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In the present study, we investigated (1) whether airway responsiveness to inhaled histamine-aerosol could be induced during 7-d exposure of guinea pigs to 4 ppm NO2 and, if so, (2) whether thromboxane A2 may be involved in such increase. Female Hartley guinea pigs were divided into 6 groups (n = 15/group). Three groups were exposed to filtered air and the other 3 groups were exposed to NO2 for 1, 3, or 7 d (24 h/d). Baseline specific airway resistance (SRaw0) did not change significantly after exposure to 4 ppm NO2 or air. Airway responsiveness was determined 1 wk before the beginning of exposure and on the day of termination of the exposure. Prior to exposure to NO2, the EC200His, the concentrations of inhaled histamine necessary to double SRawNaCl (SRaw after inhalation of 0.9% NaCl), were 1.07 +/- 0.20, 1.30 +/- 0.20, and 1.01 +/- 0.18 mM for the 3 groups later given NO2 for 1, 3, and 7 d, respectively. Following exposure to NO2 for 1, 3, or 7 d, EC200His values were 1.42 +/- 0.25, 0.66 +/- 0.10 (p < .05), and 1.05 +/- 0.22 mM, respectively. These results show that 7-d exposure to 4 ppm NO2 induced a significant increase in airway responsiveness on d 3. Exposure to air had no significant effect on the airway responsiveness. This transient hyperresponsiveness was inhibited by a specific inhibitor of thromboxane synthetase, OKY 046. These results indicated that (1) a lower concentration (4 ppm) of NO2 than that previously reported can induce transient hyperresponsiveness in guinea pigs during appropriate long-term exposure, and (2) thromboxane A2 may play an important role in this transient airway hyperresponsiveness.

We studied the concomitant effects of scavengers of reactive oxygen species (ROS) on both cardiac function and the incidence of arrhythmias. Isolated rat heart was perfused with a working mode paced at 300 beats/min. The left coronary artery was occluded for 5, 7, 15, or 60 min and reperfused thereafter for 30 min. Superoxide dismutase and catalase were infused from 5 min prior to reperfusion to the end of reperfusion in the scavenger treatment group. In the 60-min ischemia group with scavenger treatment, the cardiac output was significantly higher than that in the untreated group at both 10 and 30 min of reperfusion (P less than 0.01). In the 15-min ischemia group with scavenger treatment, the cardiac output showed a tendency toward a higher value than that in the untreated group. The incidence of reperfusion arrhythmias occurring after a short ischemic time (5, 7, or 15 min) were similar in the scavenger treated and untreated groups; but, with a preceding ischemia of 60 min, the incidence of ventricular tachycardia was higher in the scavenger treated group than in the untreated group (P less than 0.02). In conclusion, scavengers improved contractile dysfunction but did not attenuate the incidence of arrhythmias.

The surface lipids of Nicotiana umbratica contained several varieties of glycolipids. Three types of glucose esters and five types of sucrose esters were isolated and identified from this species. These glycolipids contained short-chain fatty acids such as acetic, methylpropionic, methylbutyric, 3-methylpentanoic, 4-methylpentanoic and methylhexanoic acids. The acetylated positions of each compound were determined by 2-D NMR, using the HMBC technique. The structures of the glucose esters were 1,6-di-O-acetyl-2,3-4-tri-O-acyl-alpha-D-glucopyranose (I), 6-O-acetyl-2,3,4-tri-O-acyl-alpha-D-glucopyranose (II) and 2,3,4-tri-O-acyl-alpha, beta-D-glucopyranose (III). The structures of the sucrose esters were 6-O-acetyl-2,3,4-tri-O-acyl-alpha-D-glucopyranosyl-1,3-di-O-acetyl-beta- D- fructofuranoside (IV), 2,3,4-tri-O-acyl-alpha-D-glucopyranosyl-1,3-di-O-acetyl-beta-D-fructofur anoside (V), 6-O-acetyl-2,4-di-O-acyl-alpha-D-glucopyranosyl-3-O-acetyl-beta-D- fructofuranoside (VI), 2,3,4-tri-O-acyl-alpha-D-glucopyranosyl-3-O-acetyl-beta-D-fructofuranosi de 2,3,4-tri-O-acyl-alpha-D-glucopyranosyl-3-O-acetyl-beta-D-fructofuranosi de (VII) and 2,3,4-tri-O-acyl-alpha-D-glucopyranosyl-beta-D-fructofuranoside (VIII). Among them, I, IV, V and VI were isolated for the first time from plants of the family Solanaceae. These newly isolated glycolipids were inhibitory against barnyardgrass growth.

A case of priapism following epidural anesthesia was reported. A 67 year old man received epidural anesthesia for the transurethral resection of a malignant bladder tumor. Epidural anesthesia which he had wanted to receive was given through the L3 to L4 intervertebral space with 18 ml of 2% lidocaine. The penile erection occurred while he was prepared and draped. Additional 8 ml of 1% lidocaine failed to overcome it and the operation cancelled. After this episode, he had anesthesia on 5 occasions in 2 years. General anesthesia was given 3 times without penile erection, but epidural block was tried on 2 occasions, which was followed by penile erection. For the penile erection, intracavernous injection of etilefrine hydrochloride was effective and surgical procedure could be done smoothly. The mechanism of priapism remained unclear but imbalance of the autonomic nervous system may be a involved. This case suggests that intracavernous injection of etilefrine hydrochloride is effective for treatment of penile erection during transurethral surgery.

Pressure difference (PD) across the mitral valve was analyzed by a computer-aided catheter system in dogs. Positive PD (PPD) was consistently traced in the initial phase of rapid filling. While heart rate (HR) was below 100 beat/min, a negative PD (NPD) followed the above PPD. In the period between the NPD and the 2nd PPD due to atrial contraction, PD was kept at zero, while LA and LV pressures were gradually elevated by pulmonary venous return. As HR exceeded 100, 2 positive peaks of PD merged into M-shaped or mono-peaked PD. Through higher inflow resistance produced by artificial mitral stenosis, PPD peak decayed without NPD. In mitral regurgitation with an acute volume overload, all of the PD amplitudes were exaggerated. Thus the quick reversal of PD suggested the effect in blood filling process across the mitral valve.

This study documents the value of continuous observation of nicotinamide adenine dinucleotide (NADH) fluorescence (NADH-F). NADH-F monitoring is used to identify ischemic regions for the recognition of minor technical failures associated with ischemia and reperfusion experiments in the isolated perfused heart system. The visualization of NADH-F is possible by simply irradiating the heart with ultraviolet light. Rat hearts, in the working-heart mode, were subjected to occlusion/reperfusion of the left coronary artery, and analyzed. The perfusate was filtered through a 5 micron pore membrane. Out of 281 hearts which were judged to be free of technical failures by conventional physiological indices (heart rate greater than 200/min, cardiac output greater than 34 ml/min, and coronary flow 9-14 ml/min), 43 (15%) disclosed an abnormal NADH-F area prior to the coronary intervention. During coronary intervention, 29 technical failures were detected as indicated by sparse NADH-F distribution with occlusion, delayed disappearance of NADH-F upon reperfusion, or the exhibition of an abnormal NADH-F region unassociated with the coronary artery supply area. These technical failures are not detectable without the use of NADH-F, although the actual number of failures detected may depend on the skill of the operator. We recommend NADH-F monitoring for any preparations which do not contain hemoglobin, since NADH-F is an intrinsic probe for ischemia and is easily applicable to a variety of experiments.

Subacute (7 days) exposure of guinea pigs to 4 ppm NO2 induces transient airway hyperresponsiveness to inhaled histamine (His)-aerosol as does acute exposure to higher concentration of NO2. Thromboxane A2 may play an important role in this transient airway hyperresponsiveness.

The left ventricle was removed from 76 dogs and was cast in silicone, in vitro, under three fixing pressure levels to simulate various end-diastolic pressures. This cast was designated as a silicone cast. The waxen cast was constructed by adding attachments which protrude inside the LV cavity, such as the papillary muscles and trabeculae carneae to the silicone cast. The cast volumes were compared with the volume calculated by the area-length method, including ellipsoid and paraboloid models, and by Chapman's method in which silhouettes of the silicone casts projected on 4 planes were used. Under a lower fixing pressure, the volume of papillary muscles and trabeculae carneae accounted for about 35% of the LV volume which was independent of either size of heart or weight of the dog. This ratio was reduced at higher fixing pressure levels. The relationship between the cast volume and the volume calculated by the silhouette method was linearly proportional. However, the deviation increased with higher fixing pressure levels and with larger ventricular volumes in all calculation methods, indicating the shape of the left ventricle cannot be represented by any ideal symmetrical spherical model. The calculated volume agreed with its corresponding cast volume with an error of less than 10% if either the fixing pressure level was below 5 mmHg, or the volume was less than 50 ml.

In Experiment 1 the donor hearts (group C) perfused for 24 hours with an intracellular-like solution containing perfluorochemicals, calcium antagonist, and albumin were compared with the hearts immersed for 24 hours in an intracellular-like solution to which calcium antagonist was added (group B) and the hearts in which the ischemic time was less than 1 hour (group A) followed by orthotopic heart transplantation. In Experiment 2 perfusates with (group I) and without (group II) perfluorochemicals and albumin were used for 24-hour isolated heart preservation. Periodic assessment of the hearts was performed during the perfusion. Experiment 1: All transplanted hearts started beating spontaneously. There was no statistically significant functional difference between the three groups. At the end of the preservation the creatinine phosphokinase and lactate releases of group C were at lower levels than those in group B. Electron microscopic examination revealed that the myocardium in group B was damaged more severely than in group C. Experiment 2: The level of the creatinine phosphokinase and lactate dehydrogenase released in group I was lower than that in group II. The lactate concentration was at a lower level in group I. At the end of the preservation the pyruvate concentration was higher in group I. The gain in heart weight in group II was more marked than that in group I. The passive compliance decreased only in group II. It is suggested that the perfusion method is superior to the immersion method for 24-hour isolated heart preservation and that the perfusate containing perfluorochemicals and albumin is useful.

The preparation of alcohol extracts from gamma-irradiated potatoes of the "Danshaku" variety and their chemical aspects were studied. The final concentrate of alcohol extracts from potatoes showed pH values of 3-4. The o-quinones or "radiotoxins" reported by Kuzin, et al. were not detected in the alcohol extracts from potatoes of this variety by high performance liquid chromatography (HPLC) analysis, paper chromatography and the model enzymatic experiment.

A recent study has indicated that the generation of an oxygen radical in freeze-clamped myocardium on reperfusion can be directly demonstrated using electron-spin resonance spectroscopy (ESR). However, the results need to be analyzed with caution, since artifactual radicals are misleading problems common to this method. To test whether that reported superoxide is truly the biologically existing radical or an artifactual radical, we performed experiments using isolated, perfused rat and rabbit hearts and open-chest canine hearts subjected to ischemia/reperfusion. Radicals were freeze trapped at 77 degrees K, and ESR measurements were made. The ESR spectra exhibited four free radicals. Among these, two radicals which had been previously claimed as superoxide and a nitrogen-centered radical were shown as mechanically yielded artifactual radicals. These were produced by pulverization of the frozen sample. In artifact-free samples, superoxide could not be detected. The radicals native to the myocardium were identified as coenzyme Q10-. and another radical the species of which remains unclear.

Newborn rats were intracranially inoculated with human adenovirus type 12 within 24 hours after birth and their brains were sequentially investigated by conventional histological techniques and autoradiography to clarify the early process of tumor growth. At the end of the 2nd week atypical cells having bizarre configuration first appeared singly in the tapetum. From the end of the 3rd week small clusters of slightly atypical subependymal cells ("abnormal clusters") appeared in the subependymal area. From the end of the 4th week a few "microtumors" showing compact nodular growth of atypical glial cells were observed among the "abnormal clusters". These early neoplastic changes in the rat brains had close relationship to subependymal cells. The perinatal subependymal cells showed most dense distribution in the subependymal area of lateral ventricle with open ventricular space ("open ventricular area") especially in the region of anterior horn. In contrast, the microtumors and the enlarged tumors were recognized much more in number in the subependymal area of bulbus olfactorius and tapetum where ventricular cavities closed in the young period of maturation ("closed ventricular area"). "Abnormal clusters" were located in both of the areas with more preponderence in the open ventricular area. The reasons for this discrepancy of occurrence were discussed from the viewpoint of environmental factors. Subsequent investigation revealed that the average number of microtumors, after reaching its peak at the end of the 5th week, diminished gradually and, finally, only one or two enlarged tumors were found per each tumor-bearing animal. The mechanisms for this phenomenon are open to further investigation.

Thirty patients received morphine and 27 received ketamine. Morphine anaesthesia did not influence plasma concentrations of luteinizing hormone (LH) significantly, but there was a significant increase during ketamine anaesthesia. Plasma LH increased in the early stage of surgery under both anaesthetics. A significant decrease in the plasma concentration of testosterone was found during and following both techniques of anaesthesia, the lowest concentration being detected on the first day after surgery. Ketamine anaesthesia, but not morphine, stimulated adrenocortical function significantly. Furhter stimulation was detected in the periods during and after operation with both anaesthetic techniques.

A 33-year-old woman whose left ovarian dysgerminoma had been resected presented with left axillar swelling and a right breast tumor about three years after surgery. Histological examination of the mastectomized tumor revealed primary infiltrating carcinoma into the muscle layer and a metastatic ovarian dysgerminoma showing well-defined proliferation. Despite chemotherapy, she died 7 months later of breast cancer. To our knowledge, this is the only reported case of its kind in the world literature.

The results of an autopsy of an 80-year-old Japanese male with acute myeloid leukemia who died of spontaneous rupture of the spleen are reported. The patient was admitted because of anorexia, fatigue, weight loss, and multiple skin eruptions. Hematological examinations indicated a rapid increase in myeloblasts. The patient collapsed on the 28th hospital day, immediately after complaining of severe epigastralgia and vomiting. He died ten hours later. The autopsy revealed extensive leukemic infiltration of the bone marrows, spleen, lymph nodes, skin, and other internal organs. The spleen was enlarged and was ruptured in places at the hilar portion. Massive intraperitoneal hemorrhage from the rupture was the direct cause of death. The mechanisms of splenic rupture are discussed.

The effect of gonadal steroids on basal and GnRH-stimulated hCG release was studied using collagenase-dispersed trophoblast cells from early pregnancy. Both GnRH and a GnRH superagonist, Buserelin, stimulated hCG release with a similar dose dependency. Progesterone (0.1 to 10 micrograms/ml) inhibited GnRH-stimulated hCG release in a dose dependent manner as well as basal hCG release. Relatively high concentrations of estradiol (10 micrograms/ml) stimulated both basal and GnRH-mediated hCG release and antagonized the inhibitory effect of progesterone on hCG release at 1 micrograms/ml as well as RU486 (1 microgram/ml). These results indicate that progesterone has an important role in both basal and GnRH-mediated hCG regulatory system in the placenta.