No abstract available.
Female ; Germ Cells* ; Neoplasms, Germ Cell and Embryonal* ; Ovary*

The effect of temperature on the pH-dependence of actomyosin superprecipitation was studied, using actomyosin extracted from the rabbit and frog skeletal muscle tissues. The pH optima of superprecipitation was rather broad in both the rabbit and frog actomyosin. In the frog, superprecipitation measured at 16-42 degrees C was relatively independent of pH variations between 6.7 to 8.5, but it was significantly inhibited at pHs outside of this range, showing a sharp inflection of the curve. The pH at the inflection point was inversely proportional to the incubation temperature, but the (OH-)/(H+) ratio at the inflection point was not changed with temperature. The log (OH-)/(H+) was approximately -0.6 on the acidic side and 3.16 on the alkaline side. Similarly, superprecipitation of the frog actomyosin was virtually independent of the medium pH of the intermediate range (approximately 6.0-8.5); but it was drastically inhibited at pHs below or above this range, thus revealing a sharp inflection of the curve. Again, the pH at the inflection point changed inversely with temperature, preserving a constant (OH-)/(H+) ratio. The log (OH-)/(H+) ratio at the inflection point was approximately -2 on the acidic side and 3.5 on the alkaline side. The above pH effects were not associated with irreversible protein damage or with the changes in buffer species. These results strongly suggest that suppression of the superprecipitation of rabbit and frog actomyosin gels, at a low and high pH, be due to alterations in the fractional dissociation of histidine-imidazole and cysteine-SH groups, respectively.
Actomyosin* ; Animal ; Calcium/physiology ; Hydrogen-Ion Concentration ; Muscle Contraction ; Precipitation ; Rabbits ; Temperature*

The activity of Mg++-dependent, Ca++-activated adenosine triphosphatase (Ca-ATPase) of rat liver mitochondria was studied at varying medium compositions, pH and temperatures. The enzyme system was characteristically sensitive to Ca++ concentration with a KmCa of approximately 0.06 mM. The optimal concentration of Mg was about l mM, above which the enzyme activity was progressively inhibited. The inhibitory effect of high Mg++ concentrations appeared to be due to the alteration of the Mg++/ATP ratio. Variations in the Mg++/ATP ratio affected Vmax but not the KmATP. The pH optimum for enzyme activity increased as the incubation temperature decreased, but the optimal OH-/H+ ratio of the medium was constant at around 0.1, regardless of temperature. The activity of the enzyme was not affected by La# (0.01-1 mM) and Ruthenium red (2.5-10.0 microM). These results indicate that 1) the enzymatic characteristics of the Ca-ATPase system in the rat liver mitochondria is typical of those from other tissue preparations, 2) the enzyme system maintains the most effective catalytic conformation at a fixed level of OH-/H+ ratio of 0.1 when the temperature changes, and 3) the enzyme system may not play a role in the physiological transport of Ca++ in mitochondria.
Animal ; Ca(2+)-Transporting ATPase/metabolism* ; Calcium/pharmacology ; Enzyme Activation/drug effects ; Female ; Hydrogen-Ion Concentration ; Magnesium/pharmacology ; Male ; Mitochondria, Liver/enzymology* ; Rats ; Temperature

Effects of cadmium (Cd) intoxication on renal endosomal accumulation of organic cations (OC ) were studied in rats using 14C-tetraethylammnium (TEA) as a substrate. Cd intoxication was induced by s.c. injections of 2 mg Cd/kg/day for 2-3 weeks. Renal cortical endosomes were isolated and the endosomal acidification (acridine orange fluorescence change) and TEA uptake (Millipore filtration technique) were assessed. The TEA uptake was an uphill transport mediated by H /OC antiporter driven by the pH gradient established by H -ATPase. In endosomes of Cd-intoxicated rats, the ATP-dependent TEA uptake was markedly attenuated due to inhibition of endosomal acidification as well as H /TEA antiport. In kinetic analysis of H /TEA antiport, Vmax was reduced and Km was increased in the Cd group. Inhibition of H /TEA antiport was also observed in normal endosomes directly exposed to free Cd (but not Cd-metallothionein complex, CdMt) in vitro. These data suggest that during chronic Cd exposure, free Cd ions liberated by lysosomal degradation of CdMt in proximal tubule cells may impair the endosomal accumulation of OC by directly inhibiting the H /OC antiporter activity and indirectly by reducing the intravesicular acidification, the driving force for H /OC exchange.
Animals ; Biological Transport, Active ; Cadmium ; Cations ; Citrus sinensis ; Endosomes* ; Filtration ; Fluorescence ; Ion Transport ; Ions ; Kidney ; Proton-Motive Force ; Rats* ; Tea ; Tetraethylammonium*

PURPOSE: alpha-Ketoglutarate (alphaKG), a Krebs cycle intermediate, is extensively used in the kidney as a fuel substrate and as a counter anion for organic acid secretion. It is known to be taken up by the proximal tubule cells via the brush-border as well as basolateral membranes. We explored biochemical characteristics of the brush-border and basolateral alphaKG transport systems in pars convoluta and pars recta of the proximal tubule, respectively. METHODS: Brush-border and basolateral membrane vesicles (BBMV and BLMV) were isolated from rabbit renal outer cortex and outer medulla by Percoll gradient centrifugation. Vesicular uptake of alphaKG was determined by rapid Millipore filtration method using alpha-14[C]KG as a substrate. RESULTS: Both BBMV and BLMV showed a Na-gradient dependent uphill transport of alphaKG. The systems in both membranes were similarly inhibited by Li and activated by Na (Hill coefficient of 1.4). Kinetic analyses indicated that the Na-alphaKG cotransporters in the BBMV had a lower substrate affinity as compared with those in the BLMV. The transport systems in BLMVs showed a similar Km but different Vmax between the outer cortex (Km: 34 uM, Vmax: 3.3 nmol/mg protein/10s) and outer medulla (Km: 37, Vmax: 1.8). On the other hand, the systems in BBMVs were different in both Km and Vmax between the outer cortex (Km: 194, Vmax: 3.3) and outer medulla (Km: 89, Vmax: 1.7). CONCLUSION: The findings suggest that both axial and apical to basolateral heterogeneity of the Na-alphaKG cotransport system in proximal tubules may be due to a physiological adaptation to efficiently utilize alphaKG in the kidney.
Adaptation, Physiological ; Biological Transport, Active ; Centrifugation ; Citric Acid Cycle ; Filtration ; Hand ; Ketoglutaric Acids ; Kidney Tubules ; Kidney* ; Membranes ; Population Characteristics ; Symporters

Pericarotid syndrome is the combination of a postganglionic Horner's syndrome and ipsilateral head and facial pain, which is caused by diverse pathologic processes in and around the internal carotid artery. We report a case of peri-carotid syndrome which presented Horner's syndrome and ipsilateral periodic severe hemicrania associated with malig-nant lymphma lapping internal carotid artery. After surgical removal of the mass and chemotherapy, miosis, ptosis, and ipsilateral hemicrania improved.
Carotid Artery, Internal ; Drug Therapy ; Facial Pain ; Head ; Headache ; Horner Syndrome ; Lymphoma* ; Miosis ; Pathologic Processes

Hypotensive anesthesia is widely used in an operation since 1) it minimizes bleeding and provides a good operation field, 2) it prevents massive hemorrhage in an operation which otherwise involves a large amount of b1ood loss and 3) it is useful in an operation for hypertensive patients. This procedure also involves a number of risks such as delayed awakening, reactionary bleeding, decrease in urine output and tissue hypoxia. The most dangerous complication can be hypoxia especially in the vital organs. 1t is therefore necessary to treat dehydration or blood loss before hypotensive anesthesia is induced. Since hypotensive anesthesia was introduced by Gardner (1947) for an operation of olfactory groove meningioma, various methods of deliberate hypotension have been developed. The most common method of hypotensive anesthesia in the present day is to use drugs, such as trmetaphan, nitroprusside and halothane. The effect of hypotensive anesthesia an various physiological functions of animals have been investigated is the past. Giffiths and Gillies (1948) reported that, in the hypotension induced by sympathectomy, an arterial systolic pressure of 32 mmHg is the minimum to overcome peripheral resistance. Chung (19743 observed in the halothane-induced hypotensive dogs that a systolic pressure of 30mmHg was required to assure adequate cerebral oxygenation. In the present study, we have investigated the effect of halothanie-induced hypotension on the renal function of dogs. The arterial systolic pressure was successively reduced to 60 and 30mmHg for 30min. each, and changes is various renal functions were studied during 100min. of the recovery period. The results are summarized as follows: 1. The systolic blood pressure was completely reeovered 80min. after the cessation of halothane inhalation. 2. Average renal blood flow Cestimated by Cppe) and glomerular filtration rate (estimated by Cg) during the first 20min. of the recovery phase were 26% ind 45% of the control level. However after 100min. of thy recovery period, repal blood flow was recovered to 63% and glomerular filtration rate to 74%of the control leveL 3. Average urine flow during the first 20min. of that recovery phase was approximately 40% of the control. 4. U/P osm. ratio was reduced to 90% the control level during the first 20min. of recovery, but it exceeded the control value after 20min. of recovery. 5. Thero was only 24% of the-tml value in the first 20min. of receavery phese, but there- after it gradually returned to the control level. 6. FEH2O (fractional excretion of N2) was and significantly changed- by halothane inhalation although there was a tendency to slight reduction at the beginning of the recovery phase. 7. FEK was 47% of the control value dqring ghe initial phase of recovery, but it returned to the control level after 40min. of the recovery period. 8. FE, and FEH2O were reduced to 56% and 50% of the control level after the hypotensive period, but returned to 70% and 82% of the control level after 40min. of the recovery period. These results indicate that although the systemic blood pressure completely recovered after halothane-induced hypotension, renal hemodynamics are not completely recovered with 100min. of the recovery period. However renal functions are mostly reversible, suggesting that halathane -induced hypotension did not induce irreversible damage of renal tissue.
Anesthesia ; Animals ; Anoxia ; Blood Pressure ; Dehydration ; Dogs ; Glomerular Filtration Rate ; Halothane ; Hemodynamics ; Hemorrhage ; Humans ; Hypotension ; Inhalation ; Kidney* ; Meningioma ; Nitroprusside ; Oxygen ; Renal Circulation ; Sympathectomy ; Vascular Resistance