Biomedical subjects
Publications and source records attributed to T Kumazawa.
The pH value and the DC potential in the endolymphatic sac (ES) were measured using H(+)-selective double-barreled electrodes and the intra- and extradural approach, the pH value in the ES fluid (6.65 +/- 0.12, n = 7) was markedly lower than that in the cerebrospinal fluid (7.39 +/- 0.07, n = 7). Acidity in the ES fluid, under normal (nontreated) conditions may be closely associated with metabolism in the epithelium of the ES.
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We investigated electron microscopically the changes of anionic sites of a charge barrier in the capillary basement membrane of the stria vascularis and endolymphatic sac following inner ear immune reactions. Hartley guinea pigs were immunized with bovine type II collagen, keyhole limpet hemocyanin, or horseradish peroxidase, with boosted and challenged antigens through the stylomastoid foramen. Animals were killed painlessly from several days up to 56 days after the antigen challenge. Polyethylenimine was used as a cationic tracer in order to observe the localization of anionic sites of the charge. In the animals immunized with bovine type II collagen or horseradish peroxidase, a significant decrease of anionic charge in the stria and the sac was found in the early stage of immunization. However, the keyhold limpet hemocyanin immunization group did not show any remarkable changes in the charge because of its lesser transfer into the inner ear due to of its high molecular weight and negative surface charge. A decrease of the charge under immunologic conditions may induce a hyperpermeability of vessels and a malabsorption of endolymph, and thus may cause endolymphatic hydrops.
Twenty four spontaneously hypertensive rats (SHRs) were used to assess the influence of anesthetics on myocardial and hepatic energy metabolism after hemorrhage. They were divided into four groups: a control group and three others which received pentobarbital (60 mg.kg-1 ip), 2.2% enflurane, or 1.4% isoflurane. Following a 10-min stabilisation period, blood (2 ml.100 g body weight-1) was gradually withdrawn over a 5-min period from a femoral artery. Thirty minutes after the induction of hemorrhage, the heart and liver were removed, and myocardial and hepatic metabolites (ATP, lactate, pyruvate, and glycogen) were measured by the enzymatic methods. Metabolic acidosis and decreased hematocrit were noted in all groups after hemorrhage. The mean arterial pressure in rats receiving anesthetics decreased significantly in comparison with the control group. There were significant increases of myocardial and hepatic lactate/pyruvate ratios in rats receiving enflurane when compared with controls. These results suggest that enflurane may be more detrimental than other anesthetics to the maintenance of anesthesia in hypovolemic SHRs.
Single, viable taste receptor cells were isolated from the tongue of the guinea pig by enzymatic digestion and mechanical dissociation. The cells could be classified into flask, spindle and intermediate shapes. The intracellular free calcium ion concentrations [(Ca2+)i] of these cells were determined using the Ca2+ sensitive dye fura-2 and digital imaging microscopy. All types of cells produced an irreversible increase in (Ca2+)i upon addition of Ca2+ ionophore ionomycin (1 microM) and denatonium (10 microM). There was no evidence of any increase in (Ca2+)i in the taste receptor cells in nominally Ca2+ free solution, and when stimulated by denatonium (10 microM). When 3 mM CaCl2 was added, the (Ca2+)i remarkably increased. This would suggest that the (Ca2+)i increase in the presence of denatonium mainly depended on calcium influx from the extracellular space. There was no increase in case of high potassium (50 mM and 150 mM) or saccharose (1 mM and 5 mM) stimulation. The hypothesis that the increase in (Ca2+)i controls biochemical mechanisms related to the bitter taste transduction process is worthy of further study.
The effects of several inflammatory mediators on the patency of the Eustachian tube were evaluated in 15 mongrel dogs. Histamine, leukotriene C4(LTC4) and D4(LTD4), and platelet activating factor (PAF) were perfused through the Eustachian tube of anesthetized dogs at concentrations detected in human middle ear effusion of patients with otitis media. The patency of the Eustachian tube was then evaluated by perfusion pressure and opening pressure. Histamine at concentrations of more than 10(-5) M caused increased tubal resistance and opening pressure rapidly. LTC4 and LTD4 caused a rapid increase of tubal resistance and opening pressure at far lower concentrations, i.e. 10(-12) M. Doses of PAF over 10(-9) M may cause an increase in the opening pressure. These results indicate that various inflammatory mediators are capable of affecting the Eustachian tube function.
Olfactory receptor cells were isolated from the nasal mucosa of the guinea pig, using enzymatic digestion and mechanical dissociation. Under a phase-contrast microscope, the cells can be readily distinguished from other tissues, because of morphological characteristics. The intracellular free calcium ion concentrations ([Ca2+]i) of these cells were determined using the Ca2+ sensitive dye fura-2 and digital imaging microscopy. In the presence of 1 microM ionomycin, calcium-ionophore, there was an irreversible increase in [Ca2+]i in all the cells. During prolonged stimulation by 10 mM n-Amyl acetate under standard conditions, 16 of the 40 isolated olfactory cells responded with [Ca2+]i. There was no evidence of any increase in [Ca2+]i in the olfactory receptor cells in nominally Ca2+ free solution and stimulated by amyl acetate. When 3 mM CaCl2 was added, the [Ca2+]i increased remarkably. When cells were stimulated with amyl acetate in a CaCl2-depleted extracellular fluid supplemented with 10 microM verapamil (an L-type voltage-dependent calcium channel antagonist), no change occurred in [Ca2+]i. The addition of CaCl2 to this fluid did not elevate [Ca2+]i, in any cell. This would suggest that the [Ca2+]i increase in the presence of amyl acetate may mainly depend on the influx of calcium from the extracellular space. Our finding that the influx of extracellular calcium into cells was suppressed by verapamil suggests that the calcium channel, which is opened by amyl acetate, is a voltage-dependent L-type Ca2+ channel.
The endolymphatic sac (ES) of the guinea pig was isolated from the remainder of the inner ear by means of surgical interruption of the endolymphatic duct (ED). The DC potential in the ES lumen and the morphology of the ES were studied using glass micro-electrodes and a light microscope at various time intervals after the interruption of ED. The DC potential did not significantly change 1 h postoperatively, compared to findings in the non-operated ear, but a significant decrease of the DC potential was observed after 1, 3 and 7 days postoperatively. A histologically-stainable substance in the ES lumen was enhanced on the operated side. The isolated ES shows a disturbance of mechanism(s) maintaining the DC potential and there is a secretion of a stainable substance into its lumen.
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Twelve elective abdominal surgeries were performed under epidural anesthesia with high dose fentanyl. An epidural catheter was inserted at Th9-Th12 interspace and fentanyl 10 micrograms.kg-1 with [E (+)] or without [E(-)] epinephrine 1:100,000 was given for each group of 6 patients. After the administration of epidural fentanyl, arterial blood was sampled at 5, 10, 15, 30, 60, 120, 180, 240 minutes. The serum concentrations of fentanyl were measured by gas chromatography. The peak concentration of serum fentanyl was observed in the E (-) group, while that was not seen in the E (+) group. The time of reach maximum serum concentration after epidural fentanyl administration in the E (-) group was from 10 to 15 minutes. In two cases of E (-) group, the plasma concentration-time course could be fitted to two-compartment model. The others could be fitted neither to a two-compartment nor to a three-compartment model. In both groups, we could maintain anesthesia with enflurane of less than 0. 4%, and N2O, 66%. It is suggested that analgesic effect of fentanyl on opioid receptor of spinal cord plays a major role in this anesthesia method.
Although suppression of thermoregulatory mechanisms by anesthetics is generally assumed, the extent to which thermoregulatory responses are active during general anesthesia is not known. To evaluate the effect of anesthetics on thermoregulation, we investigated the threshold body core temperatures to induce peripheral cutaneous vasoconstriction and shivering in spontaneously breathing rabbits. Rabbits are anesthetized with halothane at 0.05, 0.2 and 0.4 MAC (minimum alveolar concentration). Internal whole body cooling was performed by perfusing the cool water through an intestinal U-shaped thermode placed in the colon. Core (esophagus) and peripheral (ear) temperatures were measured with thermistors. The esophageal temperatures at the beginning of peripheral cutaneous vasoconstriction and shivering induced by internal whole body cooling were determined. Peripheral cutaneous vasoconstriction was not significantly affected by halothane. However, the incidence of shivering was significantly decreased by halothane dose-dependently. Threshold of shivering (37.3 +/- 0.8 degrees C) was significantly lower than that of peripheral cutaneous vasoconstriction (38.9 +/- 1.1 degrees C). We conclude that the halothane can exert an influence on shivering.
The effects of mexiletine on cardiac function and myocardial metabolism were assessed in the isolated rat heart-lung preparation. Mexiletine 1, 2, 4 or 8 micrograms ml-1 was administered 5 min after the start of perfusion. Heart rate decreased in the 2, 4 and 8 micrograms ml-1 groups significantly following the drug administration. The highest dose of mexiletine reduced cardiac output significantly, and this dose was associated with a higher incidence of dysrhythmias than the other groups. Although there was no significant difference in myocardial glycogen concentration among groups, ATP contents in the 4 micrograms ml-1 and 8 micrograms ml-1 groups were significantly less than in the control group. Lactate contents in the 4 micrograms ml-1 and 8 micrograms ml-1 groups were significantly higher than in the control group. Generally, the therapeutic plasma concentration of mexiletine is 0.5-2.0 micrograms ml-1. These results suggest that mexiletine may have a lesser margin of safety than lignocaine.
We studied the antitumor effect of Carboplatin on the three-dimensional tumor in vitro. First, we observed the three-dimensional growth of cultured tumor cell lines (Hep 2, KB and HT 29 cells), which were developed in the combined culture system of fibrin matrix and agar culture. The tumor cells developed a 3 x 3 mm tumor in diameter in the in vitro 10 day-culture system. This size was large enough to allow the histologic study. When we applied Carboplatin to the three-dimensional tumors, histologic change of the three-dimensional tumor developed from Hep 2 and KB cells were observed in a dose dependent manner. However, no remarkable histologic change was observed in the three-dimensional tumor developed from HT 29 cells. These results suggest the experimental system of three-dimensional tumor can predict histologically the antitumor effect of Carboplatin on various tumors at the solid tumor level.
There are many reports describing how to use epinephrine solution before nasal intubation, but there are few reports showing how much of the nasal cavity is widened by using epinephrine solution. The purpose of this study is to examine the usefulness of epinephrine solution to widen the nasal cavity before nasal intubation by measuring the decrease of the nasal concha. Twenty patients who were scheduled for nasal intubation were divided into two groups: 0.02 percent (1:5000) epinephrine solution (0.02 group, n = 10). 0.033 percent (1:3000) epinephrine solution (0.033 group, n = 10). The solutions were instilled on long cotton-tipped applicators that were slowly inserted until they reached posterior wall of the nasopharynx. We examined the area of the inferior nasal concha on X-P before and after inserting applicators in two groups. The area of the inferior nasal concha on X-P decreased 25 percent and 27 percent after using epinephrine solution in 0.02 group and 0.033 group, respectively and the decreases of the area were significant. But there was no significant difference between two groups. We conclude that 0.02 percent epinephrine solution is useful and adequate to widen the nasal cavity before nasal intubation.
Effects of exogenous prostaglandin (PG) E2 and PGI2 on testicular polymodal receptor activities were compared in in vitro recordings of single- or multi-fiber discharges from canine testis-spermatic nerve preparations. PGI2 up to 1.4 x 10(-6) mol/l (cumulative method) or 1.0 x 10(-5) mol/l (non-cumulative method) excited only weakly some of the receptors, and similar observations were made with PGE2. Both PGs applied cumulatively or non-cumulatively at concentrations above 1.4 x 10(-8) mol/l augmented the response to bradykinin (9.4 x 10(-8) mol/l) in more than half of the cases tested. The augmenting effect of PGE2 lasted longer than that of PGI2 both with the cumulative and the non-cumulative method. The degree of augmentation tended to increase dependent on concentration, but some cases showed no further increase or rather a decrease in augmentation by PGs at a ten times higher concentration, especially when PGs were applied cumulatively. A second challenge by PG after a short interval (2 min) did not induce augmentation. These phenomena were considered to be tachyphylaxis to PGs. Cross-tachyphylaxis to PGE2 and PGI2 was also observed. There was not much difference in excitatory and augmenting potencies between these two PGs, but there was a clear difference in the concentrations of the PGs necessary to induce excitation of polymodal receptors and to facilitate their response to bradykinin.
The effects of prostaglandin I(2) analogues (PGI(2)-a: op-41483 and op-2507) on oxygen toxicity during hyperoxic perfusion were evaluated in an experiment on isolated rat heart lung preparation, with the release of creatine phosphokinase (CPK) in the perfusate blood. There were no significant differences in heart rate and right atrial pressure between PGI(2)-a treated and untreated hearts. The CPK release from the heart with oxygen was significantly higher than that of the air ( P < 0.001). However, the CPK release from the PGI(2)-a treated hearts was significantly less than that from the untreated hearts ( P < 0.05). These results indicate that PGI(2)-a may prevent cell damage which was induced by hyperoxia.