Stimulation of 5-hydroxytryptamine nerve cells in dorsal and median raphe nuclei elevates blood glucose in rats

The role played by dorsal or median raphe nuclei in glucoregulation was investigated by stimulating these nuclei in normal rats and in rats with chemical ablation of the hydroxytryptamine (5-HT) nerve cells in these nuclei. Electrical stimulation of either dorsal or median raphe nuclei increased blood glucose or the in vivo voltammetric signal of hypothalamic 5-OH-indole in normal rats; the increase in blood glucose level or the hypothalamic 5-OH-indole release was proportional to the intensity of stimulation. Microinjection of kainic acid or l-glutamate at the same sites also produced hyperglycemia or stimulated the hypothalamic 5-OH-indole release. This stimulation-induced hyperglycemia was significantly reduced by pretreatment of animals with spinal transection or adrenalectomy. In addition, selective destruction of the hypothalamic 5-HT nerve fibers, produced by administration of 5,7-di-hydroxytryptamine (a 5-HT nerve depletor) into both dorsal and median raphe regions, reduced the magnitude of the hyperglycemic responses to electrical stimulation of either dorsal or median raphe nuclei. The data indicate that stimulation of ascending 5-HT pathways in the rat's brain increases the adrenal-sympathetic efferent activity and leads to hyperglycemia.     

Hypothalamic modulation of energy expenditure

The acute effects of electrical stimulation of the hypothalamus on energy expenditure as measured by indirect calorimetry were investigated in 20 unanaesthetized rats. Thirty sec of stimulation increased both O2 consumption and respiratory quotient (R.Q.). The largest magnitude hypermetabolic response (39% mean peak increase in O2 consumption) was produced by stimulation of the ventromedial hypothalamic nucleus. Stimulation of the lateral hypothalamus produced hypermetabolic effects similar to but smaller than those produced by medial stimulation. A number of considerations suggest that the hypermetabolism is not secondary to changes in motor activity, carbohydrate utilization or blood glucose levels. Consequently, these data suggest that the hypothalamus modulates energy expenditure through changes in non-shivering thermogenesis. These metabolic changes may modulate the effects of various hypothalamic manipulations on body weight.     

Glucose-dependent changes in alpha 2-noradrenergic receptors in hypothalamic nuclei

Evidence indicates that hypothalamic norepinephrine (NE), acting via alpha 2-noradrenergic receptors, and also circulating glucose both have an important role in the control of normal feeding behavior in rats. In this report, we studied the relationship between glucose and the alpha 2-noradrenergic system, by manipulating blood glucose levels and analyzing changes in the binding of [3H]p-aminoclonidine [( 3H]PAC) to alpha 2-noradrenergic receptors in discrete hypothalamic areas. Brief periods (1-3 hr) of food deprivation, at the onset of the dark cycle, produced a significant decline in serum glucose levels and a simultaneous decrease in alpha 2-receptor binding sites, specifically in the hypothalamic paraventricular nucleus (PVN) as opposed to other hypothalamic areas. Restoration of circulating glucose levels, by refeeding for 0.5 hr after 2.5 hr food deprivation or by administration of glucose to 1 hr food-deprived rats, prevented this decline in serum glucose, as well as the reduction in PVN alpha 2-noradrenergic receptor density. In each of these experiments, a strong positive correlation between circulating glucose levels and PVN alpha 2-noradrenergic receptor sites was obtained. These findings suggest that blood glucose has direct impact upon alpha 2-noradrenergic receptor activity in the PVN and may affect feeding behavior, in part, through this neurochemical system.     

An L-dopaergic relay from the posterior hypothalamic nucleus to the rostral ventrolateral medulla and its cardiovascular function in anesthetized rats.

We have proposed that L-3,4-dihydroxyphenylalanine (L-DOPA) is a neurotransmitter in the central nervous system [Misu Y. et al. (1996) Prog. Neurobiol. 49, 415-454]. Herein, we attempt to clarify whether lesions in the posterior hypothalamic nucleus decrease the tissue content of L-DOPA in the rostral ventrolateral medulla. We also attempt to clarify whether or not endogenous L-DOPA is evoked by electrical stimulation of the posterior hypothalamic nucleus. It is possible that evoked L-DOPA functions as a transmitter candidate to activate pressor sites of the rostral ventrolateral medulla in anesthetized rats. Electrolytic lesions were made in the bilateral posterior hypothalamic nucleus by a monopolar direct current of 2 mA for 10 s, 10 days before measurements. The effect of the lesions was to selectively decrease the tissue content of L-DOPA by one-half in the right rostral ventrolateral medulla. Decreases in the amounts of dopamine, noradrenaline or adrenaline were not observed. Decreases were also not evident in the right caudal ventrolateral medulla. During microdialysis of the right rostral ventrolateral medulla, extracellular basal levels of L-DOPA and three types of catecholamine were consistently detectable by high-performance liquid chromatography with electrochemical detection. Tetrodotoxin (1 microM) perfused into the right rostral ventrolateral medulla gradually decreased basal levels of L-DOPA by 25%; it decreased basal levels of noradrenaline and adrenaline by 25-30% and dopamine levels by 40%. Intensive electrical stimulation of the ipsilateral posterior hypothalamic nucleus (50 Hz, 0.3 mA, 0.1 ms duration, twice for 5 min at an interval of 5 min) selectively caused the release of L-DOPA in a repetitive and constant manner. The stimulation was accompanied by hypertension and tachycardia. However, catecholamines were not released. Tetrodotoxin suppressed the release of L-DOPA, but partially inhibited hypertension with only a slight inhibition of tachycardia evoked by stimulation of the posterior hypothalamic nucleus. L-DOPA methyl ester, a competitive L-DOPA antagonist, was bilaterally microinjected into pressor sites of the rostral ventrolateral medulla at 1.5 microg x 2 and 3 microg x 2. The antagonist dose-dependently and consistently antagonized pressor and tachycardiac responses to mild transient stimulation of the unilateral posterior hypothalamic nucleus (33 Hz, 0.2 mA, 0.1 ms duration, for 10 s). In addition, the antagonist alone (3 microg x 2) elicited hypotension and bradycardia. These results show that an L-DOPAergic relay may project from the posterior hypothalamic nucleus directly to pressor sites of the rostral ventrolateral medulla and/or indirectly to certain neurons near pressor sites in microcircuits of the same region. When released, L-DOPA appears to function tonically to activate pressor sites; it also appears to be involved in the maintenance and regulation of blood pressure and heart rate.     

Sympathetic hyperresponsiveness to hypothalamic stimulation in young hypertensive rats.

The possible occurrence of central sympathetic dysfunction during development of spontaneous hypertension was studied by recording aortic pressure and sympathetic nerve activity concurrently during electrical stimulation of the posterior hypothalamus in 9-wk-old Kyoto-Wistar rats. Even at this early age, basal levels for both measurements were already elevated significantly in those with spontaneous hypertension. Increases in sympathetic neural firing induced by graded hypothalamic stimulation were always followed by corresponding increases in blood pressure; magnitude of both effects was appreciably larger in spontaneously hypertensive than in normotensive rats, as was the vasodepression caused by blocking autonomic ganglia with pentolinium. By contrast, pressor responses to injected norepinephrine were almost equal thereby suggesting that cardiovascular reactivity was unaltered and that enhanced responsiveness to hypothalamic stimulation was directly due to the concomitant increase in sympathetic nerve activity. Although the exact site from which sympathetic hyperactivity originates was unidentified, our results support the interpretation that sympathetic mechanisms involving the posterior hypothalamus participate in elevating blood pressure during development of spontaneous hypertension in rats.     

Escape from rewarding brain stimulation of dorsal brainstem and hypothalamus

Each of 9 albino rats had two bipolar electrodes aimed at lateral hypothalamic and either of two dorsal brainstem (dorsal raphe or locus coeruleus) sites. Every rat bar-pressed for stimulation at each electrode. Then, each animal learned to treadle-press to escape from passive electrical stimulation at each elctrode site. All animals learned to escape from first dorsal brainstem and then lateral hypothalamic stimulation at current intensities which also supported self-stimulation behavior. Animals appeared hyperactive under lateral hypothalamic stimulation (active or passive), but not under dorsal brainstem stimulation.     

Dissociating the determinants of self-stimulation

Four experiments were conducted to elucidate the determinants of the initiation of and escape from electrical stimulation of the lateral hypothalamus under several different reinforcement schedules. The first experiment of this series used correlational and factor analytic techniques to show that, under continuous reinforcement, the vigour of initiation is determined more by forcement than by positive reinforcement. Forcement is defined as all of the performance changes directly elicited and potentiated by the stimulation. Escape is determined by adaptation of positive reinforcement, not by negative reinforcement or aversion. Continuous reinforcement schedules are, therefore, not appropriate for studying either the positive or negative reinforcement produced by brain stimulation. The second experiment used fixed-interval reinforcement schedules to eliminate the effects of forcement on initiation and adaptation of positive reinforcement on escape. Parametric manipulations indicate that activity in the positive reinforcement and escape systems is a simple function of stimulation charge. The combination of parameters which make up a given charge is of relatively little importance. However, the positive reinforcement system becomes maximally activated at far lower charges than does the escape system. The third experiment used a T-maze technique to show that, after 5 sec, anterior hypothalamic stimulation becomes negatively reinforcing, but posterior hypothalamic stimulation does not. Since the escape from posterior hypothalamic stimulation on a fixed-interval schedule can be dissociated from both negative reinforcement and adaptation of positive reinforcement, it is suggested that such escape is reinforced by a positive process triggered by the offset of stimulation (OFF positive reinforcement). The fourth experiment showed that stimulation trains longer than 10 sec are significantly less positively reinforcing than much shorter trains. This reduction in positive reinforcement confirms the development of negative reinforcement in long trains of hypothalamic stimulation, even at posterior electrodes. Negative reinforcement appears to be as general a property of hypothalamic stimulation as is positive reinforcement. Thus, depending on the reinforcement schedule and electrode site, the initiation of lateral hypothalamic stimulation may be determined by ON positive reinforcement, OFF positive reinforcement and forcement. Escape may be determined by OFF positive reinforcement, adaptation of positive reinforcement and negative reinforcement.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of midbrain reticular formation,hippocampal, and lateral hypothalamic stimulation upon recovery from neophobia and taste aversion learning

In a neophobia paradigm midbrain reticular formation (MRF) electrical stimulation applied after consumption of a novel flavor produced a time-dependent disruption in recovery from neophobia (learned safety), while hippocampal and lateral hypothalamic stimulation had no disruptive effects. In a learned aversion paradigm neither MRF nor hippocampal or lateral hypothalamic stimulation applied after the illness experience produced a disruptive effect. In conjunction with previously reported effects of amygdala stimulation [12] the data support the existence of separate information processing systems mediating learned aversion and learned safety.     

Biphasic modulation of spinal visceral nociceptive transmission from the rostroventral medial medulla in the rat

Descending inhibitory and facilitatory influences from the rostroventral medulla (RVM) on responses of lumbosacral spinal neurons to noxious colorectal distension (CRD, 80 mmHg, 20 s) were studied. At 25 sites in the RVM, electrical stimulation produced biphasic effects, facilitating responses of spinal neurons to CRD at lesser intensities of stimulation (5-25 microA) and inhibiting responses of the same neurons at greater intensities of stimulation (50-100 microA). At 38 other sites in the RVM, electrical stimulation produced only intensity-dependent inhibition of neuron responses to CRD. At another 13 sites in the RVM, electrical stimulation (5-100 microA) produced only facilitatory effects on responses to CRD. Descending modulatory effects were selective for distension-evoked activity; spontaneous activities of the same spinal neurons were not significantly affected by electrical stimulation that either facilitated or inhibited neuron responses to CRD. Neuron responses to graded CRD (20-100 mmHg) were positively accelerating functions that were shifted leftward or rightward, respectively, by lesser, facilitatory intensities or greater, inhibitory intensities of RVM stimulation. L-glutamate microinjection into the RVM replicated the effects of electrical stimulation, producing similar biphasic modulatory effects as produced by electrical stimulation. Microinjection of glutamate into the RVM at a low dose (5 nmoles) facilitated responses of spinal neurons to CRD and inhibited responses of the same neurons at a greater dose (50 nmoles). In some experiments, microinjection of lidocaine (0.5 microl of 4% solution) or the neurotoxin ibotenic acid (0.5 microl, 10 microg) into the RVM produced reversible or long-lasting, respectively, decreases in spontaneous activity and responses of spinal neurons to CRD. These results reveal that spinal visceral nociceptive transmission is subject to a tonic descending excitatory influence from the RVM and that descending modulatory effects from the RVM on visceral nociceptive transmission are qualitatively similar to modulation of cutaneous nociceptive transmission.     

Preabsorptive insulin release and hypoglycemia in rats.

Peripheral blood glucose and immunologically reactive insulin levels were determined in freely moving normal rats which were submitted either to a free oral glucose load or to a gastric administration of the glucose load. Identical determinations were performed in ventromedial hypothalamic nucleus-(VMH) lesioned and vagotomized rats after the same oral intake. It was demonstrated that: 1) a free oral glucose intake was immediately followed by two peaks of insulun release and a resultant decrease in blood glucose; 2) a gastric glucose load resulted in a single peak of insulin release and the concomitant decline in blood glucose; 3) the recorded blood glucose level was the resultant of the insulin-induced hypoglycemia and the postabsorptive hyperglycemia; and 4) the responses were largely exaggerated in VMH-lesioned rats and abolished by vagotomy. It is concluded that the early prandial insulin release reflexly induced by food-related stimuli temporarily enhances the metabolic conditions which provoke feeding.     

Involvement of a humoral factor in regulation of body weight in parabiotic rats.

Excessive food intake and obesity was induced in one member of parabiotic pairs by electrical stimulation (three 30-min sessions/day for 2 wk) of the lateral hypothalamus (LH). The nonstimulated partners reduced spontaneous food intake the fatter the stimulated animals became. This reduced food intake resulted in a decreased body weight, fat content, and fat-free solid body mass. The decrease of food intake was not due to changed social behavior of the obese partner. It must be attributed to transmission of a humoral satiety factor. The very first stimulation of the LH in the stimulated partners resulted in a large increase in blood glucose and glucagon level without much change in the insulin level. These changes in blood parameters were probably due to strong sympathetic arousal. In the nonstimulated animals there were practically no changes in these parameters. One week of fattening resulted in increased basal glucose and insulin levels in the stimulated animals and decreased glucose levels in the nonstimulated partners, in which the basal insulin levels remained nearly normal. Basal glucagon levels were the same in both partners and did not differ from the prefattening situation. At that time during stimulation the obese animals showed a large increase in glucose and glucagon levels and a decrease in insulin level. On the other hand the nonstimulated animals showed a slow gradual increase in glucose and insulin level due to transmission from their fat partners because of the large gradient in these substances between the animals. These phenomena were still more pronounced after 2 wk of fattening. It is tentatively concluded that the humoral satiety factor is neither circulating insulin nor glucagon nor one of the major circulating nutrients.     

The effects of chronic ventromedial hypothalamic stimulation on weight gain in rats

The effects of chronic stimulation of the ventromedial hypothalamus and adjacent structures on body weight, food intake, and epididymal fat pad weight were examined in normophagic rats. Three hours of intermittent low level electrical stimulation were delivered threetimes per week for four weeks; body weight and food intake were monitored for an additional ten days after stimulation trials had ceased. Animals receiving ventromedial hypothalamic stimulation had the shallowest growth curves while stimulation of other structures produced a rate of growth that fell between that of the ventromedial hypothalamic and the implanted control group. This pattern persisted during the poststimulation phase. Food intake, while initially depressed in the stimulated groups, began to approach control levels by the third week of stimulation. Efficiency of food utilization (weight gain/consumption) was significantly reduced during the first week of stimulation in the ventromedial hypothalamic stimulated group. Fat pad weight was slightly decreased in this group as well. These findings suggest that chronic stimulation of the ventromedial hypothalamus causes a persistent shift in metabolic rate that results in a long-term inhibition of weight gain.     

Cardiovascular effects of septal,thalamic, hypothalamic and midbrain self-stimulation

A positive correlation was found between the lever-pressing rate and the variability in the cardiovascular and respiratory effects elicited by septal, thalamic, hypothalamic and midbrain self-stimulation in cats. This correlation showed that all electrode placements which support self-stimulation are also capable of eliciting appropriate cardiovascular effects. The common characteristic of these effects was an increase in blood pressure, average respiratory and heart rates, and a decrease in pulse pressure during stimulation. Up to an unfavourably high level in the cardiovascular functions, self-stimulation at high rates was regularly assocaited with higher amplitude cardiovascular effects as compared to self-stimulation at low rates. Nonrewarding stimulation sites failed to evoke statistically significant changes in the cardiovascular responses. The instrumental alimentary behaviour was accompanied by an increase in blood pressure of about the same magnitude as self-stimulation at high rates. It was concluded that the cardiovascular effects are essential components of the behavioural pattern elicited by self-stimulation.     

慢性束缚应激致大鼠持续性高血糖症与孤束核损伤有关

目的 探讨孤束核联合亚核前部（acNTS）损伤在慢性束缚应激（CRS）所致的胰岛素抵抗性高血糖症发生中的作用。 方法 采用CRS大鼠模型（n=20;7 d束缚+3 d自由活动，共40 d），检测葡萄糖代谢相关指标。 结果 CRS导致约1/3的个体（n=7）持续性的中度胰岛素抵抗性高血糖（空腹血糖不超过11 mmol/L）。CRS高血糖鼠acNTS可观察到神经元染色浓缩，Caspase-3表达和TUNEL阳性染色，提示出现神经元凋亡样改变。机械损伤acNTS（n=6），空腹血糖水平逐渐升高，也能导致胰岛素抵抗性高血糖, 且高胰岛素血症、胰岛平均体积增大和血清皮质酮水平不变等特点与CRS小鼠一致。 结论 CRS损伤了acNTS的葡萄糖敏感神经元，从而使血糖调节紊乱。     

Quantitative characterization of ceruleospinal inhibition of nociceptive transmission in the rat

A total of 51 dorsal horn units responsive to heat were isolated and their receptive fields characterized (i.e., response properties and adequate stimuli determined) in pentobarbital-anesthetized, paralyzed rats. In 39 of the 51 units, the descending inhibition of heat-evoked activity produced by focal electrical stimulation in the locus ceruleus/subceruleus (LC/SC) was examined. All units studied responded to mechanical stimulation, to electrical stimulation of the ipsilateral tibial nerve at intensities supramaximal to activate A-alpha, delta- and C-fibers, and to noxious heating (50 degrees C) of the footpad. The cutaneous receptive fields of all units were confined to the glabrous skin of the toes and footpad. All neurons examined were located in the dorsal horn of the spinal cord in laminae I-VI. Tracking experiments established that inhibition of heat-evoked dorsal horn unit activity could be reliably produced by focal electrical stimulation in both the contralateral and ipsilateral LC/SC. The inhibition produced by electrical stimulation in the LC/SC was intensity-, pulse duration-, and frequency-dependent. In six experiments, the efficacy of LC/SC stimulation-produced inhibition of heat-evoked activity was compared using two pulse durations (100 and 400 microseconds); greater inhibition of heat-evoked activity was produced at lower intensities of stimulation at the 400-microseconds pulse duration. In 10 experiments, the frequency of stimulation was varied (25-200 Hz); stimulation at a frequency of 100 Hz resulted in maximal inhibition of heat-evoked activity for stimulation sites both inside (n = 7) and outside (n = 3) the LC/SC. Inhibition of heat-evoked dorsal horn unit activity could be reliably produced by focal electrical stimulation in sites inside the LC/SC (n = 18). Significant descending inhibition of noxious heat-evoked spinal neuronal activity could also be produced by stimulation in pontine sites located outside the LC/SC, however, not as reliably. Systematic electrode tracks were made through the pons, using a searching stimulus of 100 microA, to locate sites medial, lateral, and ventral to the LC/SC from which significant descending inhibition could be produced. Stimulation in 156 sites outside the LC/SC at 100 microA produced inhibition of heat-evoked spinal unit activity to 50% of control or less in only 37 sites. Descending inhibition was characterized quantitatively from 14 of these 37 sites; the mean intensities of stimulation to inhibit heat-evoked activity to 50% of control were experimentally determined, and the mean thresholds of stimulation for inhibition and the mean recruitment indices were calculated.(ABSTRACT TRUNCATED AT 400 WORDS)     

Modulation of noxious and non-noxious spinal mechanical transmission from the rostral medial medulla in the rat

Modulatory influences on spinal mechanical transmission from the rostral medial medulla (RMM) were studied. Noxious stimulation, produced by von Frey-like monofilaments, and non-noxious stimulation, produced by a soft brush, was applied to the glabrous skin of the hind foot. At 28 sites in RMM, electrical stimulation facilitated responses to noxious mechanical stimulation at low intensities (5-25 microA) and inhibited responses of the same neurons at greater intensities (50-100 microA) of stimulation. At 24 and 9 other sites in RMM, stimulation at all intensities only inhibited or only facilitated, respectively, responses to noxious mechanical stimulation of the hind foot. Stimulus-response functions to mechanical stimulation were shifted leftward by low intensities and decreased by high intensities of stimulation. Inhibitory influences were found to descend in the dorsolateral funiculi; facilitatory effects were contained in the ventral spinal cord. Descending modulation of non-noxious brush stimulation revealed biphasic facilitatory-inhibitory effects (9 sites in RMM), only inhibitory effects (14 sites) and only facilitatory effects (8 sites). The effects of electrical stimulation were replicated by intra-RMM administration of glutamate; a low concentration (0.25 nmol) facilitated and a greater concentration (2.5 nmol) inhibited spinal mechanical transmission, providing evidence that cells in RMM are sufficient to engage descending influences. Descending modulatory effects were specific for the site of stimulation, not for the spinal neuron, because modulation of the same neuron was different from different sites in RMM. These results show that spinal mechanical transmission, both noxious and non-noxious, is subject to descending influences, including facilitatory influences that may contribute to exaggerated responses to peripheral stimuli in some chronic pain states.     

Characterization of descending facilitation and inhibition of spinal nociceptive transmission from the nuclei reticularis gigantocellularis and gigantocellularis pars alpha in the rat.

1. Descending influences produced by focal electrical stimulation in the nuclei reticularis gigantocellularis (NGC) and gigantocellularis pars alpha (NGC alpha) on spinal nociceptive transmission and the dorsoventral region of spinal white matter mediating stimulation-produced modulation were examined in pentobarbital sodium-anesthetized, paralyzed rats. Spinal units studied responded to mechanical stimuli and noxious heating (50 degrees C) of cutaneous receptive fields confined to the glabrous skin of the ipsilateral hind foot. Recording sites were located in laminae I-VI of the L3-L5 spinal segments. 2. Electrical stimulation in the NGC or NGC alpha produced both facilitation and inhibition of responses of spinal units to noxious heating of the skin. At 33 of 57 stimulation sites in the NGC and NGC alpha, electrical stimulation produced biphasic effects, facilitating responses at lesser intensities (5-25 microA) and inhibiting responses at greater intensities (50-100 microA). At 21 other sites in the NGC and NGC alpha, electrical stimulation (5-100 microA) only inhibited, and at 3 sites stimulation (5-100 microA) only facilitated responses of spinal units to noxious heating of the skin. 3. Electrical stimulation in the NGC or NGC alpha contralateral to the spinal recording site produced the same magnitude of facilitation/inhibition or inhibition of spinal nociceptive transmission as did stimulation in the ipsilateral NGC and NGC alpha. 4. The latencies to descending facilitation and inhibition of spinal nociceptive transmission from the NGC and NGC alpha were estimated by a cumulative sum technique to be 232 and 80 ms, respectively. 5. Responses of spinal units to graded heating (42-50 degrees C) of the skin exhibited positively accelerating stimulus-response functions (SRF) throughout the temperature range tested. Electrical stimulation at lesser, "facilitating" intensities produced a parallel, leftward shift of the SRF, whereas stimulation at greater, "inhibitory" intensities significantly decreased the slope of the SRF without affecting the threshold for response. 6. To determine whether activation of cell bodies in the NGC or NGC alpha were capable of replicating the effects of electrical stimulation, L-glutamate was microinjected into sites where electrical stimulation facilitated at lesser and inhibited at greater intensities the responses of spinal units to 50 degrees C heating of the skin. L-Glutamate (5 nmol) produced a rapid onset, short-lasting and reproducible facilitation of nociceptive transmission; glutamate microinjection into the same site at a greater dosage (50 nmol) inhibited responses of the same spinal units.(ABSTRACT TRUNCATED AT 400 WORDS)     

脑卒中患者血糖水平变化及其原因

探讨脑卒中患者血糖变化的原因。采用葡萄糖氧化酶-过氧化酶法和放射免疫分析法分别对90例脑卒中患者的血糖水平和血清促肾上腺皮质激素(ACTH)、胰高血糖素(GCG)、胰岛素(INS)、生长激素(GH)、皮质醇(COR)、甲状腺素(T4)及三碘甲状腺原氨酸(T3)浓度做动态检测；采用CT扫描确定病灶大小及脑组织病理改变情况(有无脑中线移位、脑室受压和血肿破入脑室等)；对血糖水平与激素浓度和脑组织病理改变之间的关系做相关研究。结果表明：90例脑卒中患者中有38例发生高血糖，发生率为42．22％；血糖水平与GCG和COR浓度成正相关，与T3成负相关；发病10天后高血糖组的血糖水平和相关激素浓度均恢复正常。高血糖组ACTH浓度和脑组织病理改变的发生率均显著高于正常血糖组和对照组，而ACTH升高组脑组织病理改变的发生率显著高于ACTH正常组。结论：脑卒中血糖升高的原因可能与下丘脑受刺激后引起ACTH和GCG释放因子分泌增加，继而与血清COR和GCG水平升高、T3水平降低有关。     

The glycogenolytic response to stimulation of the splanchnic nerves in adrenalectomized calves, sheep, dogs, cats and pigs

1. The effects of stimulation of the peripheral ends of one or both splanchnic nerves have been investigated in calves, sheep, dogs, cats and pigs after removal of both adrenal glands.2. Stimulation of both splanchnic nerves produced comparable hyperglycaemic and glycogenolytic effects in sheep, dogs and cats; the mean liver glycogen concentration was reduced by between 7.0 and 10.5 mg/g, five min after stimulation was discontinued, at which time the mean plasma glucose concentration had risen by between 126 and 137 mg/100 ml.3. In five 3-5 week-old calves which were tested under identical conditions the mean liver glycogen concentration was reduced by 13.3 +/- 1.9 mg/g and the plasma glucose concentration raised by 216 +/- 1.9 mg/100 ml., 5 min after stimulation was terminated.4. In pigs, stimulation of both splanchnic nerves invariably produced a rise in the plasma glucose concentration, even when the concentration of glycogen in the liver was less than 5 mg/g before stimulation. The response was, nevertheless, considerably smaller in these animals than in any of the other species investigated.5. Splanchnic nerve stimulation also caused a rise in mean aortic blood pressure and blood haematocrit during the period of stimulation; changes of approximately the same order of magnitude were encountered in all five species.6. Dogs were found to resemble calves in that the hyperglycaemic response to stimulation of a single splanchnic nerve did not differ significantly from that obtained when both were stimulated simultaneously; furthermore, either nerve was found to be equally effective.7. In cats the change in plasma glucose concentration in response to stimulation of a single splanchnic nerve was always less than that which occurred in response to bilateral stimulation although comparable changes in blood haematocrit occurred in both groups of animals.8. It is concluded that stimulation of the splanchnic nerves causes break-down of glycogen in the livers of various unrelated species of adult animals but that the magnitude of the hyperglycaemic response in the young calf provides further evidence of the importance of the sympathetic system in the control of metabolism in the young animal.     

Gonadotrophin secretion in the ovariectomized guinea-pig: effects of electrical stimulation of the hypothalamus and of LH-RH.

1. Serial blood samples were collected from anaesthetized spayed guinea-pigs subjected to anterior hypothalamic stimulation or injected with luteinizing hormone-releasing hormone (LH-RH), and the effect on the secretion of follicle-stimulating hormone (FSH) and LH followed. 2. Hypothalamic stimulation enhanced LH secretion, although the response waned during the course of the 1 hr period of stimulation; the secretion of FSH was not increased. After stimulation, FSH and LH levels fell below control values. 3. The response to stimulation of the hypothalamus was greater 2 weeks after spaying than after 1 week. 4. Since repeated periods of hypothalamic stimulation induced repeated surges of LH secretion, the decline in LH secretion during stimulation was not likely to have resulted from hypothalamic damage, while the observation that the plasma concentration of FSH and LH declined below control values after brain stimulation implies the operation of inhibitory mechanisms. 5. Pre-treatment of spayed guinea-pigs with progesterone depressed the resting plasma concentration of LH but did not affect the immediate response to hypothalamic stimulation. After hypothalamic stimulation the plasma gonadotrophin levels did not fall below control values. 6. Pre-treatment with oestradiol benzoate depressed the resting plasma level of LH and slightly reduced the size of the LH surge produced by hypothalamic stimulation. However, the raised plasma LH concentration was sustained after stimulation ended. 7. The response to hypothalamic stimulation after pre-treatment with progesterone and oestradiol benzoate showed features of the reaction to each steroid given singly. 8. The I.V. injection of 0-5 microng LH-RH induced a surge of LH secretions without affecting FSH discharge. 9. Pre-treatment with progesterone did not greatly modify the response to LH-RH but after an injection of oestradiol the high level of LH produced by the releasing factor was sustained for about 2 hr. 10. Injections of LH-RH during the phase of depressed LH release after hypothalamic stimulation produced a surge of LH secretion which matched that seen in non-stimulated animals.