Selective brain cooling in desert animals: the camel (Camelus dromedarius).

1. Animals living in the Arabian desert are subjected to extremely high temperatures during the day in summer and very cold nights in winter. They have developed various adaptive mechanisms in order to cope with these severe heat conditions. 2. The camel (Camelus dromedarius), like many other land animals, resorts to selective brain cooling when it is subjected to heat stress. 3. This mechanism protects the heat-sensitive brain tissue from heat stress and at the same time increases the animals' tolerance to high temperatures. 4. The blood cooled in the nasal cavity by evaporative heat loss is diverted to the brain sinuses via the nasal and angular veins. 5. In the cavernous sinus, the arterial blood in the carotid rete is cooled by the cold venous blood before entering the brain. This will lead to significant cooling of the brain tissue. 6. Active myogenic tone was mainly observed in the facial, nasal and angular oculi veins of the camels head. This tone was found to be sensitive to small changes in temperature in the range 33-45 degrees C. 7. The facial veins constricted, while the nasal and angular oculi veins relaxed to increasing temperatures. This leads to a coursing of cold venous return to the brain's sinuses for selective brain cooling. 8. It is concluded that this myogenic vasoactive mechanism is a major factor in the control of blood flow in the facial area of the camel during heat stress.

Facial vessels of desert camel (Camelus dromedarius): role in brain cooling.

The reactivity of the superficial veins of the camel was investigated in vitro in response to stretch, heat, norepinephrine, and transmural nerve stimulation (TNS). Stretch at 30 degrees C or 37 degrees C produced a maintained tone and phasic contractions of the facial and nasal veins. The developed tone increased significantly with increasing the temperature (from 30 to 45 degrees C), especially in the proximal part of the buccal facial vein. Norepinephrine caused a constrictor response in the facial vein with the proximal part showing a lower maximum. TNS evoked a constrictor response in proximal segment and a dilator response in the more proximal segment of the buccal facial vein. Either responses were blocked by bretylium or tetrodotoxin. Morphological examination of the vasoactive segment of the facial vein showed a thick muscular layer and a valve in the proximal segment of the buccal facial vein. These results show functional variation in the distribution of adrenoceptors in the facial vein. The high-temperature sensitivity of the buccal facial vein suggests that this part could serve as a temperature-sensitive sphincter that diverts cool nasal blood to the brain for selective cooling of the camel brain during heat stress.

Heterogeneity of the histological features along the course of the facial vein of the desert camel (Camelus dromedarius): relevance to brain cooling.

Sections from different parts along the facial vein of the camel (Camelus dromedarius) were examined by light microscopy. The results demonstrated heterogeneity among the various segments. Particular attention was paid to a specific area in the buccal region which was previously shown by physiological experiments to have a temperature-dependent myogenic tone. The morphology of that area showed highly thickened media with prominent bands of circularly disposed smooth muscles infiltrating both the intima and the adventitia. The morphology described in this study correlates well with the function and gives further credence to the proposed role of the facial vein in cranial thermoregulation particularly under heat stress.

Ethanol-induced sleeping time in mice: age and sex differences.

Ethanol-induced sleeping time was determined in mice of both sexes at ages ranging from 3 weeks to just over 1 year. A progressive increase in sleeping time was seen in both sexes up to 26 weeks of age; no subsequent changes were observed, except for a modest decrease in the oldest female group. In the majority of age groups, sleeping time values were higher in females, but few statistically significant sex differences were found.

Taurine and ethanol-induced sleeping time in mice: route and time course effects.

Taurine was given to mice: (i) intracerebroventricularly (i.c.v.) 20 min prior to 4.5 g/kg of ethanol intraperitoneally (i.p.); (ii) i.p. 10 min-5 days prior to ethanol; or (iii) orally (p.o.) as drinking fluid for 30 days prior to ethanol. Ethanol-induced sleeping time was increased by i.c.v. taurine and also by i.p. taurine when the pretreatment interval was 4-5 days. The long i.p. pretreatment time probably reflects the slow uptake of taurine by the brain. Sleeping time was decreased by p.o. taurine and by i.p. taurine when the pretreatment interval was 10-20 min. The mechanism of this attenuation remains unclear.

Vascular effects of hyperthermia on isolated blood vessels.

1. The contractile response of isolated human umbilical and sheep renal arteries to 5-hydroxytryptamine (5-HT) with increasing temperatures was investigated. 2. In the umbilical artery the threshold value was lowest at 30 degrees C and increased with increasing temperature, the maximal response being lower at temperatures above 30 degrees C. 3. Spontaneous rhythmic contractions of the umbilical artery were not augmented by warming above 37 degrees C. 4. The sheep renal artery exhibited an opposite response pattern: increasing temperature lowered the threshold and increased the maximal response. 5. Addition of indomethacin to the bathing fluid resulted in increased responsiveness of the umbilical arteries to 5-HT. With lower threshold, ED50 and higher maximal response.

Vascular effects of potassium cardioplegic solutions.

Experiments have been performed on isolated human umbilical and sheep coronary arteries, studying the effects of increasing potassium concentration in steps from 10 to 160 mM. Comparative studies were also done on rat-heart papillary-muscle preparations. The results revealed a dose-dependent increase in smooth muscle tone of the blood vessels. Maximal contraction was reached at 80 mM K+. Papillary-muscle preparations showed a dose-dependent decrease in contractile activity. Complete stoppage of contractile activity was observed at 30 mM K+. The corresponding increase in the vascular smooth muscle tone at 30 mM K+ was 10-25%, showing that vascular smooth muscle cells are less easily affected by increasing K+ than the heart. Further confirmation of the results were obtained by exposing the preparations (papillary muscle and arteries) to a locally-developed depolarizing K+-cardioplegic solution.

Adrenergic and cholinergic induced contractions of tracheal smooth muscle in the rabbit as demonstrated by a new in vivo method.

An in vivo tracheal muscle preparation in the rabbit was developed which enabled us to measure changes in the isometric tension of the trachealis muscle in response to electrical stimulation of autonomic nerves and to i.v. administration of autonomic agonists and antagonists. The preparation was very sensitive to injections of carbachol, and showed graded contractions to stimulation of the caudal end of the cut cervical vagus as frequency and strength of stimulation were increased. Stimulation of the rostral end of the cut cervical sympathetic nerve fibers produced contractions in all preparations. This effect was mimicked by the alpha-adrenoceptor agonist, phenylephrine. The effects of both sympathetic stimulation and phenylephrine were blocked by phentolamine and not inhibited by pretreatment with atropine or propranolol. Sympathetic stimulation produced contractions of the trachealis muscle whether the initial tone was normal or actively increased by carbachol, while adrenaline produced relaxation when the initial tone was high. Using this new in vivo trachealis muscle preparation in the rabbit, we could show that sympathetic stimulation produced contractions of the trachealis muscle. This effect is consistent with the existence of smooth muscle activating alpha adrenoceptors.

Effects of dopamine receptor stimulants on locomotor activity of rats with electrolytic or 6-hydroxydopamine-induced lesions of the nucleus accumbens.

Ergometrine (8 mg/kg) injected intraperitoneally into normal rats had little effect on locomotor activity. In contrast, rats with selective 6-hydroxydopamine-induced lesions of dopamine terminals in the nucleus accumbens showed a strong stimulation of locomotor activity following injection of this dose or ergometrine. The dopamine analogue 2-amino-6-7-dihydroxy-1, 2, 3, 4-tetrahydronaphthalene (ADTN) (150 mug), caused strong and long lasting stimulation of locomotor activity when injected intracerebroventricularly into rats. The ADTN response was markedly reduced in rats with bilateral electrolytic lesions of the nucleus accumbens, but unchanged in rats with bilateral electrolytic lesions of the caudate nucleus. At a lower dose level (50 mug) ADTN, injected intracerebroventricularly, had little effect on the locomotor activity of normal or sham-operated rats. This dose of ADTN was, however, effective in causing locomotor stimulation of rats with bilateral 6-hydroxydopamine-induced lesions of the nucleus accumbens. These results support the view that the dopamine receptors in the nucleus accumbens are involved in the actions of locomotor stimulant drugs.

Studies on the behavioural pharmacology of a cyclic analogue of dopamine following its injection into the brains of conscious rats.

1. The cyclic analogue of dopamine, 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (ADTN) was injected into the lateral ventricle or bilaterally into the nucleus accumbens or caudate nucleus of conscious rats and its effect on locomotor activity was investigated. 2. When given intraventricularly, ADTN produced some stereotyped responses which were followed by a strong and long lasting stimulation of locomotor activity. When administered bilaterally into the nucleus accumbens a similar stimulation of locomotor activity was observed. ADTN had no effect on locomotor activity when injected bilaterally into the caudate nucleus. 3. The ADTN-induced locomotor stimulation following its intraventricular injection was completely abolished by a low dose of pimozide (0.01 mg/kg, i.p.) or haloperidol (0.5 mg/kg, i.p.). Pimozide (1 mg/kg, i.p.) given 30 min before ADTN injected bilaterally into the nucleus accumbens completely blocked locomotor stimulation. 4. Unilateral injections of ADTN (5 mug) into the nucleus accumbens caused locomotor stimulation but no turning. 5. Bilateral injections into the nucleus accumbens of 2-amino-6,7-dimethoxy-1,2,3,4-tetrahydronaphthalene or 0.9 percent w/v NaCl solution had no effect on locomotor activity. 6. It is concluded that the central stimulant action of ADTN is due to an effect on the dopamine receptors in the nucleus accumbens.