[Treatment of hypertension complicated by diabetes mellitus and obesity].
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Biomedical subjects
Publications and source records attributed to N Kajiwara.
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Ergometer two-dimensional echocardiography was performed in 28 subjects complaining of chest pain but without myocardial infarction. Sequential ergometer loading was initiated at 50 or 75 watts, and increased in several stages. Apical four-chamber view two-dimensional echocardiograms were recorded onto video tape, and video images were converted into digital computer signals. After cine-loop display, computer image processing included noise reduction and edge enhancement, M-mode measurements were made at a designated level on the two-dimensional echo images. Wall motion was also analyzed directly from the two-dimensional echo images, using an auto-edge detection method. The derived data were compared with results from coronary angiograms. No echo abnormality was observed at rest, whereas during exercise wall motion was depressed at the diseased site of the angiogram; the amplitude of excursion and the changes in systolic and diastolic velocity were disturbed at the septum in LAD-involved patients, and in the posterolateral wall in both Cx and RCA patients. The imaging success rate using the computer-aided analysis was found to be 92.9%. Sensitivity for diagnosis of coronary artery disease was 82.1% and specificity 89.3%. Ergometer two-dimensional echocardiography with assisted computer image processing appears to be one of the most valuable tools for clinical real time evaluation of coronary artery disease.
A simple procedure was developed for detection of Theileria sergenti infection on the basis of hybridization of parasite DNA with a specific probe. A genomic DNA library of T. sergenti constructed in pUC-18 was screened to detect clones containing the parasite's DNA sequences by colony and Southern hybridizations. Two positive DNA inserts were purified from the recombinant plasmids and used as probes labelled with 32P or non-isotopic reagent, biotin-11-dUTP. 32P-radiolabelled and non-radioactive probes appear to be sensitive enough to detect 15 pg (equivalent to 1,200 parasites) and 125 pg (equivalent to 10,000 parasites) of purified T. sergenti DNA, and in diluted T. sergenti-infected red blood cells, they are able to detect 8,000 parasites and 16,000 parasites, respectively.
Dipyridamole-stress two-dimensional echocardiography (2DE) was performed in 25 subjects, 14 with stenotic and 11 with normal coronary arteries by coronary angiography, to assess the sites and severity of coronary artery stenosis noninvasively. Dipyridamole was administered intravenously with a dose of 0.56 mg/kg for 4 min. 2DE was recorded at the lower papillary muscle level and the percent fractional area change (% FAC) of the left ventricular segments was computed (FV). In all cases with an echocardiographic regional wall motion abnormality in the interventricular septum, a significant stenosis (greater than or equal to 75%) was documented angiographically in the left anterior descending coronary artery (LAD). In seven of eight patients with a segmental abnormality in the inferolateral wall, a significant stenosis was observed in the left circumflex coronary artery (Cx). The sensitivity and specificity of dipyridamole-stress echocardiography were 100% and 92%, respectively, for an LAD stenosis, and and 87.5% and 71%, respectively, for a Cx stenosis. The segmental wall motion abnormality induced by dipyridamole resolved within four to five min after terminating the infusion in patients with coronary artery narrowing of 75%; whereas, it persisted up to six to seven min in patients with 90% narrowing. There was no improvement in the LV wall motion 15 min after the termination of the infusion in patients with severe narrowing (99%). In conclusion, dipyridamole-stress echocardiography proved to be one of the most useful methods, not only for detecting coronary artery disease, but for predicting the severity and for localizing the sites of lesions as well.
A 76-year-old male admitted to Surugadai Nihon University hospital complaining of general fatigue, slight fever and anorexia. The laboratory examination revealed anemia and an appearance of a few myeloblasts and 7% of monocytes in the peripheral blood. The nucleated cell count was 2 x 10(4)/microliters with 43% myeloblasts in the bone marrow aspirate. He was diagnosed as acute myelomonocytic leukemia. He did not receive any chemotherapy for leukemia because of his old age and smoldering disease. Pyoderma gangrenosum developed in the left submandibular and axillary regions about 6 months later. Three more month later, significant increase of myeloblast was recognized in the peripheral blood and the bone marrow. It has been reported that pyoderma gangrenosum precedes a remarkable increase of leukemic cells in the patients with acute leukemia in complete remission and with myelodysplastic syndrome. In our case, to, the same process was strongly suggested.
Histamine H2-receptor antagonists administered into the central nervous system have been shown to increase arterial pressure (AP) in anaesthetized animals (Paakkari et al., 1982). Few studies have been reported on the effects of centrally administered cimetidine (CIM), one of the histamine H2-receptor antagonists, in conscious animals. However, the mechanism of the pressor action of histamine H2-receptor antagonists remains unclear. The present study was designed to investigate the hemodynamic effects of intracerebroventricular (i.c.v.) CIM and the interaction between the sympathetic nervous system and histamine receptor system in conscious rats. Male Wistar rats weighing 200 gr were prepared for the experiment under a conscious and minimally restricted state. Five micrograms of i.c.v. saline (SAL-ICV group, n = 5) did not produce significant changes in mean arterial pressure (MAP) or heart rate (HR) (MAP from 85.6 +/- 3.4 to 86.0 +/- 4.3 mmHg and HR from 395.0 +/- 13.9 to 395.2 +/- 8.2 bpm, respectively). Twenty micrograms of i.c.v. phenoxybenzamine (POB-ICV group, n = 6) decreased MAP from 95.8 +/- 4.1 to 85.2 +/- 3.1 mmHg, -10.7 +/- 2.2 mmHg as delta MAP, and increased HR from 392.5 +/- 8.5 to 435.3 +/- 13.9 bpm, +42.8 +/- 6.8 bpm as delta HR. Two-hundred micrograms of intravenous (i.v.) POB (POB-IV group, n = 5) also decreased MAP from 96.0 +/- 4.3 to 71.0 +/- 5.1 mmHg, -25.0 +/- 2.7 mmHg as delta MAP, and increased HR from 395.8 +/- 10.5 to 473.0 +/- 12.4 bpm, +77.2 +/- 7.6 bpm as delta HR. The changes in MAP and HR were much greater in the POB-IV group than those in the other two groups. The subsequent i.c.v. administration of 250 micrograms of CIM induced an increase in MAP (+19.4 +/- 1.7 mmHg as delta MAP) and a decrease in HR (-36.4 +/- 3.1 bpm as delta HR) in the SAL-ICV group, which continued for at least 30 minutes producing peak effects 2 minutes after i.c.v. administration of CIM. However, an elevation of MAP caused by i.c.v. CIM was much more inhibited in the POB-ICV group than in the POB-IV group (+2.5 +/- 0.7 mmHg as delta MAP in the POB-ICV group and +5.0 +/- 1.3 mmHg as delta MAP in the POB-IV group, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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Coronary thrombolysis with plasminogen proactivator, GE-0943, was undertaken in patients with acute myocardial infarction and compared with urokinase. Fifty patients were given 6000 units of GE-0943 intracoronary and the totally occluded infarct-related arteries were recanalized in 92.0%. Fifty-four patients who were given 3000 units of GE-0943 intracoronary demonstrated a recanalization rate of 68.2%, while intracoronary administration of urokinase in 54 patients showed a recanalization rate of 70.4%. There was only one patient with hemorrhagic complication among GE-0943 3000-units group, none among GE-0943 6000-units group, and 5 among urokinase group. Thus, intracoronary administration of GE-0943 is very effective and safe with a dose up to 6000 units.
The purpose of this study was to assess the effects of chronic insulin infusion on blood pressure and urinary sodium excretion in Wistar rats. Fifteen Male Wistar rats weighing about 220 g were used. The rats were housed in metabolic cage and measured urine volume. Osmotic minipumps filled with insulin (0.57 U/day, Insulin group, n = 9) or saline (0.014 cc/day, Control group, n = 6) were implanted subcutaneously under ether anaesthesia, and blood pressure, urine volume, urinary sodium excretion (UNaV), plasma renin activity (PRA), plasma norepinephrine concentration (PNE) were measured for 4 weeks. In insulin group, there were no significant changes on plasma glucose levels, but systolic blood pressure rose significantly from 119 mmHg to 140 mmHg after 4 weeks. In this group, urine volume, UNaV, and PRA were significantly lower than those of control group and PNE was tended higher but not significant (P less than 0.1). Exogenous NE was given intravenously to assess the endogenous NE activity. Blood pressure elevation caused by exogenous NE in insulin group was suppressed significantly than that of control group. On the basis of these findings, we conclude that insulin can cause high blood pressure due to sodium retention and activation of endogenous NE.
In order to elucidate the relation between the serotonergic nervous system and the hypothalamus-pituitary system in hemodynamic regulation, the effects of a serotonin S2 receptor antagonist, ketanserin, on hemodynamic changes after intracerebroventricularly (i.c.v.) administrated corticotropin releasing factor (CRF) were investigated. Male Wistar rats (n = 19) weighing approximately 200 g were used. Thirty minutes after either intravenous (i.v.) (KET-IV group) or intracerebroventricular (KET-IC group) administration of 100 micrograms of ketanserin, 10 micrograms of CRF was given i.c.v. and mean arterial pressure (MAP) and heart rate (HR) were observed for 40 minutes, which was followed by blood sampling for plasma norepinephrine (PNE). The experiment was performed under conscious state. Resting MAP and HR were similar in both groups. Neither i.v. or i.c.v. ketanserin alone induced significant changes in MAP and HR. Although there was consistent pressor responses (+10 +/- 1.7 mmHg) and increase in HR (+31 +/- 13 bpm) after CRF administration in KET-IV group, there was not significant changes in MAP (+17 +/- 1.0 mmHg) and HR (+4.3 +/- 5.7 bpm) in KET-IC group. PNE was significantly higher in KET-IV group than that in KET-IC group, 489 +/- 71 pg/ml and 179 +/- 57 pg/ml, respectively. These data suggest that the pressor response to i.c.v. CRF is related to the increased peripheral sympathetic tone, and that the central serotonergic nervous system may play an important role in the hemodynamic changes.
For determination of the responses of sodium balance, blood pressure, and other relevant variables to Na loading in people with a low intake of Na, 10 male Papua New Guinea highland subjects were given additional Na at two levels (128 and 256 mmol/d) for 10 d after a 3-d control period of low-Na diet. Na loading caused a marked positive balance of Na, decreases of aldosterone concentration and renin activity in the plasma, and a decrease of urinary aldosterone excretion. The blood pressure, particularly that measured at noon, increased in the latter half of the Na-loading period, the increase being significant in the group given 256 mmol of sodium daily: the systolic and diastolic blood pressure increased from 92 +/- 8 over 56 +/- 7 mm Hg in the control period to 102 +/- 7 over 60 +/- 4 mm Hg in the latter half of the test period (p less than 0.05).
To investigate the predictive value of exercise tests and diastolic function measurements for the progression of left ventricular hypertrophy, symptom-limited treadmill stress testing and echocardiography were performed before and after a follow-up period of 3.5 years in 47 mild hypertensive men aged 42 +/- 2 years. The men were classified into three groups by the progression of the left ventricular mass index (%LVMI) during the observation, i.e. (LVMI after follow-up) - (LVMI before follow-up)/(LVMI before follow-up). The high-progression group (n = 13) had a %LVMI exceeding mean +/- 2/3s.d. of all subjects; the low-progression group (n = 21) had a %LVMI within mean +/- 2/3s.d. and the non-progression group (n = 13) had a %LVMI less than mean -2/3s.d. At the beginning of the observation, age, blood pressure at rest, LVMI, ejection fraction, mean velocity of circumferential fibre shortening, peak shortening rate and systolic time intervals (ET/PEP, ratio of ejection time to pre-ejection period) were similar among the three groups. However, the high-progression group showed a higher systolic pressure at peak exercise, a lower peak filling rate and a longer time to peak filling rate (TPFR) as corrected by the R-R interval of the ECG. These data suggest that systolic pressure at peak exercise and echocardiographically assessed diastolic function are useful in predicting the progression of cardiac involvement in mild hypertension.
Coronary recanalization rates and changes in the coagulation and fibrinolysis system were evaluated in a randomized fashion in patients with acute myocardial infarction after intracoronary administration of single-chain urokinase-type plasminogen activator (pro-urokinase: GE-0943) or urokinase. Three groups of patients were studied: group H (n = 50), 6,000 units pro-urokinase i.c.; group L (n = 44), 3,000 units pro-urokinase i.c.; and group U (n = 54), 960,000 IU urokinase i.c. Coronary recanalization rates determined angiographically after 45 minutes of intracoronary infusion averaged 90% in group H, 59% in group L, and 61% in group U. The differences were statistically significant between group H and the latter two groups. Pro-urokinase affected plasma proteins of the fibrinolytic system to a lesser degree than urokinase. Bleeding complications were present in one patient in group L, in none in group H, and in five in group U. Thus, intracoronary administration of 6,000 units pro-urokinase is more effective in coronary thrombolysis and causes less systemic fibrinogenolysis than intracoronary administration of urokinase.
To clarify the relationship between time interval from the onset of coronary occlusion to the reperfusion and reperfusion rates or left ventricular function, an experiment with 113 mongrel dogs was carried out. Coronary thrombi experimentally induced within 4 hours in 63 dogs were rapidly lysed by intracoronary thrombolytic agent (Experiment 1). Infarct size was investigated in 17 dogs. The infarct size (% of left ventricle) in 9 dogs with 4-hour reperfusion following 2-hour coronary occlusion was significantly smaller than that in 8 dogs with 6-hour occlusion (12.0 +/- 7.9 vs 19.1 +/- 8.7% respectively p less than 0.05) (Experiment 2). The infarct size in 8 dogs with 7-day reperfusion following 2-hour occlusion was also significantly reduced compared to that in 7 dogs with 7-day occlusion (16.3 +/- 7.4 vs 28.5 +/- 8.9%, respectively p less than 0.02) (Experiment 3). The infarct size in 11 dogs with 4-hour reperfusion with verapamil administration following 2-hour occlusion was significantly reduced compared to that in 7 dogs with 6-hour occlusion without verapamil (5.5 +/- 1.9 vs 20.3 +/- 3.3%, respectively p less than 0.01) (Experiment 4). In experiment 3, anterior wall motion also was assessed by contrast ventriculography and infarct related areas in reperfused group was found to be improved compared to non-reperfused group at 7 days after infarction. In clinical studies, 121 patients who were admitted within 12 hour of onset of symptoms, were investigated to evaluate reperfusion rates and left ventricular function. The reperfusion rate of young age thrombus within 3 hours was 89% of 18 patients with completely occluded coronary artery. It was 77% of the 52 patients with 3 to 6 hour occlusion and 72% of the 18 patients with over 6 hour occlusion. There was a tendency towards high reperfusion rates in younger thrombus. In patients who were recanalized within 3 hours from the onset of symptoms ejection fraction of left ventricle at the chronic stage had a significantly higher percentage when compared to the unsuccessful group. Wall motion of infarct-related areas in patients who were thrombolysed within 6 hours was improved compared to the unsuccessful group. Administration of verapamil during reperfusion in patients with acute myocardial infarction suppressed rapid CK release and sigma CK. Thus, young age thrombus can be lysed easily, earlier recanalization after coronary occlusion can reduce infarct size and improve left ventricular function. Reinforced administration of verapamil during reperfusion can also reduce infarct size.
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