A comparative study of the role of the cerebral arterial blood in the regulation of brain temperature in five mammals

Hayward, James N.; Baker, M. A.

doi:10.1016/0006-8993(69)90236-4

Cited by 264 publications

(144 citation statements)

References 34 publications

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“…The effective dose of PGD2 for induction of sleep was as little as 60 fmol/min, which might be physiologically feasible, because the preoptic/hypothalamic area, the site of action of PGD2 in inducing sleep (7), contained 4-6 pmol of PGD2/g (wet weight) of tissue after sacrifice of the rats by microwave radiation (3,4). It has been reported that monoamines (12) and several peptides such as 8-sleep-inducing peptide (13), factor S (14, 15), and muramyl peptides (16) (4,7) as observed in physiological sleep (19)(20)(21)(22)(23). In support of this hypothesis, Krueger et aL (16) have reported that indomethacin, a potent inhibitor of PG synthetase (17,18), blocks normal sleep.…”

Section: Resultsmentioning

confidence: 99%

Prostaglandin D2, a cerebral sleep-inducing substance in rats.

Ueno¹,

Honda²,

Inoue³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

131

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We continuously monitored the circadian sleep patterns of unrestrained rats for more than 96 hr and infused various prostaglandins into their third ventricles for 10 hr to study the effects on inducing sleep. Prostaglandin D2 at 6 fmol/min had no effect on either slow wave sleep or paradoxical sleep. However, prostaglandin D2 at as little as 60 fmol/min caused a significant amount of excess slow wave sleep as compared with the control level during saline infusion. Paradoxical sleep was induced by prostaglandin D2 at doses greater than 600 fmol/min. Prostaglandin D2 (600 fmol/min) increased slow wave sleep by 33% and paradoxical sleep by 56%. Although prostaglandin F2a (600 fmol/min) increased the amount of slow wave sleep, its activity was less than that of the same amount of prostaglandin D2. Prostaglandin E2 (600 fmol/min) had no effect on increasing the amounts of both slow wave sleep and paradoxical sleep. During the infusion of prostaglandin D2, rats were easily aroused by clap sound stimulation and their sleeping and waking postures remained normal. Further, their sleep was episodic, as observed in the physiological sleep of rats.Prostaglandin D2 (PGD2) has been identified as a natural constituent in brains of various mammals (1-4) and its synthesis and degradation in brain have been investigated in detail (2, 5, 6). Recently, Ueno et aL (4,7,8) reported that the use of the intracerebral microinjection technique to administer nmol doses of PGD2 elicits several central actions. One of the prominent actions of PGD2 was the induction of sleep (7,8). A site of action of PGD2 on inducing sleep was the preoptic area and 0.3 nmol of PGD2 induced excess slow wave sleep (SWS) (7). However, the PGD2 content in the preoptic/hypothalamic area in rat brain was 4-6 pmol/g (wet weight) of tissue (3, 4), indicating that even the doses we used before were not physiologically feasible. In the present study, we continuously infused small amounts of various PGs into the third ventricles of conscious rats and found that PGD2 at as little as 60 fmol/min induced excess sleep.MATERIALS AND METHODS Experimental Animals. Male Sprague-Dawley rats, 300-350 g, 70-80 days old were used. Rats were housed in a 12-hr light (08:00-20:00)/dark (20:00-08:00) cycle for at least 2 wk prior to surgery. Under pentobarbital anesthesia (50 mg/kg), rats were mounted on a stereotaxic instrument with the head fixed according to the coordinate system of Pellegrino et aL (9). For electroencephalogram (EEG) recordings, three silver ball electrodes were placed on the cortex and a silver plate over the frontal skull served as the indifferent electrode. The electromyogram (EMG) electrodes were inserted into the neck muscle. For intracerebral infusion to the third ventricle, a stainless steel cannula (o.d., 0.35 mm) was placed 3.4 mm lateral and 0.6 mm anterior from the bregma and inserted about 9 mm from the surface of the cortex at an angle of 20°from the midsagittal plane. The position of the cannula was determined by x-ray photographs. The ele...

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Section: Resultsmentioning

confidence: 99%

Prostaglandin D2, a cerebral sleep-inducing substance in rats.

Ueno¹,

Honda²,

Inoue³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

131

View full text Add to dashboard Cite

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“…Our finding of a substantial difference between striate nucleus and temporal muscle temperatures in animals with spontaneous brain cooling during ischemia confirms similar observations by Busto et al (1987), who also observed a discrepancy of up to 2°C after 30 min of four-vessel occlusion. This dif ference may be caused by the faster arrest of cere bral metabolic activity caused by selective brain cooling through fluid evaporation from the nasal mucosa (Hayward and Baker, 1969;Bamford and Eccles, 1983), or some residual blood flow in the temporal muscle after vascular occlusion. Busto et al (1987) proposed to correct this tem perature difference by introducing an empirical cor rection factor derived from the correlation of brain and muscle temperatures during spontaneous brain cooling.…”

Section: Discussionmentioning

confidence: 99%

Methodological Requirements for Accurate Measurements of Brain and Body Temperature during Global Forebrain Ischemia of Rat

Miyazawa

Hossmann

1992

J Cereb Blood Flow Metab

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Summary:The methodological requirements for accurate measurements of brain and body temperature during brain ischemia have been validated in Wistar rats submit ted to 30 min of four-vessel occlusion. During ischemia, brains were exposed to three different temperature pro files: spontaneous cooling from 36 to 31°C (n = 10), con stant hypothermia at 30°C (n = 19), and constant normo thermia at 36°C (n = 21). Direct and indirect brain tem perature recordings were carried out by placing fine thermocouples (200 !-Lm diameter) into the striate nucleus, the temporal muscle, and the epidural space. Body tem perature was measured with a flexible thermocouple in serted at various depths into the rectum. Accurate mea surements of body temperature required insertion of the The severity of brain damage after global cere brocirculatory arrest is markedly affected by slight variations of brain temperature (Busto et a!., 1987(Busto et a!., , 1989a. Investigations of ischemic injury, therefore, require precise measurements of brain temperature, particularly for the evaluation of pharmacological intervention (Buchan and Pulsinelli, 1990;Corbett et a!., 1990). A methodological problem associated with such measurements is the placement of the temperature probes. Measurements on the surface of the brain require exposure of the cortex and are greatly affected by changes in ambient temperature. Insertion of the probe into the brain produces a pen etrating lesion that may affect the ischemic injury (Takahata and Shimoji, 1986; Mushiroi et aI., 1989 817rectal probe to a depth of at least 6 cm; lesser insertion resulted in an underestimation of up to 6°C, Accurate estimates of brain temperature were obtained in all three experimental conditions by recording of the epidural tem perature. The temperature in the temporal muscle, by contrast, differed from the brain temperature by up to 2°C, depending upon the experimental condition and the duration of ischemia. We therefore suggest that indirect measurements of brain temperature during ischemia are carried out in the epidural space in order to avoid misin terpretations of temperature-sensitive pathological changes.

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“…Brooks and co-workers usually used a choloralosane anaesthetized, immobilized, hemispherectomized cat with ligated cerebral arteries on the hemispherectomized side. Intracarotid injections, given into the common carotid artery on the hemispherectomized side, must traverse the carotid rete (Baker & Hayward, 1967;Hayward & Baker, 1969) to reach the opposite circle of Willis and the supraoptic nucleus. Perhaps some aspect of their experimental design, such as disinhibition by removal of the opposite NSO, or after-discharge related to chloralosane, or delayed passage of the osmotic injection or prolonged behavioural arousal may account for their observed delayed responses.…”

Section: Discussionmentioning

confidence: 99%

“…17, L 2-5 (Snider & Lee, 1961). We cemented this cylinder to an elevated lucite platform (Baker et al 1968;Hayward & Baker, 1969) which was in turn cemented to four additional stainless-steel epidural skull screws. We sealed the margins of the opening around the cylinder with dental cement, and filled the cylinder, which subsequently supported the micro-electrode carrier, with bone wax and capped it.…”

Section: Introductionmentioning

confidence: 99%

Osmosensitive single neurones in the hypothalamus of unanaesthetized monkeys

Hayward¹,

Vincent²

1970

The Journal of Physiology

Self Cite

101

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SUMMARY1. We recorded with tungsten micro-electrodes the activity of single neurones in the supraoptic nucleus (NSO) and adjacent regions of the hypothalamus while repeatedly injecting solutions of varying tonicity into the common carotid artery of trained, unanaesthetized monkeys who accepted the experimental restraints without anxiety.2. Intracarotid injections of mildly hypertonic solutions of sodium chloride produced a characteristic behavioural response during and immediately after injection: e.e.g. 'arousal,' lip and tongue smacking, chewing, irregular sniffing respiration and associated mildly increased movement of face, eyes and body.3. Of the 130 cells analysed during hypertonic intracarotid injections, 105 (81 %) were osmosensitive. Twenty-five (19 %) of the cells studied during similar injections were non-osmosensitive. On the basis of the anatomical location of the cells, the pattern of discharge to intracarotid osmotic stimuli and the response to arousing sensory stimuli, we divided the osmosensitive cells into two major groups, 'specific' and 'non-specific' osmosensitive cells.4. Fifty-two (50 %) of the osmosensitive cells we labelled 'specific' because they responded to an intracarotid injection of hypertonic sodium chloride, generally did not respond to non-noxious arousing sensory stimuli and were located in or near the supraoptic nucleus. We found two subtypes of these 'specific' osmosensitive cells: (a) twenty-one (20 %) NSO cells with 'biphasic' responses, that is, acceleration followed by inhibition; (b) thirty-one (30 %) cells in the immediate perinuclear zone of the NSO with 'monophasic' responses, subdivided into twenty-one (20 %) cells that accelerated and ten (10 %) that were inhibited. lateral hypothalamus, were 'non-specific', responding both to intracarotid injections of hypertonic sodium chloride and also to sensory stimuli that were mildly arousing. Two groups of 'non-specific' osmosensitive cells showed monophasic responses; thirty-five (34 %) cells accelerated and seventeen (16 %) of them were inhibited.6. The 'monophasic' specific osmosensitive neurones lying in the immediate perinuclear zone of the supraoptic nucleus in the primate could conceivably be the 'osmoreceptors' of Verney. The 'biphasic' specific osmosensitive neurones in the NSO may well represent the secretary cells of this system. From our data, the 'non-specific' osmosensitive neurones, scattered diffusely in the anterolateral hypothalamus, have little to do with osmoregulation. Some of these cells located in the perinuclear zone of the NSO could act as interneurones, however, conveying afferent input to the osmoreceptor-secretory complex of the supraoptic nucleus.

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A comparative study of the role of the cerebral arterial blood in the regulation of brain temperature in five mammals

Cited by 264 publications

References 34 publications

Prostaglandin D2, a cerebral sleep-inducing substance in rats.

Prostaglandin D2, a cerebral sleep-inducing substance in rats.

Methodological Requirements for Accurate Measurements of Brain and Body Temperature during Global Forebrain Ischemia of Rat

Osmosensitive single neurones in the hypothalamus of unanaesthetized monkeys

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