Mode-conversion process and overdense-plasma heating in the electron cyclotron range of frequencies.
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Biomedical subjects
Publications and source records attributed to H Abe.
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Forty-one patients who underwent cardiac surgery under conditions of systemic hypothermia and intermittent cold crystalloid potassium cardioplegia were studied, in order to elucidate the effects of ventricular fibrillation and reperfusion on the myocardium, by using the intramyocardial pCO2 and temperature sensor. All patients were assigned to 2 groups, namely; group A (21 cases), in which the time between the aorta declamping and defibrillation was under 10 minutes, and group B (20 cases) in which the time was over 10 minutes. In both groups A and B, myocardial pCO2 increased at the rate of 3.58 +/- 1.70 and 2.16 +/- 0.62 mmHg/min (p less than 0.05) after aorta declamping, respectively and the myocardial pCO2 decreased at the rate of 5.59 +/- 0.60 and 4.18 +/- 0.76 mmHg/min (p less than 0.05) after defibrillation, respectively. In group A, the myocardial calcium content, pre-CPB (cardio pulmonary bypass) was 10.98 +/- 1.62 nmol/mg/dry weight and at the time of aorta declamping it was 15.90 +/- 1.81 nmol/mg/dry weight (p less than 0.05). In group B, the myocardial calcium content, pre-CPB, was 14.62 +/- 2.15 nmol/mg/dry weight and at the time of aorta declamping it was 18.23 +/- 4.36 nmol/mg/dry weight (p less than 0.05). At both three and six hours after the operation, the left ventricular work index per minute (LVWI) in group A showed better cardiac pump function than that in group B. We therefore conclude that when reperfusion is encountered, acidosis can be minimized by prompt defibrillation.
Twenty-six patients with fulminant hepatic failure were treated with daily infusions of antithrombin III concentrate until recovery of consciousness or death. Seven patients were alive (group A), 7 survived 17 to 47 days after treatment (group B), and 12 died within 9 days (group C). Decreased plasma antithrombin III levels increased on the day after treatment, irrespective of the pretreatment levels in all patients. Continuous or temporary normalization was seen in all patients in groups A and B, but in only 5 in group C patients whose bleeding was extensive (p less than 0.05). An abrupt drop in peripheral platelet counts occurred when plasma antithrombin III levels were below normal. General bleeding accompanied this drop. These results suggest that maintained normal plasma antithrombin III levels are beneficial for prolonged survival time in fulminant hepatic failure, probably through controlling intravascular coagulation, and that antithrombin III infusion may be useful for such treatment.
Isovolumic perfused rat hearts containing an intraventricular balloon were used to assess the effects of incremental balloon volumes on developed pressure, oxygen consumption, coronary flow, phosphorylation potential obtained by P-31 nuclear magnetic resonance, wall thickness obtained by two-dimensional echocardiography, and diastolic wall stress. Three phases in developed pressure were noted: (1) volumes from 0 to 150 microliter resulted in a continuous increase in developed pressure; (2) with volumes from 150 to 250 microliter, developed pressure remained constant whereas developed (systolic) and diastolic wall stress rose sharply; and (3) with volumes from 250 to 400 microliter, developed pressure fell whereas developed (systolic) and diastolic wall stress continued to rise. The ln [(PCr)/(Pi)] was in synchrony with oxygen consumption at 0 and 50 microliter balloon volumes, and then diverged at volumes greater than 100 microliter. Oxygen consumption increased from 0 to 50 microliter, was constant from 50 to 250 microliter balloon volume, and then declined. The ln [(PCr)/(Pi)] fell precipitously at balloon volumes greater than 100 microliter, most likely limited by oxygen consumption. Coronary flow did not change significantly until 250 microliter or more of water was added to the balloon, and then it started to decline. Volumes greater than 100 microliter result in overstretch of myofibers, as observed by the precipitous decline in ln [(PCr)/(Pi)], and the steep increase in diastolic wall stress. With excessive volume loading, the drop in phosphorylation potential, ln [(PCr)/(Pi)], appears to contribute to the decrease in developed pressure.
We report on 2 cases of renal cell carcinoma with solitary contralateral adrenal metastasis which was demonstrated six months and one year, respectively, after radical nephrectomy. Pulmonary metastases developed six months after adrenalectomy in 1 patient; the other patient is alive without any evidence of disease twenty-two months after adrenalectomy.
The concept of left atrial systolic time intervals and Doppler echocardiography were used in a quantitative assessment of left atrial function in relation to the presence or absence of a fourth heart sound and to left ventricular hypertrophy in 47 patients with hypertension. Left atrial systolic time interval indexes included atrial pre-ejection period (the time between the onset of an electrocardiographic P wave and the onset of left ventricular inflow during atrial systole [A wave]), corrected atrial pre-ejection period (the atrial pre-ejection period divided by the duration of the P wave), and atrial ejection time (the time between the onset and cessation of the A wave). Twenty-one patients with a fourth heart sound on the phonocardiogram had a shorter atrial pre-ejection period (81 +/- 10 versus 89 +/- 14 ms p less than 0.05) and a corrected atrial pre-ejection period (66 +/- 17 versus 83 +/- 18 ms, p less than 0.01), as well as a longer atrial ejection time (147 +/- 15 versus 126 +/- 13 ms, p less than 0.001) than did 26 patients without a fourth heart sound. The ratio of atrial pre-ejection period to atrial ejection time and that of corrected atrial pre-ejection period to atrial ejection time was smaller in patients with than in patients without a fourth heart sound (0.56 +/- 0.08 versus 0.71 +/- 0.11, p less than 0.001; 0.46 +/- 0.16 ms-1 versus 0.67 +/- 0.17 ms-1, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Moyamoya disease is a disease characterized by chronic occlusion of the circle of Willis with subsequent development of fine vascular networks in the ganglionic region, which is common in Japanese people. The term of 'moyamoya' means puff of smoke in the Japanese language and represents the characteristic angiographic findings of subsequent development of fine vascular networks in the ganglionic region. Although reconstructive surgery for moyamoya disease has been widely accepted nowadays, there is still no definite consensus as to a surgical indication for patients with an haemorrhagic attack and as to the selection of an operative method for each individual patient. This paper presents our overall surgical results and introduces a new operation, devised by Y. Nakagawa (i.e. EMAS). It refers also to surgical intervention for patients with haemorrhagic attacks.
The hypotensive effects of some antihypertensive drugs are augmented under sodium restriction, while those of others are not. The mechanisms of these interactions were theoretically analyzed based on the arterial pressure-natriuresis relationship. Four-week studies were performed in 24 patients with essential hypertension who were given a regular sodium diet (12-15 g of NaCl/d) in the first and third weeks and a sodium-restricted diet (1-3 g/d) in the second and fourth weeks. One of three antihypertensive drugs, 60 mg/d of nicardipine (Ca-antagonist), 120 mg/d of propranolol (beta-blocker) or 150 mg/d of captopril (converting-enzyme inhibitor) was administered in the third and fourth weeks. The mean arterial pressure and urinary sodium excretion were measured on the last three days of each week. The degree of interaction between the antihypertensive drugs and sodium restriction was statistically compared. The hypotensive effect of nicardipine and propranolol did not differ with the change in sodium intake, whereas that of captopril was greater under sodium restriction than under the regular sodium diet. Urinary sodium excretion was plotted on the ordinate as a function of arterial pressure before and after administration of the antihypertensive drugs. The pressure-natriuresis curve was shifted left, without a change in the slope, by nicardipine and propranolol and also left, but with a decrease in the slope, by captopril. The hypotensive effect of nicardipine and propranolol, being independent of the amount of sodium intake, was based on the leftward shift of the pressure-natriuresis curve that was probably due to the decrease in renal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Isolated rat heart preparations were studied to characterise the alterations in high energy phosphates that occur during reversible regional ischaemia and to determine whether pyruvate, as the sole exogenous energy substrate, would attenuate the ischaemia induced depletion of the nucleotide pool when compared with glucose. Using phosphorus-31 magnetic resonance spectroscopy baseline concentrations of adenosine triphosphate, phosphocreatine, inorganic phosphate, and intracellular pH were compared with values during 30 min of left coronary artery occlusion followed by 30 min of reperfusion. These variables were related to changes in developed pressure, coronary flow, and oxygen consumption. In addition, the total nucleotide pool was evaluated by biochemical analysis of myocardial tissue extracts and coronary effluent. The ischaemic region was characterised by a dye staining technique and cross sectional echocardiographic measurements of regional myocardial wall thinning. In both glucose and pyruvate perfused groups, coronary flow and oxygen consumption decreased to 50-60% of control within 1 min of ischaemia and returned to baseline values with reflow. Developed pressure decreased to 50(9) and 74(8)% (mean(SEM] of control after 30 min of ischaemia in glucose and pyruvate perfused groups respectively. Reperfusion resulted in complete recovery of developed pressure in hearts perfused with pyruvate but not in the glucose group. Glucose perfused hearts had a greater decrease in intracellular pH during ischaemia (7.07(0.01) to 6.36(0.1] than pyruvate perfused hearts (7.06(0.02) to 6.83(0.04]. Reperfusion resulted in a rapid return to baseline intracellular pH in both groups. During ischaemia, adenosine triphosphate values decreased to a greater degree in glucose than in pyruvate perfused hearts (57(4) and 79(5)% of baseline respectively). Thirty minutes of reperfusion did not significantly improve adenosine triphosphate concentrations in either group. Phosphocreatine concentrations decreased to 52(7) and 75(6)% of baseline in glucose and pyruvate perfused groups respectively after the ischaemic period. Reperfusion resulted in normalisation of phosphocreatine values in the pyruvate but not in the glucose perfused group. Biochemical analysis of myocardial tissue extracts confirmed the spectroscopy data and showed that pyruvate inhibits the efflux of adenine nucleotide derivatives. Tissue concentrations of adenosine monophosphate were three times greater and adenosine 50% less after 30 min of ischaemia in the pyruvate perfused group.(ABSTRACT TRUNCATED AT 400 WORDS)
Elongating shoots of rapidly growing clones of Salix viminalis L. (clone 683-4) and Salix dasyclados Wimm. (clone 908) harvested in early August were analyzed for endogenous gibberellins (GA). Distribution of GA-like activity, determined by Tan-ginbozu dwarf rice microdrop bioassay after reverse phase C(18) high performance chromatography, was similar for both species. For S. dasyclados, combined gas chromatography-selected ion monotoring (GC-SIM) yielded identifications of GA(1), GA(8), GA(19), GA(20), and GA(29). Identifications of GA(4) and GA(9) were also made using co-injections of known amounts of [17, 17-(2)H(2)]GAs. By bioassay, the main activity was GA(19)-like in both species. Gibberellin A(1), GA(19), and GA(20) concentrations were approximated by GC-SIM using co-injections of known amounts of [17,17-(2)H(2)]GAs. Both bioassay and GC-SIM results indicated very high concentrations of GA(19) and GA(20) (about 6000 nanograms per kilogram fresh weight shoot tissue using GC-SIM: 800 ng using bioassay), compared to the concentration of GA(1) (about 130 nanograms per kilogram fresh weight using either GC-SIM or bioassay).
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A total of 104 isolates of enterotoxigenic Escherichia coli derived from diarrheal patients from more than 10 countries were examined for serotype and toxigenicity. The transferability and molecular structure of the enterotoxin plasmids from each isolate were also examined. Enterotoxin plasmids from serotypes such as O6, O25, O27, O126, O128, and O159, which are frequently associated with E. coli diarrhea (classical strains) generally did not transfer by conjugation from clinical isolates, whereas those from serotypes such as O7, O17, O80, O98, O139, O150, and O153, which are rarely associated with diarrhea (rare strains) transferred almost always from the clinical isolates by conjugation. Analyses of enterotoxin plasmids by restriction endonucleases and DNA-DNA hybridization with the enterotoxin probes revealed that the strains with the same O serotype and toxigenicity carry closely related enterotoxin plasmids. These results suggest that classical strains resulted from the dissemination of ancestral clones which received enterotoxin plasmids long ago, while the rare strains acquired the enterotoxin plasmids recently by conjugation and have not yet been spread to the same degree as the ancestral clones.
Responses in muscle sympathetic activity (MSA) to acute hypoxia were studied in 13 healthy male subjects under hypobaric hypoxic conditions at a simulated altitude of 4,000, 5,000, and 6,000 m. Efferent postganglionic MSA was recorded directly with a tungsten microelectrode inserted percutaneously into the tibial nerve. Heart rate (HR) and respiratory rate (RR) were counted respectively from the R wave of an electrocardiogram and from the respiratory tracing recorded by the strain-gauge method. The average values of the MSA burst rate and total activity of MSA (burst rate x mean burst amplitude) at 4,000, 5,000, and 6,000 m were 36.4 +/- 2.6, 39.1 +/- 3.1, and 40.2 +/- 4.2 (SE) bursts/min and 616 +/- 138, 794 +/- 190, and 764 +/- 227 arbitrary units, respectively. These values were significantly higher than the values of 27.1 +/- 2.9 bursts/min and 446 +/- 28 at sea level. HR increased significantly at altitudes, but RR did not show significant change. Under severe hypoxic conditions beyond 5,000 m, there were large interindividual differences in the MSA responsiveness to hypoxia. The results indicate that MSA is activated under hypoxia by stimulating the chemoreceptors. However, the central controlling mechanisms that would be affected by hypoxia may also influence the MSA responsiveness under severe hypoxia.
Whether obliteration of glomerular epithelial foot processes and increases in urinary N-acetyl-beta-D-glucosaminidase (NAG) activity are the consequence or the cause of proteinuria after administrations of the aminonucleoside of puromycin was examined using Nagase analbuminemic rats. The administration of puromycin aminonucleoside to Nagase analbuminemic rats did not induce proteinuria. However, the increase in urinary NAG activity and the degree of abnormality of foot processes in the glomerular cells were similar to those in control Sprague-Dawley rats. These findings suggest that NAG excretion and the morphological alterations of epithelial cells in nephrosis are not the consequence of massive proteinuria.
Plasma GH responses to human GHRH, arginine, L-dopa, and insulin-induced hypoglycemia were determined in seven myotonic dystrophy (MD) patients. An iv bolus injection of GHRH-(1-44)-NH2 (1 microgram/kg BW) only slightly increased plasma GH concentrations in MD patients. The mean peak plasma GH level after GHRH injection [4.2 +/- 0.8 (+/- SE) micrograms/L] was significantly lower than that in 10 age-matched normal subjects (26.7 +/- 4.3 micrograms/L) or that in 6 patients with progressive muscular dystrophy (22.8 +/- 6.6 micrograms/L) whose nutritional status was similar to that of the MD patients. Even with a larger dose of GHRH (3 micrograms/kg BW), the plasma GH rises were minimal in the MD patients (mean peak, 5.9 +/- 1.8 micrograms/L). The plasma GH responses to a 30-min iv infusion of arginine (0.5 g/kg BW) and oral ingestion of L-dopa (0.5 g) were attenuated to a similar extent, whereas insulin-induced hypoglycemia caused a significant increase in plasma GH in all seven MD patients [mean peak, 17.4 +/- 4.1 (+/- SE) microgram/L]. The plasma TSH responses to TRH and plasma insulin-like growth factor I levels were similar in the MD patients and normal subjects. These findings suggest that 1) the impaired GH release after GHRH, arginine, and L-dopa administration in MD patients is not due to somatotroph deficiency, since the GH response to hypoglycemia is well preserved; and 2) insulin-induced hypoglycemia may stimulate GH release at least in part via inhibition of somatostatin release.
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The present experiments were designed to find a method to facilitate methotrexate (MTX) transfer into rat brain tissue. Adult male Wistar-Kyoto strain rats, anesthetized with pentobarbital-Na, received an infusion of the drug solution to be tested into the right internal carotid artery (5 ml/min, 30 sec) 5 min before injection of MTX (7 mg/kg). After 10 min, the MTX levels in the cerebral hemispheres were estimated as a peak height ratio unit of MTX vs. the internal standard by high performance liquid chromatography. MTX was undetectable in either hemisphere after the pretreatment with saline alone or 15% mannitol-saline. The MTX levels in the right hemisphere were about 10 after the pretreatment with 20% mannitol-saline, while MTX was undetectable in the left hemisphere. In contrast, the MTX levels in the right hemisphere were dose-dependently increased to about 25, 130 and 60, 100, respectively, when nitroglycerin (NTG, 2.5 or 7.5 micrograms/rat) or nicardipine-HCl (NIC, 1.25 or 2.5 micrograms/rat) was administered together with 20% mannitol-saline. These vasodilator drugs, however, had no effect when tested in combination with saline or 15% mannitol-saline. It is assumed that an increase in cerebrovascular blood flow induced by NTG or NIC enhances the MTX transfer into the brain once the blood brain barrier is opened by hypertonic solutions.