摘要:

Prolonged exercise of a sufficiently high intensity is thought to create physiological stress and to disturb cellular homeostasis, ultimately inducing cellular adaptations which enable the organism to better deal with any future exercise challenge. Heat shock proteins (hsp) are expressed when cells are exposed to different types of stress. In this study, we have investigated whether the expression of the heat inducible form of hsp70 is increased in human skeletal muscle cells after a single bout of exercise. Five untrained subjects performed an exercise bout at their individual anaerobic threshold for 30 min on a treadmill. Hsp70 mRNA concentration was significantly increased by a factor of four at 4 min post‐exercise. Similarly high levels were also observed 30 min and 3 h after the end of exercise. Hsp70 protein concentration, on the contrary, did not change within 3 h after cessation of exercise. Thus, a single exercise bout in humans is able to increase the steady state concentration of hsp70 mRNA, but is probably not sufficient to have an effect on the already high basal level of its protein. The analysis of hsp70 mRNA is potentially useful as a method to detect stress in tissues with a high basal level of heat shock protein

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.512270000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

Myogenic tone and reactivity were studied in isolated, cannulated and pressurized small branches of the femoral artery of the rat. Myogenic tone developed spontaneously under control conditions (1.5 mmCa2+), reducing the diameter at 80 mmHg to 64±6% of the ‘max 80’, i.e. the diameter in Ca2+free solution, which was 221±23 μm (mean±SD,n=18). The calcium channel blockers verapamil and diltiazem, dose‐dependently, decreased this myogenic tone with pIC50values of 6.9±0.2 (n=7) and 6.6±0.1 (n=6), respectively. Myogenic reactivity was demonstrated under control conditions as a sustained decrease in diameter, by 5±3% of max 80 (after an initial, transient distension), in response to a step increase in transmural pressure from 80 to 140 mmHg. This response to the pressure increase was markedly inhibited when myogenic tone had been reduced by 50% with verapamil or diltiazem resulting, in fact, in an increased steady state diameter by 2±1 and 1±1% at 140 compared with 80 mmHg. However, if myogenic tone was reduced to the same extent by low extracellular Ca2+(∼0.3 mm) the vessels constricted by 6±1% in response to the pressure increase, an effect comparable to that in control Ca2+. Moreover, 50% reductions in myogenic tone by ACh (∼0.1 μm) or pinacidil (∼0.3 μm) were associated with significantly enhanced reactivity; steady state diameter decreased by as much as 11±4 and 15±5% of max 80. These results suggest that voltage dependentl‐type Ca2+channels are involved both in myogenic tone and in the myogenic response to a rise in vascular transmural pressure in skeletal muscle arteries. Partial inhibition of myogenic tone by other pharmacological routes do not necessarily interfere with myogenic reactivity since the response was, in fact, enhanced in the p

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.514269000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

During recovery from high intensity exercise, substantial and rapid muscle glycogen repletion from endogenous carbon sources is reported in a variety of vertebrate species, the rat being the only reported exception. The major aim of this study was to re‐examine the process of glycogen repletion during recovery from high intensity exercise in the rat. In response to 3 min of vigorous swimming, muscle glycogen concentrations decrease markedly from initial levels of 20.2±1.5 and 21.2±0.9 μmol g‐1to 6.4±1.1 and 7.9±1.4 μmol g‐1in the tibialis anterior and plantaris muscles respectively. The equivalent of 58% of the glycogen carbons mobilized during exercise by the plantaris and 73% of that mobilized by the tibialis anterior muscle is repleted within 1 h following exercise. Using the hepatectomized rat as experimental model, a secondary aim of the study was to evaluate whether the liver is essential for the repletion of muscle glycogen. Although the absence of significant differences in the magnitude of post‐exercise muscle glycogen repletion between sham‐operated and hepatectomized rats suggests that the resynthesis of muscle glycogen can take place in the absence of hepatic gluconeogenesis, the present study identifies several limitations in the use of acute hepatectomy. Overall, the present study indicates that, in contrast to published views, the rat resembles other vertebrates in that it can support extensive muscle glycogen repletion from endogenous carbon sources during the recovery phase following high int

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.507273000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

In the present study, we determined both anaerobic capacity (the maximal accumulated oxygen deficit) and maximal oxygen uptake (VPo2max) during arm stroke (A), leg kicking (K), and whole body swimming (S), and compared them. The subjects were six trained college swimmers (two male and four female), aged 20±1 years. To determineVPo2maxfor A, K and S,VPo2maxwas measured during a 6‐min swim at constant water flow rates.VPo2was measured by the Douglas bag method. Anaerobic capacity was determined by accumulated oxygen deficit during exercise lasting 2–3 min according to the methods of Medbøet al. Mean values ofVPo2maxduring A, K and S were 2.53±0.37 L min‐1, 2.93±0.37 L min‐1, and 3.23±0.43 L min‐1, respectively. Those in A and K corresponded to 78.2% and 91.0% of that in S. Mean values of anaerobic capacity during A, K and S were 2.15±0.31 L, 2.52±1.08 L and 2.99±0.52 L, respectively. Those in A and K corresponded to 73.3% and 81.7% of that in S. BothVPo2maxand anaerobic capacity in S were much lower than the sum of A and K, corresponding to only 59.3% and 65.9%, respectively. These results suggest that the total energy production during S is lower than simply the sum of A and K because the potentials of both the anaerobic and aerobic energy releasing processes in the muscle groups involved in A and K cannot be fully

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.490237000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

The influence of acute mental stress and the effect of electrically induced skeletal muscle contractions on natural cytotoxicityin vivowas investigated in spontaneously hypertensive rats. Natural cytotoxicityin vivowas measured as the clearance of injected51Cr‐labelled YAC‐1 lymphoma cells from the lungs, which are specifically lysed by natural killer cells. The mental stress consisted of an air jet directed towards the animals in their cage for 25 min. During the mental stress there was a significant increase in natural cytotoxicity. Thus, retained radioactivity in the lungs was decreased to 74±6% of the control levels which was set to 100% (P<0.01). This augmentation of YAC‐1‐cell clearance could be blocked with the β‐adrenergic receptor antagonist Timolol. Two hours after termination of the air stress,in vivocytotoxicity had returned to control levels. In contrast, acute physical stress, consisting of electrically induced muscle contractions for 60 min, had no significant effects onin vivocytotoxicity, either during the stimulation or 1, 2 or 24 h after the stimulation. Further, significantly increased plasma levels of adrenaline were seen after the air jet stress, but not after muscle stimulation. There were no significant changes in plasma noradrenaline levels either after air stress or muscle stimulation. These results indicate that changes inin vivocytotoxicity after mild mental stress are dependent on increased plasma catecholamine levels while acute physical stress, without changes in catecholamine levels, does not influencein vivoc

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.515276000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

Endothelin‐1 (ET‐1) is known to act via G‐protein coupled receptors. It has therefore been suggested that any mitogenic activity it may possess, is due to activation of phospholipase C and protein kinase C (PKC). We have therefore examined both the ability of ET‐1 to act as a mitogen and its ability to activate PKC. We found that ET‐1 significantly increased thymidine incorporation and enhanced platelet‐derived growth factor‐induced DNA synthesis, as well as causing a prolonged translocation of PKC to the cell membrane. ET‐1 significantly increased PKC dependent phosphorylation of two specific substrates. The phosphorylation of MBP4–14(from myelin basic protein) was partially dependent on extracellular Ca2+, implicating activation of PKC‐α, whereas phosphorylation of the so called ε‐peptide was Ca2+‐independent and prolonged. This could be due either to the δ or ζ isoform of PKC, known to be present in these cells. However, ET‐1 induced little proliferation or PKC activity in a transformed smooth muscle cell line, DDT1MF‐2, which lacks expression of the PKC‐αisoform, but expresses the ζ‐isoform. Thus, it would appear that ET‐1‐induced mitogenicity in smooth muscle cells may be related to the sustai

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.511285000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

Previous studies by electron microscopy and laser confocal microscopy of immuno‐histochemically stained sections have shown that during pregnancy the extent of gap junction formation in human myometrium is low, but that an increase occurs in the active stages of labour despite a high concentration of progesterone in maternal blood. The present investigation focused on the effect ofin vitroexposure of isolated myometrical tissue to progesterone, oestradiol and oxytocin, on the number of gap junction plaques in human myometrium at term. Myometrial biopsies were obtained at term from 13 pregnant women who had an elective caesarean section in the 37th or 40th week of pregnancy. The biopsies were immersed immediately in Hepes buffer and buffer containing 0.5, 5.0 μg mL‐1of progesterone, and 0.1 μg mL‐1of oestradiol. The muscle biopsies were trimmed under a stereo microscope into strips along the bundles of smooth muscle cells and mounted in tissue baths, superfused with Hepes buffer supplemented with glucose (0.01 mm); subsequently the strips were exposed to buffer containing different concentrations of progesterone, oestradiol and oxytocin. Incubation of the muscle strips for 180 min resulted in a significant decrease of the number of gap junctions (P<0.01). Neither oestradiol or oxytocin, alone or in combination, had a significant effect on the maintenance of the number of gap junctions. The progesterone concentration of 5.0 μg mL‐1, combined with oxytocin, and with or without oestradiol had a significantly positive effect on the number of gap junction plaques in strips of human myometrium at term (P<0.05 vs. buffer alone). The high concentration of progesterone in the superfusion medium duringin vitroexperiments may be responsible for the maintenance of high numbers of gap junction complexes in term human myometrium. This finding is of interest in the light of findings of persisting high progesterone levels in maternal blood dur

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.500247000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

The problem whether endogenous nitric oxide (NO) may serve as a true physiological regulator of vascular tonein vivowas approached by testing its role during graded acute haemorrhage with the aid of the nitric oxide synthase (NOS) inhibitorl‐NAME. The study was performed on the vascular bed of cat skeletal muscle with a technique permitting quantitative recordings of vascular resistance in the whole vascular bed (RT) and in its consecutive sections, the proximal arterial resistance (‘feeder’) vessels (>25 μm;Ra,prox), the small arterioles (<25 μm) and the veins. NO blockade by close‐arteriall‐NAME infusion in the control situation increasedRTfrom 16.3 to 33.0 PRU (+102%), because of a selective increase inRa,proxby 16.7 PRU. A 35% blood lossper seraisedRTfrom 13.6 to 21.7 PRU. Superimposed NO blockade in this state caused a much stronger vasoconstriction than in the control situation, increasingRTto 60.9 PRU (+181%) andRa,proxby 40.5 PRU, which indicated an ∼2.4‐fold increase (P<0.001) in the NO dilator influence in theRa,proxsection above control. The effect was independent of autonomic nerves. The increased NO dilator influence during haemorrhage most likely was caused by an increased production of endothelium‐derived nitric oxide (EDNO). The constrictor response tol‐NAME was graded in relation to the blood loss (17.5 vs. 35%). The results indicate that EDNO functions as a physiological regulator of vascular tone in the arterial ‘feeder’ vessels during haemorrhage, serving to counterbalance to a significant extent the concomitant adrenergic constriction, and thereby preventing critical reduction of blood flow and untoward heterogeneous flow distrib

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.516275000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

To compare plasma NT‐proANP, a stable and biologically inactive N‐terminal portion of ANP prohormone, with the known plasma ANP response to increased right atrial pressure a Swan–Ganz catheter was inserted into the right atrium of five normal healthy male volunteers. The elevation of right atrial pressure was produced by a head‐down tilt after a hypertonic saline infusion. Blood samples were drawn from the lumen of the right atrium. After 5 min of starting the tilt the right atrial pressure had increased from 7.0±1.0 to 11.6±0.9 mmHg (P<0.05) and then began to normalize in spite of the constant tilt. Atrial plasma ANP increased in relation to the pressure increase and peaked at 15 min after the start of the tilt. The change was from 27.9±6.5 to 53.9±9.7 pmol L‐1(P<0.05). Atrial plasma NT‐proANP increased significantly from 357±91.2 to 529.1±116.0 pmol L‐1(P<0.05) at 10 min and remained high throughout the experiment. The molar ratio of NT‐proANP to ANP varied in atrial plasma from 9.5±1.2 to 13.9±2.7 showing that the plasma clearance of ANP from plasma was much higher

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.280000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY

摘要:

The present study examines the applicability of the isolated, acid‐secreting vascularly perfused rat stomach for long‐term physiological and pharmacological studies. The model was used to study the fade of acid secretion during gastrin stimulation. The stomachs were stimulated by exogenous gastrin or histamine alone or in succession. Acid secretion and venous histamine concentrations were measured. Gastrin and histamine potently stimulated acid output, histamine‐stimulated acid secretion was sustained for 300 min while gastrin‐stimulated secretion peaked at 120 min and declined towards basal output at 300 min. Stomachs rendered tachyphylactic to gastrin could be re‐stimulated by exogenous histamine. Venous histamine output during gastrin stimulation decreased in parallel to acid secretion. Thus, the acid‐secreting, isolated vascularly perfused rat stomach can be used for physiological and pharmacological studies with histamine as stimulant for at least 300 min. The present results strongly indicate that the effect of gastrin on acid secretion is mediated by histamine, and that fade of acid secretion during stimulation with gastrin is due to depletion of releasable mucosa

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1996.506272000.x

出版商:Blackwell Science    

年代:1996

数据来源: WILEY