Evidence for the involvement of alpha-2 adrenoceptors in the sedation but not REM sleep inhibition by clonidine in the rat

Rats with implanted electrodes for recording of EEG and EMG underwent 12-h recordings during the light period starting after i.p. injections of clonidine (0.1 mg/kg) alone or in combination with different alpha-adrenoceptor antagonists. Clonidine increased the proportion of time the rats spent in the drowsy stage of wakefulness which corresponds to behavioural sedation and inhibited both deep slow wave sleep and REM sleep for 6-9 hours. The amount of active wakefulness or light slow wave sleep were unaffected by clonidine. Yohimbine (1 mg/kg) reversed the increase in drowsy wakefulness by clonidine and increased active wakefulness without affecting sleep. Phentolamine (10 mg/kg) was ineffective against clonidine. Phenoxybenzamine (20 mg/kg) accentuated the sedative effect and prolonged the REM sleep inhibiting effect of clonidine. Prazosin (3 mg/kg) prolonged both the drowsy stage inducing and deep slow wave plus REM sleep inhibiting effects of clonidine. These electrophysiological results support the view that the sedative effect of clonidine in the rat is mediated by alpha-2 adrenoceptors, whereas in this species other mechanisms, possibly another population of alpha-2 receptors, may be involved in the clonidine-induced suppression of deep slow wave sleep and REM sleep.     

Fluid balance in exercise dehydration and rehydration with different glucose-electrolyte drinks

After exercise dehydration (3% of body weight) the restoration of water and electrolyte balance was followed in 6 male subjects. During a 2 h rest period after exercise, a drink of one of four solutions was given as 9 X 300 ml portions at 15 min intervals: control (C-drink), high potassium (K-drink), high sodium (Na-drink) or high sugar (S-drink). An exercise test (submaximal and supramaximal work) was performed before dehydration and after rehydration. Dehydration reduced plasma volume by 16%, a process reversed on resting even before fluid ingestion began, due to release of water accumulated in the muscles during exercise. After 2 h rehydration, plasma volume was above the initial resting value with all 4 drinks. The final plasma volumes after the Na-drink (+14%) and C-drink (+9%) were significantly higher than after the K- and S-drinks. The Na-drink favoured filling of the extracellular compartment, whereas the K- and S-drinks favoured intracellular rehydration. In spite of the higher than normal plasma volume after rehydration, mean heart rate during the submaximal test was 10 bpm higher after rest and rehydration than in the initial test, and was not different between the drinks. The amount of work which could be performed in the supramaximal test (105% VO2max) was 20% less after exercise dehydration and subsequent rest and rehydration than before. This reduction was similar for all drinks, and may be due to a decreased muscle glycogen content (70% of initial) at the time of the second test.     

Effects of fatigue and recovery on electromyographic and isometric force- and relaxation-time characteristics of human skeletal muscle

Effects of fatigue produced by a maintained 60% isometric loading on electromyographic and isometric force-time and relaxation-time characteristics of human skeletal muscle were studied in 21 males accustomed to strength training. Fatigue loading resulted in a slight but not significant change in the maximal integrated EMG of a maximal isometric contraction, and a large decrease (20.4 +/- 6.3%, p less than 0.001) in maximal force. Fatigue loading increased (p less than 0.05-0.01) neural activation of the muscles during rapidly produced submaximal isometric forces, but had a considerable adverse effect (p less than 0.001) on the corresponding force-time characteristics. Correlations between the relative changes after fatigue in the IEMG/force ratio at the maximal force level, and in the IEMG/force ratios of the early phases of the force-time curve were not significant, but gradually became significant (p less than 0.01) at higher force levels. The average IEMG of the muscles in the relaxation phase of contraction remained unaltered by fatigue, while a marked deleterious change in the relaxation-time variables (p less than 0.001) occurred concomitantly. During the subsequent 3 min rest period considerable (12.1 +/- 7.0%, p less than 0.001) recovery was noted in the maximal force, with smaller (insignificant or p less than 0.05-0.01) changes in the force-time and relaxation-time variables, while the average IEMG of force production decreased (p less than 0.01-0.001). The present findings suggest that fatigue leading to a worsening in force-time, in maximal force and in the relaxation-time parts of a maximal isometric contraction might take place primarily in the contractile processes.     

Swelling of the foot, its vascular volume and systemic hemoconcentration during long-term constrained sitting

Swelling of the left foot and changes in its vascular volume (VV) were studied in seven healthy subjects during 8 h of seated work without leg movements. Changes in total plasma volume (PV) were calculated from hematocrit values. Reference values (r.v.) were obtained during a working day requiring intermittent physical activity (walking). Significant changes during the first 4 h: the foot swelled by 3.5% (r.v.: 2.2%) and VV was reduced by 0.5% of the foot volume (r.v.: increased by 0.3%). Accordingly, the interstitial fluid volume (IFV) of the foot increased by 4.0% (r.v.: 1.9%). The loss of PV was 6.3%. During the last 4 h the only significant change was an increase in foot volume by 1.9%. It is concluded that (1) foot swelling should be corrected for changes in VV to obtain an exact measure of the change in IFV, (2) prolonged elevated pressure, assumed to occur in the feet during relaxed sitting, does not imply distension ("delayed compliance") of the vascular system as previously suggested, (3) hemoconcentration seems to reach complete stability during the initial period of quiet sitting, (4) loss of PV during sedentary work may be avoided by a modest increase in leg activity.     

Nucleotide sequence of the CytR regulatory gene of E. coli K-12.

We have determined the nucleotide sequence of the cytR gene, which codes for the Cyt repressor (CytR). The coding region consists of 1023 or 1029 bp. The subunits of CytR are thus predicted to consist of 341 or 343 residues. It is shown that the N-terminal segment of the polypeptide is structurally similar to the DNA-binding region of known DNA-binding proteins. In addition, there exists an exceptionally high amino acid sequence homology between CytR and the Gal repressor, indicating a common origin of evolution.     

Experimental reovirus myocarditis in newborn mice. Electron microscopic observations

Reovirus is a double-stranded RNA-virus which induces myocarditis in newborn mice. Due to the large diameter of the viral particles (70-75 nm) it can be detected by electron microscopy. Subcutaneous inoculation of 0.05 ml reovirus type 3 (TCID50-titer: 10(8.5)/ml) into newborn NMRI-mice (12-18 h after birth) caused a grey-yellow mottling on the ventricular surface first seen on the 5th day after birth. At the same time muscle fiber necrosis was observed which increased with time. Electron microscopic investigations of the diseased heart muscle disclosed a marked interstitial oedema, swelling of the tubular system and sarcoplasmic reticulum, and degenerative changes in the mitochondria of individual myocardiocytes as early as the 2nd post-inoculation day. Simultaneously, an enlarged Golgi-apparatus and an increasing number of lysosomes, partially exhibiting acid phosphatase activity, was detected in the perinuclear region of ventricular myocardiocytes. On the 5th day after infection, viruses were detected either within single membrane vesicles, dispersed in cytoplasm or as aggregated clusters in the perinuclear region. These in vivo electron microscopic findings correspond with observations of virus propagation in cell-culture systems.     

In vitro interactions of murine peritoneal macrophages and sarcoma cells. I. Promotion of tumor cells proliferation by macrophages

An ascites subline (AA) of the murine sarcoma MC1M grows in vivo in the peritoneal cavity but dies in vitro when cultured on glass or collagen. The viability of AA cells in vitro is not influenced in cocultures with fibroblast cell line L929, and is diminished in cocultures supplemented with macrophage culture supernatant or in cocultures with non-adherent peritoneal cells. However, AA cells proliferate in vitro on glass or collagen when cocultured with syngeneic, semisyngeneic, and allogeneic peritoneal macrophages. This was demonstrated by tritiated thymidine incorporation assay, by AA cell number counting, and by measuring AA cell protein content. Proliferation also occurs when AA cells are separated from the macrophage monolayer by millipore filters.