Biomedical subjects

M Yanase-Fujiwara

Publications and source records attributed to M Yanase-Fujiwara.

9 recordsLinked to original sources

PubMed2001

Effects of estrogen on thermoregulatory tail vasomotion and heat-escape behavior in freely moving female rats.

Effects of estrogen on thermoregulatory vasomotion and heat-escape behavior were investigated in ovariectomized female rats supplemented with estrogen (replaced estrogen rats) or control saline (low estrogen rats). First, we measured tail temperature of freely moving rats at ambient temperatures (T(a)) between 13 and 31 degrees C. Tail temperature of the low estrogen rats was higher than that of the replaced estrogen rats at T(a) between 19 and 25 degrees C, indicating that the low estrogen rats exhibit more skin vasodilation than the replaced estrogen rats. There was no significant difference in oxygen consumption and core temperature between the two groups. Second, we analyzed heat-escape behaviors in a hot chamber where rats could obtain cold air by moving in and out of a reward area. The low estrogen rats kept T(a) at a lower level than did the replaced estrogen rats. These results imply that the lack of estrogen facilitates heat dissipation both by skin vasodilation and by heat-escape behavior. Ovariectomized rats may mimic climacteric hot flushes not only for autonomic skin vasomotor activity but also for thermoregulatory behavior.

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PubMed2001

Hypothalamic region facilitating shivering in rats.

Although the posterior part of the hypothalamus has long been considered important for thermoregulatory shivering, it is unknown whether the neurons there or the passing fibers are implicated in the response. Exposure of urethane-anesthetized rats to cold (15-21 degrees C) elicits shivering. An injection of muscimol (0.5 mM), a GABA(A) receptor agonist, into the medial part of the hypothalamus, including the dorsomedial and posterior nuclei, suppressed the cold-induced shivering. This result suggests that neurons having an excitatory effect on shivering are in this region of the hypothalamus.

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PubMed1997

Effect of midbrain stimulations on thermoregulatory vasomotor responses in rats.

1. Efferent projections eliciting vasodilatation when the preoptic area is warmed were investigated by monitoring tail vasomotor responses of ketamine-anaesthetized rats when brain areas were stimulated electrically (0.2 mA, 200 microseconds, 30 Hz) or with the excitatory amino acid D,L-homocysteic acid (1 mM, 0.3 microliter). 2. Both stimulations elicited vasodilatation when applied within a region extending from the most caudal part of the lateral hypothalamus to the ventrolateral periaqueductal grey matter (PAG) and the reticular formation ventrolateral to the PAG. 3. Vasodilatation elicited by preoptic warming was suppressed when either stimulation was applied within the rostral part of the ventral tegmental area (VTA). 4. Sustained vasodilatation was elicited by knife cuts caudal to the VTA, and vasodilatation elicited by preoptic warming was suppressed by cuts either rostral to the VTA or in the region including the PAG and the reticular formation ventrolateral to it. 5. These results, together with the results of earlier physiological and histological studies, suggest that warm-sensitive neurones in the preoptic area send excitatory signals to vasodilatative neurones in the caudal part of the lateral hypothalamus, ventrolateral PAG and reticular formation, and send inhibitory signals to vasoconstrictive neurones in the rostral part of the VTA.

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PubMed1997

Effect of gonadotropin releasing hormone on thermoregulatory vasomotor activity in ovariectomized female rats.

To investigate the effect of gonadotropin releasing hormone (GnRH) on thermoregulatory skin vasomotion, we injected GnRH into various brain regions in both anesthetized and unanesthetized ovariectomized female rats. Local warming of preoptic area (PO) elicited skin vasodilation in anesthetized rats. Injection of 2 microg GnRH into the septal area lowered the threshold hypothalamic temperature for skin vasodilation at least for 2 h. Similar injections of 2 microg GnRH into the lateral ventricle (LV) and PO were ineffective. Although this vasodilative effect was also obtained after the injection of 20 ng GnRH into the septal area, injections of 2 ng GnRH were without effect. Not only injections of 20 ng Antide, a potent GnRH antagonist, but also injections of the mixed solution of 20 ng GnRH and 20 ng Antide were also without effect. In unanesthetized and unrestrained rats at an ambient temperature of 17 degrees C, injections of 20 ng GnRH into the septal area elicited tail vasodilation lasting for 30 minutes, whereas vehicle injections were ineffective. Injections of 20 ng GnRH into LV and PO were also ineffective. These results indicate that GnRH can elicit thermoregulatory skin vasomotion by acting on GnRH receptors in the septal area. This thermoregulatory vasodilative effect of GnRH might be possibly related to the etiology of climacteric hot flush.

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PubMed1995

Warm and cold signals from the preoptic area: which contribute more to the control of shivering in rats?

1. To find out whether the thermosensitive neurones in the preoptic area that control shivering are predominantly warm or cold sensitive, we tested the effects of injecting the excitatory amino acid L-glutamate at various sites in and adjacent to the preoptic area of anaesthetized rats shivering at ambient temperatures of 15-21 degrees C. 2. L-Glutamate injections (0.2 mM in 0.5-1.0 microliter), as well as preoptic warming and electrical stimulation, suppressed shivering, whereas control saline injections had no effect. Effective sites were restricted to the anterior part of the preoptic area, and a tenfold lower concentration of L-glutamate did not influence shivering. 3. Injections of procaine (0.2 M) into the sites where L-glutamate suppressed shivering did not affect strong shivering activity, but facilitated shivering in three out of seven cases when shivering was weak or absent at higher ambient temperatures (25-30 degrees C). 4. L-Glutamate injections, as well as preoptic warming and electrical stimulation, also elicited vasodilatation of the paw skin and the tail. Procaine elicited vasoconstriction when it was applied during vasodilatation induced by local preoptic warming. 5. These results indicate that the contribution of the preoptic area to the control of shivering and vasomotion is influenced more by signals from warm-sensitive neurones than by signals from cold-sensitive neurones.

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PubMed1994

Hypothalamic network for thermoregulatory shivering.

Warming one side of a rat's preoptic area and anterior hypothalamus (POAH) suppresses shivering on both sides of the body, and the present study evaluated the extent to which signals mediating this suppression cross the midline within and below the POAH. Hind paw shivering during unilateral POAH thermal stimulation was measured for rats in which the POAH had been midsagittally transected and for rats in which one side of the hypothalamus had been coronally transected just caudal to the POAH. In midsagittally transected rats, unilateral warming on either side of the POAH suppressed shivering equally on both sides of the body. In unilaterally transected rats, POAH warming on the transected side did not affect shivering, but warming the intact side suppressed shivering equally on both sides of the body. When a unilateral transection of only the lateral part of the hypothalamus included the medial forebrain bundle, the effect was the same as that of a unilateral transection of the whole hypothalamus. These results indicate that no information controlling shivering is exchanged between the left and right POAH and that efferent signals from the POAH, descending through the medial forebrain bundle, cross the midline somewhere below the hypothalamus to innervate both sides of the body equally.

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PubMed1994

Hypothalamic network for thermoregulatory vasomotor control.

Warming one side of a rat's preoptic area and anterior hypothalamus (POAH) causes skin vasodilation on both sides of the body, and the present study evaluated the extent to which signals mediating this vasodilation cross the midline within and below the POAH. Hind paw vasomotion during unilateral POAH thermal or electrical stimulation was measured for rats in which the POAH had been midsagittally transected and for rats in which one side of the hypothalamus had been coronally transected just below the POAH. In midsagittally transected rats, unilateral POAH thermal or electrical stimulation produced bilateral paw vasodilation, but the ipsilateral dilation occurred at a hypothalamic temperature lower than that at which contralateral dilation occurred. In the unilaterally transected rats, unilateral POAH warming produced bilateral vasodilation and, regardless of which side of the POAH was warmed, the threshold stimulus temperature was always lower for vasodilation on the intact side. Unilateral transection of a part of the hypothalamus that included the medial forebrain bundle had the same effect as did unilateral transection of the whole hypothalamus. Information controlling thermoregulatory vasomotion thus crosses the midline both within and below the POAH. Although efferent signals descending through the medial forebrain bundle innervate skin blood vessels on both sides of the body, this innervation is stronger on the ipsilateral side.

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PubMed1993

Marked reduction of acyl-CoA synthetase activity and mRNA in intra-abdominal visceral fat by physical exercise.

Several reports have suggested that the reduction of intra-abdominal visceral fat after physical exercise is more prominent than that of subcutaneous fat. We compared some parameters in mesenteric and subcutaneous fats between sedentary and exercised rats (treadmill running; 10-20 m/min, 60 min/day, 7 days). Tissue weight and cell volume were decreased in mesenteric fat by the exercise. The exercise reduced activity and mRNA levels of acyl-CoA synthetase (ACS; 67 and 26% of those of the sedentary group, respectively), mRNA levels of lipoprotein lipase (LPL; 49% of those of the sedentary group), and GLUT-4 (38% of those of the sedentary group) in the mesenteric fat. In contrast, all of these parameters did not change significantly in the subcutaneous fat. Gastrocnemius muscle was heavier in exercised rats. ACS activity was elevated in the gastrocnemius muscle of the exercised rats (137% of those of sedentary group), although mRNA levels of ACS, LPL, and GLUT-4 did not change in the muscle by the exercise. These observations suggest that mesenteric fat may contribute to switching of distribution of plasma energy flux, including lipid and glucose, from fat tissue to muscle in physical exercise.

Abdomen↗

PubMed1993

Effects of centrally and systemically administered indomethacin on body temperature in exercising rats.

Subcutaneous and intracerebroventricular (icv) injections of indomethacin were used to test whether prostaglandin synthesis is essential for the exercise-induced increase in a rat's body temperature. At an air temperature of 24 degrees C, male Wistar rats ran on a treadmill at 10-15 m/min 20 min after 300-micrograms icv injection or 60 min after 15-mg/kg sc injection of indomethacin or of control vehicle. The rectal temperature (Tre) of control rats in 17 control experiments increased by 1.0 degree C during exercise, whereas the Tre of the rats pretreated with intracerebroventricular indomethacin increased by only 0.4 degrees C. Threshold Tre for tail vasodilation was significantly lower in rats pretreated with indomethacin than the control rats (38.4 +/- 0.1 vs. 38.9 +/- 0.1 degrees C), but O2 uptake did not differ between indomethacin-pretreated and control rats. Subcutaneous injection of indomethacin did not affect the body temperature, tail vasomotor activity, or O2 uptake of exercising rats. Intracerebroventricular indomethacin did not affect Tre or tail vasomotor activity of rats resting at ambient temperatures of 24 and 28 degrees C. Present results suggest that prostaglandin synthesis is required for the vasoconstrictive effect of exercise on skin blood vessels and thus for the exercise-induced elevation of body temperature.

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