Biomedical subjects

K T Sato

Publications and source records attributed to K T Sato.

7 recordsLinked to original sources

PubMed1996

Reexamination of tympanic membrane temperature as a core temperature.

Controversies surrounding tympanic temperature (Tty) itself and techniques for measuring it have dampened the potential usefulness of Tty in determining core temperature (operationally defined here as the body temperature taken at a deep body site). The present study was designed to address the following questions. 1) Can a tympanic membrane probe be made that is safer and more reliable than its predecessors? 2) Why is the effect of facial cooling and heating on Tty so inconsistent in reports from different laboratories? 3) Is Tty still useful as a measure of core temperature? Data from this study, obtained with a modified thermocouple probe, suggest that the widely reported facial skin cooling effect on Tty is most probably due to thermal contamination from the surrounding ear canal wall and/or suboptimal contact of the probe sensor with the tympanic membrane because 1) Tty that fell during facial cooling was increased to the precooling level by the repositioning of the probe sensor; 2) Tty determined by using a probe with a larger sensor area (the sensor soldered to a steel wire ring)tended to fall in response to facial cooling, whereas Tty determined with a thermally insulated probe ring did not; and 3) Tty obtained under careful positioning of the insulated probe was relatively insensitive to facial cooling or heating. Because Tty was practically identical to esophageal temperature (Tes) in the steady state, i.e., 36.83 +/- 0.20 (SD) degrees C for Tty and 36.87 +/- 0.16 degrees C for Tes at room temperature (n = 11), and because facial cooling had little effect on both Tty and Tes (36.86 +/- 0.17 degrees C for Tty and 36.86 +/- 0.26 degrees C for Tes during facial or scalp skin cooling), we support the postulate that Tty is a good measure of core temperature. The temperature transient in response to foot warming was detected 5 min (n = 2) faster with Tty than with Tes. Thus, with further improvements in the design of the probe. Tty can become a standard for determination of core body temperature.

Adult↗

PubMed1994

Secretion of ions and pharmacological responsiveness in the mouse paw sweat gland.

1. Some of the basic functional features of the mouse paw eccrine sweat gland were delineated to allow comparison with those of transgenic mice in the future. 2. The mouse sweat secretory coil responds to methacholine, elaborating a K(+)-rich (> 120 mmol/l), Na(+)-poor (< 70 mmol/l) primary fluid as does the rat paw sweat gland, as previously reported. The methacholine-induced sweat rate increases with age in parallel with the growth of the sweat gland over the first 6 weeks of life. 3. The sweating response to cyclic AMP-elevating agents, such as isoprenaline or forskolin, is as much as 40% of the methacholine-induced sweat rate at 1 week of age, but falls to 10% by 6 weeks of age despite the fact that the agonist-induced tissue accumulation of cyclic AMP expressed on a per microgram of protein basis triples with age over the same period. 4. A marked K+ outflux was also noted in response to methacholine and a small K+ outflux was seen in response to cyclic AMP-elevating agonists in superfused adult mouse secretory coils in vitro. 5. Since sweat secretion is usually associated with activation of either K+ channels or Cl- channels or both, and since the sweating occurred in response to cyclic AMP-elevating agonists, we speculate that the cyclic AMP-activated Cl- channels (the mouse version of the cystic fibrosis transmembrane conductance regulator) may also occur in the mouse sweat gland, but that the degree of their expression may be influenced by the age of the mice.

Aging↗

PubMed1991

Roles of Ca and cAMP on C1 channel activity in cystic fibrosis sweat clear cells as studied by microsuperfusion and cell volume analysis.

In an attempt to study regulation of C1 channels in intact sweat secretory coils in cystic fibrosis and controls in the least invasive manner, isolated secretory coils were superfused with various drugs and K-efflux was determined as an indirect measure of C1 movement. C1 channel activity was also determined from the drug-induced cell volume increase in gramicidin (GC)-treated dissociated eccrine clear cells. We observed that while MCh-induced K-efflux from the CF secretory coils was entirely normal, K-efflux in the presence of isoproterenol (ISO), forskolin (FK), or IBMX was absent in CF, suggesting that these agents failed to stimulate C1 movement. C1 channel activity of dissociated CF clear cells, as studied by cell volume analysis, was entirely normal when stimulated by Ca-elevating agents but was defective when stimulated by cAMP-elevating agents. TPA (phorbol ester) does not appear to stimulate C1 channel activity nor does it modify the effect of other agents. The following observations from the present and previous studies are not necessarily consistent with the traditional thesis that the observed C1 movement is due to cAMP: CT-cAMP had no effect on cell swelling or on K-efflux; ISO is more potent in accumulating tissue cAMP than IBMX yet the latter is more potent in stimulating K-efflux; IBMX increases cytoplasmic [Ca] yet is unable to stimulate K-efflux in CF; K-efflux stimulated by cAMP-elevating agents was inhibited by removal of Ca from the bath; and, cell swelling of GC-treated cells in response to cAMP elevating agents was inhibited by removal of Ca. The inability of IBMX to stimulate C1 channels in the face of elevated cytoplasmic [Ca] and cAMP in CF cells deserves further scrutiny.

1-Methyl-3-isobutylxanthine↗

PubMed1991

Movement of cellular ions during stimulation with isoproterenol in simian eccrine clear cells.

The ionic mechanism of beta-adrenergic sweating is unknown. In isolated rhesus eccrine secretory coils, K efflux was determined by an extracellular K electrode and cellular monovalent ions by X-ray microanalysis. Isoproterenol (Iso) induced a small (dose-dependent propranolol-inhibitable) K efflux followed by net K reuptake. Similar K response was seen with forskolin, theophylline, or isobutyl-methylxanthine (IBMX). The net K uptake often exceeded the net K efflux, causing a small net accumulation of K. Bumetanide (BT) and ouabain not only abolished the Iso (with or without IBMX) -induced net K uptake but increased the Iso-induced initial K efflux about threefold. BT and ouabain drastically decreased K and Cl concentrations in the clear cell (by X-ray microanalysis) only in the presence of Iso plus IBMX, suggesting that adenosine 3',5'-cyclic monophosphate (cAMP) may simultaneously stimulate both KCl efflux (by unknown mechanisms) and K reuptake (presumably by BT-sensitive cotransporters and ouabain-sensitive Na pumps). Thus the cAMP-mediated ion movement is different from the cholinergic mechanism that is characterized by the net KCl loss, cell shrinkage (Saga et al., J. Membr. Biol. 107: 13-24, 1989; Takemura et al., J. Membr. Biol. In press), and no augmentation of methacholine-induced K efflux by BT or ouabain.

1-Methyl-3-isobutylxanthine↗

PubMed1989

Biology of sweat glands and their disorders. I. Normal sweat gland function.

The basic mechanisms of sweat gland function and an updated review of some relatively common disorders of sweat secretion, are presented. Although sweat secretion and ductal absorption are basically biophysical and biologic cellular processes, a detailed description of the basic biophysical principles of membrane transport has been avoided to make the discussion more readable. The cited references will, however, help those readers primarily interested in the basic details of sweat gland function. Part I of this article includes a discussion of morphologic characteristics, central and peripheral nervous control of sweat secretion, neurotransmitters, intracellular mediators and stimulus secretion coupling, Na-K-Cl cotransport model for the ionic mechanism of sweat secretion, ingredients of sweat, ductal function, the pathogenesis of abnormal sweat gland function in cystic fibrosis, and the discovery of the apoeccrine sweat gland. Part II, to be published in the May issue of the Journal, reviews reports of all those major disorders of hyperhidrosis and hypohidrosis that have appeared in the literature during the past 10 years. It is hoped that this review will serve as a resource for clinicians who encounter puzzling disorders of sweating in their patients, as well as for investigators who wish to obtain a quick update on sweat gland function.

Humans↗

PubMed1989

Biology of sweat glands and their disorders. II. Disorders of sweat gland function.

Part I of this article (J Am Acad Dermatol 1989; 20:537-63) focused on normal sweat gland function. Part II provides a discussion of hyperhidrosis and hypohidrosis. Hyperhidrotic disorders affect the palms and soles and the axillae and are associated with previous spinal cord injuries, peripheral neuropathies, brain lesions, intrathoracic neoplasms, systemic illness, and gustatory sweating. Hypohidrotic disorders include anhidrotic ectodermal dysplasia, hereditary sensory neuropathy, Holmes-Adie syndrome, and generalized anhidrosis.

Humans↗

PubMed1988

One-step iodine starch method for direct visualization of sweating.

Despite recent progress in eccrine sweat gland physiology, simple, safe and reliable methods of visualizing local and generalized sweating are not available for clinicians and physiologists. We developed a simple one-step method for visualizing sweating that requires only soluble starch previously treated with iodine. When the powder is sprayed on the skin, sweat droplets are visualized as discrete dark purple dots. Since visualized dots are easily wiped off without staining the skin, sweating patterns can be obtained consecutively on the same skin site. The method is far superior to the classical Minor's method and is useful for clinical diagnosis of disorders of sweating and for visualization of the total body sweating for physiological studies. Two simple devices for spraying powder also have been presented.

Female↗