Sleep disorders in relation to coronary heart disease.

In a cross-sectional study of 5419 Finnish adult men, a higher prevalence of diagnosed myocardial infarction was found among those who slept more than 9 hours, whilst those sleeping less than 6 hours per night had more symptomatic coronary heart disease (CHD). This relationship held after controlling by multivariate analysis for age, sleep quality, use of sleeping pills and tranquilizers, smoking, alcohol use, Type A score, neuroticism, use of cardiovascular drug and history of hypertension. The cardiovascular physiology and pathophysiology of sleep is reviewed and the relationship of some specific sleep disorders to CHD is discussed.

Prazosin increases paradoxical sheep.

Prazosin 0.5 and 1.0 mg/kg i.p. induced a prompt and enduring increase in paradoxical sleep in the cat. The maximal effect, 140 percent above control was observed during the first 4 h after 1 mg/kg. In 16 h polygraphic records the respective increment was 69%. After 10 mg/kg paradoxical sleep was inhibited but it returned to control levels in 16 h. These results are discussed with reference to our previous experiments with agents having different alpha 1- and alpha 2-antagonist or agonist potency. It is concluded that selective, moderate blockade of alpha 1-receptors favours paradoxical sleep.

Alpha-adrenoceptive influences on the control of the sleep-waking cycle in the cat.

Polygraphic 16 h sleep recording were carried out in 35 adult cats following i.p. injections of various alpha-adrenoceptors agonists, antagonists and their combinations. The direct alpha-agonists, clonidine (CLO 0.005, 0.01 and 0.02 mg/kg) and xylazine (XYL 0.5, 1 and 2 mg/kg), dose-dependently decreased paradoxical sleep (PS) and deep slow wave sleep (S2), with a respective increase mainly in drowsy waking (D). alpha-Methyldopa, precursor of the potent alpha-agonist, alpha-m-noradrenaline (alpha-m-NA) suppressed PS, with little effect on other vigilance stages. Of the alpha-antagonists only phentolamine (PHE 10 and 20 mg/kg) increased significantly the 16 h mean of PS. Thymoxamine (THY 5 mg/kg) gave a modest, temporary increment in PS between 4 and 8 h after the injection, but the effect diminished with 10 mg/kg THY. Yohimbine (YOH 2 mg/kg) induced an early increment in aroused waking (A). Tolazoline (TOL 6 mg/kg) and THY (5 and 10 mg/kg) increased D in the first 4 h epoch. Phenoxybenzamine (PBZ 10 mg/kg) significantly decreased the 16 h mean of S2 and PS. PHE antagonized the PS suppressing effect of CLO (0.01 mg/kg) already at the dose of 5 mg/kg and with 10 and 20 mg/kg its PS increasing character prevailed. TOL (6 mg/kg) and YOH (2 mg/kg) were also effective antagonists to CLO. THY (5 and 10 mg/kg) was ineffective in this respect and clearly potentiated the S2 inhibiting effect of CLO. PBZ (10 mg/kg) powerfully potentiated both PS and S2 suppressing effects of CLO. PHE (20 mg/kg) was tested against XYL (0.5 and 1 mg/kg) and alpha-methyldopa (100 mg/kg). It also antagonized the PS inhibiting action of these drugs. All the three agonists preferentially stimulate presynaptic (alpha 2) type of alpha-adrenoceptors, inhibitory to noradrenaline (NA) transmission. Furthermore, as only antagonists possessing presynaptic potency inhibited PS suppression by alpha 2-agonists, while preferential alpha 1-antagonists were either ineffective or potentiated this effect, the results favor the hypothesis of a positive involvement of NA in the mechanisms of PS. The optimal level of NA transmission for PS may, however, be postulated to lie below that for arousal, in which case the balanced blockade of alpha 1- and alpha 2-adrenoceptors by PHE might be exceptionally favorable to PS. The possible role of alpha-adrenoceptive influences on cholinergic and 5-HT neurons and their relevance to alpha 2-agonist-induced sedation and inhibition of PS and S2 are discussed.

Effects of two adrenergic beta-receptor blockers on the sleep cycle of the cat.

Sixteen hour polygraphic recordings (EEG, EOG and EMG) were obtained from 14 adult cats after intraperitoneal injections of propranolol (5 mg/kg) or pindolol (0.1 or 0.5 mg/kg). All injections moderately increased waking, which consisted mainly of a sedated drowsy stage. Both drugs also decreased deep slow wave sleep, while light slow wave sleep remained at control levels. The changes were more marked after propranolol, which also significantly reduced paradoxical sleep (PS). The decrease in the deeper stages of sleep and PS is suggested as being due to blockade of the central adrenergic beta-receptors per se and/or antagonistic effects of the beta-blockers on 5-HT receptors. The results agree with the finding that beta-blockers cause insomnia in susceptible patients, but they do not suggest that intensified dreaming or nightmares reported by others are likely to be caused by increased PS.

A new vestibular thalamic area: electrophysiological study of the thalamic reticular nucleus and of the ventral lateral geniculate complex of the cat.

Single unit recordings were carried out in the reticularis thalamic nucleus (RT) and the ventral lateral geniculate body (LGv) of chronically prepared alert cats under sinusoidal vestibular stimulation in the horizontal plane. Optokinetic stimulation was also used. Of the 57 recorded neurons, 12 present vestibular modulation in the dark, analogous to Duensing's and Schaefer's (1958) type I response in the vestibular nuclei. Responses of 26 cells are similar to response of type II vestibular neurons and 14 units have a type III response; the 5 remaining cells were activated by vestibular stimulation in the vertical sagittal plane. The majority of these cells does not present detectable direct visual responses, but 50% can be driven by optokinetic stimulation. 74% of types I, II and III neurons show saccadic resonses to vestibular nystagmic saccades in the dark. About 60% present similar saccadic modulations during optokinetic nystagmus and 55% keep this response for spontaneous saccades in the dark or in front of a striped background. The saccadic responses are constant for a given neuron in all cases of stimulation with latencies ranging from 30 msec prior to the beginning of the saccade to 120 msec after its onset. The histological localization of these units falls on one hand into the caudal part of the RT nucleus (type III neurons) above the dorsal lateral geniculate nucleus and on the other hand within the internal subdivision of the LGv and its rostral limit (all other types). The significance of this new, saccadic and vestibular focus in the feline thalamus is discussed in relation with the two previously known vestibular thalamic relays in terms of interrelations between the vestibular and the visual systems.

Compensation of postural effects of hemilabyrinthectomy in the cat. A sensory substitution process?

A photographic technique was used to study the evolution of lateral head-tilt following hemilabyrinthectomy in adult cats. Animals were maintained post-operatively in normally lit conditions (LM cats), in total darkness (DM cats), or in stroboscopic light. In LM casts, the head tilt peaked at 45 degrees (with the lesionned side down) on the second post-operative day, and decreased to about 0 degree within about 10 days. This evolution was followed by rebounds of head-tilt to large angles before a stable compensated head postion could be maintained (approximately at the end of the third post-operative month). In DM cats the head remained tilted by a large angle throughout the duration of the dark period. Re-exposure to light was followed by a rapid decrease of head-tilt. In stroboscopic light, the evolution of head-tilt was found to be closely similar to that in the normally lit condition. Finally, when put back in the dark at a late post-operative stage, already compensated animals were found to loose their symmetrical head position, and to re-acquire a strong head tilt. This effect resumed on re-exposure to light. It is inferred that static visual input is a necessary condition for compensation of the postural deficits of hemi-labyrinthctomy in the cat. Maintenance of a stable head posture also depends upon continuous availability of visual input.

Sleep-waking cycle in rabbits after cerebral ischemia.

In rabbits experimental cerebral ischemia of 4-6 min was followed by degradation of the electroencephalographic sleep-waking cycle, as determined from 3 h afternoon records: I. Hyposomnia i.e., reduction of slow wave and paradoxical sleep lasting for about 2 days, was seen, with gradual normalization in case of survival. II. In the first postischemic days abundant 14-17 c/sec spindles appeared in the motor cortex against a low voltage desynchronized background, making the EEG of waking qualitatively different from control records. The results are discussed with reference to polygraphic studies in comatose patients, EEG phenomenology of drowsiness, and cerebral monoamines.