutter by causing block of the orthodromic wave front of the premature beat in an area of slow conduction. The mean coupling interval that caused orthodromic block was 113 +/- 5 ms (recorded at the site just proximal to the area of block), and it was always longer than the delivered stimulus coupling interval at the pacing site (96 +/- 8 ms, P < .001). CONCLUSIONS: We conclude that in this functionally determined atrial flutter reentrant circuit in the canine sterile pericarditis model, (1) a fully excitable gap is present in at least part of the reentrant circuit; (2) the duration of the excitable gap in the reentrant circuit is shortest in areas of slow conduction; and (3) when a premature beat encounters the partially excitable gap of the reentrant circuit, it results in changes in conduction such that the coupling intervals are not uniform throughout in the reentrant circuit.

Animals↗
PubMed1994

Mapping the conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter. Insights into mechanisms.

It is not generally believed that there is a relation between atrial flutter, thought to be due to a single reentrant circuit, and atrial fibrillation, thought to be due to simultaneously circulating multiple-reentrant wave fronts. However, there are many reasons to suggest that these rhythms are more closely related than previously thought. To test the hypothesis that the length of an area of functional block in the right atrial free wall is critical to the conversion of atrial flutter to atrial fibrillation and of atrial fibrillation to atrial flutter, we studied spontaneous and ATP-induced conversion of stable atrial flutter to sustained atrial fibrillation and spontaneous conversion of sustained atrial fibrillation to stable atrial flutter. We studied 13 episodes of the conversion of stable atrial flutter to sustained atrial fibrillation and sustained atrial fibrillation to stable atrial flutter in seven dogs with sterile pericarditis. Six episodes were spontaneous and seven were ATP related. All episodes were studied by using a multisite mapping system to record 190 unipolar electrograms (converted in the software to 95 bipolar electrograms) from the right atrial free wall along with ECG lead II. Atrial flutter induction was attempted by atrial stimulation (S1S2 or S1S2S3) or by rapid atrial pacing for > or = 20 beats from selected sites at selected rates. For both the spontaneous and the ATP-related episodes, stable atrial flutter was defined as any episode of > or = 5 minutes, and sustained atrial fibrillation was any episode of > or = 1 minute. During all the episodes of stable atrial flutter, a line of functional block with a mean length of 24 +/- 4 mm was localized on the right atrial free wall. When the previously stable line of functional block decreased to a mean of 16 +/- 3 mm (P < .05), either spontaneously or after ATP administration (40 mg i.v.), the new line of functional block was not long enough to maintain stable atrial flutter, and conversion to atrial fibrillation resulted. This shortened line of functional block continued to change and migrate over the right atrial free wall throughout sustained atrial fibrillation. These observations were similar for both spontaneous and ATP-induced conversions. When sustained atrial fibrillation evolved to stable atrial flutter, there was reformation of a long line of functional block, long enough (> or = prior length) to create a stable reentrant circuit, which then captured the right atrial free wall and subsequently both atria.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1994

Diagnosis of moyamoya disease with magnetic resonance angiography.

BACKGROUND AND PURPOSE: Present criteria for the diagnosis of moyamoya disease emphasize the use of conventional cerebral angiography as an indispensable requirement. However, magnetic resonance angiography (MRA) is fast becoming a reliable diagnostic modality for occlusive cerebrovascular diseases. The purpose of this study is to assess the accuracy of MRA compared with conventional angiography. METHODS: Thirty-nine patients (23 children and 16 adults) with moyamoya disease confirmed by conventional angiography (78 side views) were examined with MRA (three-dimensional time-of-flight technique with a 256 x 256 or 256 x 512 matrix). T1- and T2-weighted MR images were also taken. RESULTS: The stenotic or occlusive change at the carotid fork was clearly revealed by MRA, which correlated well with conventional angiography (83% good correlation, 17% overestimation). Apparent moyamoya vessels were clearly shown as a signal void on the MR image and fine unusual vessels on MRA, particularly in children with moyamoya disease (82%). However, small moyamoya vessels were poorly shown on both MR images and MRA, particularly in adults (63%). CONCLUSIONS: MRA can be an alternative to conventional angiography in typical moyamoya disease cases (the bilateral type of moyamoya disease in children). However, in the early or the end stages of moyamoya disease, diagnosis by means of MRA should be carefully evaluated.

Adolescent↗
PubMed1994

A case of acute myocardial infarction. Intracoronary thrombosis in two major coronary arteries due to hormone therapy.

A fifty-four-year-old woman was admitted to the hospital for a sensation of tightness in the chest of one hour's duration. She had undergone surgery for breast cancer two years previously and had been taking 30 mg of tamoxifen and 1200 mg of medroxyprogesterone daily after surgery. Emergency coronary angiography on admission revealed thrombi in both the right coronary artery and the left anterior descending coronary artery. Tissue-type plasminogen activator was injected into both coronary arteries, resulting in diminution of thrombus size. Repeat coronary angiography on the next day disclosed no thrombus in either artery and no significant stenosis. Electrocardiographic and laboratory data indicated myocardial infarction. These findings strongly suggest that the combination hormone therapy altered the patient's blood coagulability and played an important role in the formation of the intracoronary thrombi and subsequent acute myocardial infarction.

Acetylcholine↗
PubMed1994

Benefits of rate-responsive pacing in patients with sick sinus syndrome.

The effect of changing a rate-responsive pacemaker program (which reacts to evoked QT interval) to fixed-rate ventricular pacing was studied in 10 patients with sick sinus syndrome (SSS). After the patients had been in the rate-responsive mode (VVIR) for at least one year, the exercise capacity (maximal oxygen consumption [peak VO2], anaerobic threshold [AT], and cardiac output [CO] at these points) was examined. Three hours later on the same day, the pacemaker was reprogrammed to the fixed-rate pacing (VVI) and the exercise capacity was examined again (VVI-S). One month later, a similar exercise test was also done in the VVI mode (VVI-L). There was no significant difference in peak VO2 and AT between VVIR and VVI-S, but both peak VO2 and AT were significantly lower in VVI-L than in VVIR. However, there were no significant differences in the CO at peak VO2 or AT between any of the pacing modes. These findings indicate that a VVIR pacemaker should not be reprogrammed to the VVI mode in SSS patients, because the change can cause the exercise capacity to deteriorate.

Aged↗
PubMed1994

Posttraumatic syringomyelia: its characteristic magnetic resonance imaging findings and surgical management.

Posttraumatic syringomyelia should be considered in any patient showing a delayed neurological deterioration after spinal cord injury. The purpose of this article is to assess the posttraumatic syringomyelia on magnetic resonance images and to evaluate the results of its surgical treatment. Fourteen patients with posttraumatic syringomyelia were studied. There were 10 men and 4 women ranging in age from 25 to 67 years. Eleven patients with syringomyelia were symptomatic, and the three others were asymptomatic. The periods from spinal cord injury to onset of symptoms due to syringomyelia ranged from 3 to 33 years with a mean of 14 years. On magnetic resonance images, the mean length of the syrinx was 14 vertebral levels and ranged from 3 to 20 levels. At the rostral part of the injured cord, the syrinx was located off center. In contrast, at the caudal part of the injury, the syrinx was markedly large in size and its location was central. In 6 of 13 patients, the syringes extended into the medulla oblongata. Eleven symptomatic patients underwent surgical treatments: a syringosubarachnoid shunt was done in six patients, a syringoperitoneal shunt was done in four, and a ventriculoperitoneal shunt was carried out in one. Shunt malfunction was encountered in three of the four syringoperitoneal shunts and in the one ventriculoperitoneal shunt. Final neurological outcomes were satisfactory in all 11 patients who underwent surgery. Motor function improved in eight of nine patients, sensory disturbance improved in five of five patients, and relief of local pain or numbness was obtained in four of four patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

A simple method for predicting the cyclosporin A erythrocyte-to-plasma distribution ratio in blood, and its clinical assessment.

To adapt the monitoring of cyclosporin A (CyA) to clinical practice, we have developed a model to predict the CyA erythrocyte-to-plasma distribution ratio (CyA-EP), and evaluated its utility in clinical practice. We monitored CyA trough concentrations in whole blood and performed a series of biochemical tests during disease states in patients undergoing immunosuppressive therapy with CyA after transplantation. An estimate of CyA-EP (EPpr) was thus given by the following equation: EPpr = 6.0831 - 0.2944 x (TG+CHO) - 0.0037 x (CyAblood) - 0.0553 x (HCT) + 0.0463 x (BW) + 0.4447 x (CRE) - 0.0366 x (AGE). In this predictive model, EPpr is given as a function of the plasma lipid levels (TG+CHO, mM), the CyA concentration in whole blood (CyAblood, ng/ml), and the hematocrit (HCT, %), as well as the patient's body weight (BW, kg), serum creatinine (CRE, mg/dl) and age (AGE, years). The parameters TG+CHO, CyAblood, HCT, and AGE were negatively correlated with the CyA-EP, whereas BW and CRE exhibited a positive correlation. The predictive performance of this model was satisfactory for clinical use and changes in CyA-EP in transplant patients were obtained from monitoring CyA in whole blood and routine biochemical tests, without directly measuring CyA-EP. Since CyA-EP is an useful indicator for predicting a shift of CyA into tissues and its systemic clearance in plasma, our model to predict the CyA-EP will help the physician select a CyA regimen during immunosuppressive therapy in a variety of disease states after transplantation.

Adult↗
PubMed1994

Complete atrioventricular block during left heart catheterization.

A 75-year-old male underwent cardiac catheterization for frequent ventricular premature contractions and reduced left ventricular function. ECG on admission showed complete right bundle branch block (RBBB) and left anterior hemiblock. Right heart catheterization was performed uneventfully, but complete atrioventricular block (CAVB) occurred suddenly when a pig-tail catheter was inserted into the left ventricle. Electrophysiological study identified this CAVB as HV block, and demonstrated HV prolongation in sinus rhythm. The coronary angiogram revealed no obstructive lesion or spasm with ergonovine. The reproducibility of the CAVB was demonstrated. The final CAVB developed and persisted for more than one week, requiring the implantation of a permanent pacemaker (DDD). Complete atrioventricular block induced during left heart catheterization is very rare. Pre-existing RBBB with left anterior or posterior hemiblock and reduced left ventricular function may be common factors in patients with this condition. Emergency pacing equipment should always be on-line when left heart catheterization is conducted in such patients.

Aged↗
PubMed1994

Atrioventricular (AV) nodal reentry associated with 2:1 infra-His conduction block during tachycardia in a patient with AV nodal triple pathways.

We report a patient with atrioventricular (AV) nodal reentry in which a 2:1 infra-His conduction block was demonstrated during tachycardia. The electrocardiogram (ECG) at the time of attack showed two types of supraventricular tachycardias. The first type was a narrow QRS tachycardia associated with 1:1 AV conduction at a rate of 170 beats/minute. The second type was a narrow QRS associated with 2:1 AV block at a rate of 85 beats/minute. Electrophysiological study revealed AV nodal reentry based on AV nodal triple pathways. The AV conduction curve obtained by atrial premature stimulation showed two discontinuous points at two different basic cycle lengths (500 msec, 400 msec) and from two different pacing sites (high right atrium, distal coronary sinus). These two types of tachycardias were induced by both atrial premature and overdrive stimulation. In the first type, the impulse conducted in the slow pathway antegradely with 1:1 AV conduction and in the fast pathway retrogradely. In the second type, the impulse was conducted beat-to-beat by either a slow pathway or a very slow pathway antegradely with the retrograde limb being the fast pathway and 2:1 infra-His conduction block. Only when the impulse was conducted in the slow pathway antegradely was the infra-His conduction block observed during the tachycardia. The tachycardia in this patient was drug refractory and controlled by an anti-tachycardia pacemaker.

Aged↗
PubMed1994

Cytoarchitecture of periendothelial cells in human cerebral venous vessels as compared with the scalp vein. A scanning electron microscopic study.

Three-dimensional cytoarchitectures of the periendothelial cells of human cerebral venous vessels as well as a scalp vein were studied by scanning electron microscopy after removal of extra-cellular connective tissue matrices with a KOH-collagenase digestion method. Postcapillary venules appeared covered with pericytes, while collecting venules had stellate periendothelial cells which formed a basket-like network around the vessel wall. As the size of the venous vessels increased, the stellate periendothelial cells became flat in shape and dense in arrangement. Although they had some characteristics similar to the smooth muscle cells in surface structure, no spindle-shaped smooth muscle cells were recognizable even in the superficial cerebral veins. On the other hand, the scalp vein was densely covered with spindle-shaped smooth muscle cells running circularly. These findings suggest that the cerebral venous vessels cannot constrict strongly as compared with the scalp vein, but probably regulate blood volume by mildly changing the caliber of the vessels.

Adult↗
PubMed1994

Scanning electron microscopic studies of the medial smooth muscles in human major intracranial arteries.

The three-dimensional arrangement of the medial smooth muscle cells of human major intracranial arteries was studied by scanning electron microscopy after removal of extracellular connective tissue matrices with a KOH-collagenase digestion method. In the straight portion of the major arteries, the smooth muscle cells were arranged roughly circularly, whereas the arrangement was somewhat random in the vertebral, basilar, and internal carotid arteries. Groups of the longitudinal muscle cells were also found in the vertebral, basilar, and internal carotid arteries, but were absent in the anterior, middle, and posterior cerebral arteries. At a higher magnification, smooth muscle cells in these arteries formed anastomosed bundles about 5-30 micrograms in diameter. The smooth muscle cells in the dichotomous branching and the uniting portions were arranged circularly, but multidirectionally and longitudinally oriented smooth muscle cell groups were present in the facial and dorsal walls of the forked vessels. These multidirectional muscle cell groups were small in number in the portion where the major arteries gave off lateral branches at a right angle. So called "medial defects" were found at the crotch of the bifurcating region in two cases out of four. Smooth muscle cells near the defects tapered off toward the center of the defect where internal elastic lamina with oval fenestrations were exposed. However, no special arrangement of the smooth muscle cells was observed around the "medial defects" as compared with that in the ordinary bifurcating region.

Adult↗
PubMed1994

Lymphocytic hypophysitis, pustulosis palmaris et plantaris and eosinophilia.

We describe here a unique case of lymphocytic hypophysitis accompanied by pustulosis palmaris et plantaris and eosinophilia. The patient also suffered from panhypopituitarism with hyperprolactinemia and pituitary diabetes insipidus caused by lymphocytic hypophysitis. Complications of pustulosis palmaris et plantaris and eosinophilia with lymphocytic hypophysitis have not been reported previously. In the present case, the activities of the three diseases correlated well throughout the patient's course, suggesting that a common mechanism might possibly participate in their pathogenesis.

Adult↗
PubMed1994

Adrenogenital syndrome caused by an androgen-producing adrenocortical tumor.

We describe here a typical case of virilizing adrenocortical tumor. A 23-year-old Japanese woman had her male-like musculature, hirsutism, the absence of breast development and marked clitoromegaly. Adrenal androgens were remarkably elevated, with plasma dehydroepiandrosterone sulfate 2,752 micrograms/dl, plasma testosterone 250 ng/dl and urinary 17-ketosteroids 203.4 mg/day. A well-encapsulated tumor approximately 7 cm in diameter was detected in the left adrenal gland by computed tomography, magnetic resonance imaging and arteriography. The tumor was surgically resected and histologically diagnosed as a benign adrenocortical adenoma. The elevated adrenal androgens returned to normal postoperatively with amelioration of her masculinized clinical features.

Adenoma↗
PubMed1994

Temporary neurological deterioration caused by hyperperfusion after extracranial-intracranial bypass--case report and study of cerebral hemodynamics.

A 64-year-old female with occlusion of the left internal carotid artery (ICA) developed temporary neurological deterioration after superficial temporal artery to middle cerebral artery anastomosis. Preoperative single photon emission computed tomography (SPECT) showed marked reduction of the cerebral perfusion reserve in the left ICA territory. She suddenly developed aphasia 18 hours after operation. Follow-up SPECT revealed temporary hyperperfusion in the left temporal lobe, strongly suggesting that this unusual complication resulted from bypass flow into the brain tissue with chronic severe ischemia and impaired autoregulation.

Aged↗