摘要:

This study examines lactate and K+fluxes from muscle to blood during and after intense exercise. Ten men performed exhaustive dynamic exercise (mean load 65 W, mean duration 3.18 min) with the knee extensors of one leg. The mean lactate efflux was 15.5 (range 8.9–24.0) mmol min‐1at exhaustion, and it was linearly related to the lactate gradient. A linear relationship was also obtained if the H+gradient was taken into account. Muscle pH decreased from 7.14 at rest to 6.71 (range 6.50–6.87) at exhaustion. At rest and during late recovery blood lactate was distributed across the erythrocyte membrane according to the membrane potential (intra‐/extracellular ratio of 0.5), but during rapid lactate release this ratio decreased to 0.2.In‐vitroexperiments demonstrated a time constant of 1.2 min for lactate efflux from the erythrocytes.Approximately 70% of the K+ions released from the muscle to the blood accumulated in the plasma; the rest were taken up by other tissues. However, erythrocytes were not involved as a dilution space. The small change in erythrocyte K+concentration was due to cellular volume changes. During recovery the kinetics of K+reuptake by the muscle were described by a very fast (1 min): the magnitude of the former was equivalent to what had accumulated in the plasma. Individuals displayed a wide range of intramuscular lactate concentrations and pH values at exhaustion. Further, the pH changes were not as extreme as previously reported, suggesting that pH may not be the only factor involved in the fatigue process. A possible role for the potassium shifts as a limiting factor for muscle function is

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08986.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

To evaluate the importance of right atrial filling pressure versus central blood volume for the plasma concentration of atrial natriuretic peptide in man, head‐up tilt to 50± maintained until the appearance of presyncopal symptoms was carried out in six healthy males. Head‐up tilt increased thoracic electrical impedance from 35± 0.9 (mean and SE) to 39.2 ± 0.9 ohm, mean arterial pressure from 64.5 ± 3.6 to 76.6 ± 3.0 mmHg and heart rate from 51± 3 to 85 ± 4 beats min‐l(P<0.01). After 35 ± 7 min presyncopal symptoms appeared, together with a decrease in mean arterial pressure to 51 ± 4 mmHg and in heart rate to 59 ± 7 beats min‐1(P<0.01). Central venous pressure (2.1 ±1.0 mmHg) did not change significantly, but atrial natriuretic peptide decreased from 9.4 ± 1.6 to 4.2 ± 1.3pmol l‐1(P<0.01) and was inversely related to thoracic impedance (r= ‐0.65,n= 44,P<0.001). The results indicate that changes in the central blood volume rather than in central venous pressure determine the secretion of atrial na

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08987.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Cardiac output at rest increased by 11–63 % in a group of healthy individuals after the consumption of a medium‐sized, mixed meal. The maximum post‐prandial levels of cardiac output were reached from 10 to 30 min after termination of the meal. Cardiac output values at rest fluctuate around a mean level, and this fluctuation was considerably more marked after a meal, when changes in cardiac output from one 15–s period to another could be of the order of 1–1.5 1 min‐l.Recording of flow in the superior mesenteric artery before and also after a meal was successful in two subjects in whom anatomical conditions were favourable. Flow in the artery was approximately doubled from the fasting to the post‐prandial situation, an augmentation that accounted for about 50% of the concomitant increase in cardiac output.The increases in cardiac output caused by 2–min bouts of standardized, moderate and rhythmic exercise were consistently larger in the post‐prandial than in the fasting situation. It thus appears that any tendency for redistribution of blood flow, for example from the gastrointestinal tract to the working muscles, during moderately intense exercise is less marked after a

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08988.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

The myosin heavy chain (MHC) composition of single fibres from m. biceps brachii of young sedentary men (28 ± 0.4 years, mean ± SE,n= 4) and male body builders (25 ± 2.0 years,n= 4) was analysed with a sensitive one‐dimensional electrophoretic technique. Compared with sedentary men, the body builders had a higher proportion of fibres containing only MHC type IIa (36 ± 4us12 ±2%;P<0.05), but a lower proportion of fibres with a coexistence of MHC types IIa and IIb (16 ± 3us34 ± 2%;P<0.05) and nearly no fibres containing only MHC type IIb(1 ±1vs12 ±1%;P<0.05). Myofibrillar ATPase histochemistry only demonstrated a trend towards a higher proportion of type IIa fibres (31 ± 6us25 ± 6%)and a lower proportion of type IIb fibres (18 ± 5us26 ± 6%) within the body builders. These results, therefore, suggest an altered expression of MHC isoforms within histochemical type II fibres of human skeletal muscle with body building. Furthermore, in human skeletal muscle differences in expression of MHC isoforms may not always be reflected in the traditional histochemical classification of types I, IIa, IIb

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08989.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

This study concerns the function of aortic baroreceptors during slow haemorrhage, in particular the mechanisms by which baroreceptors respond to hypovolaemia in the absence of hypotension and the manner in which haemodynamic information is encoded in the aortic nerve discharge. Beagle dogs, anaesthetized with morphine and chloralose, were instrumented for the recording of aortic pressure, aortic diameter, aortic flow and aortic nerve activity. The animals were subjected to slow haemorrhage (0.4 ml kg‐1min‐1) of 20% of the estimated blood volume. Mean aortic pressure remained unchanged, whereas mean aortic diameter, mean aortic tension and aortic baroreceptor activity decreased during the haemorrhage. Baroreceptor sensitivity to mean aortic pressure, mean aortic diameter and mean aortic tension decreased as the haemorrhage proceeded. Also, the sensitivity of baroreceptors to mean aortic pressure and mean aortic diameter during acute pressure stimulation was attenuated. The results indicate that during non‐hypotensive haemorrhage aortic baroreceptor discharge is reduced by two mechanisms: firstly, via constriction and stiffening of aortic smooth muscle and, secondly, via direct effects of the compensatory mechanisms on the baroreceptors. The reduced sensitivity renders the baroreceptors capable of responding to hypovolaemia prior to the onset of hypotension. In the regression analysis, systolic aortic diameter proved to be the best determinant of baroreceptor activity (r =0.877). Of the neural variables, impulses per cardiac cycle and average discharge rate were the most reliable, but no difference in the relative importance of these two parameters could be obs

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08990.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

In a previous study, electrically induced contractions of the gastrocnemius muscle in conscious spontaneously hypertensive rats were shown to induce a blood pressure reduction of 15–20 mmHg lasting several hours. We showed in that study that endogenous opioid systems were involved.In this study, drugs with selective affinity for different opioid receptors were used to analyse further the involvement of endogenous opioid systems in the post‐stimulatory drop in blood pressure in spontaneously hypertensive rats. Prestimulatory intra‐cerebroventricular administration of β‐FNA (a preceptor antagonist) did not significantly influence the response at all, nor did a lower intravenous dose of naloxone reverse the post‐stimulatory drop in blood pressure. High‐dose naloxone (15 mg kg‐') increased post‐stimulatory blood pressure by around 10 mmHg. About 50% of the drop thus remained after this treatment. A similar, partial reversal of the decreased blood pressure was seen after intravenous administration of a&receptor antagonist, ICI 154, 129. However, the depressor response was completely reversed by a low intravenous dose of MR 2266 BS (a K‐receptor antagonist).These results suggest that the reduction in blood pressure after muscle stimulation is mainly mediated by the opioid k‐receptor. A certain involvement of the δ‐rec

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08991.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

In the present study we have examined the action of the phorbol diester tetradecanoyl phorbol acetate, an activator of protein kinase C, on the transepithelial transport of sodium, chloride and water and the production of cAMP in the isolated frog skin epithelium (Rana esculenta).Addition of tetradecanoyl phorbol acetate to the mucosal solution resulted initially in an increase in the short‐circuit current, which was followed by a progressive decrease. If the short‐circuit current was first activated by addition of the antidiuretic hormone, arginine vasotocin, then the addition of tetradecanoyl phorbol acetate resulted only in a pronounced inhibition. The changes in the short‐circuit current were the result of changes in the active influx of Na+.The effect of tetradecanoyl phorbol acetate on the intracellular potential measured under short‐circuited conditions (Vscc) was time‐dependent. Just after addition of tetradecanoyl phorbol acetate to the mucosal solution.Vsccdepolarized; this was followed by a slight hyperpolarization, after whichVscccontinued to decline.The inhibition of the Na+transport by tetradecanoyl phorbol acetate was associated with a decline in the response to the antidiuretic hormone (arginine vasotocin), but the ability of arginine vasotocin to increase the cellular level of cAMP and to stimulate the osmotic water flow was not affected by the presence of tetradecanoyl phorbol acetate.In skin halves in which the short‐circuit current was stimulated with arginine vasotocin, addition of tetradecanoyl phorbol acetate resulted in a dose‐dependent inhibition of the short‐circuit current, but only minor changes inVsccwere observed.The results presented suggest that the addition of tetradecanoyl phorbol acetate to the isolated frog skin first increases and then decreases the arginine vasotocin‐sensitive sodium permeability of the apical membrane. This might be due to a stimulating effect of tetradecanoyl phorbol acetate on both the activation and deactivation (turnover) of th

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08992.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

The inhibitors of the cGMP‐inhibited, low‐KmcAMP phosphodiesterase—milrinone and OPC 3911‐and an inhibitor of a non‐cGMP‐inhibited low‐KmcAMP phosphodiesterase—rolipram—were used to evaluate the functional importance of the two cAMP phosphodiesterase activities in vascular smooth muscle and in platelets. Vinpocetine, an inhibitor of a calcium‐calmodulin‐dependent phosphodiesterase was also studied. OPC 3911 and milrinone relaxed the contracted rat aorta, inhibited ADP‐induced platelet aggregation and also enhanced isoprenaline‐induced relaxation as well as the antiaggregatory effects of adenosine. In platelets, OPC 3911 and milrinone increased cAMP levels, but in the rat aorta the increase was significant only for milrinone (OPC 3911P= 0.062). In both tissues OPC 3911 and milrinone enhanced the increase in cAMP caused by activators of adenylate cyclase (isoprenaline/adenosine). Rolipram had no effects on aggregation or cAMP levels in platelets and no overadditive effects in combination with adenosine. Rolipram had little effect on relaxation and cAMP levels, did not alter isoprenaline‐induced relaxation of guanfacin‐contracted rat aorta, but showed synergistic effects with isoprenaline in raising cAMP levels. In PGF2α‐contracted aorta rolipram enhanced relaxation caused by isoprenaline. Vinpocetine had a relaxant effect without affecting cAMP levels, but had no effect on platelets. These results support the concept that the cGMP‐inhibited phosphodiesterase is an important modulator of vascular smooth muscle tone and platelet function. The role of the non‐cGMP‐inhibited phosphodiest

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08993.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Average capillary pressure (Pe) close to the venous end (fluid equilibrium point) of the exchange vessels (denotedPev) arterial (PA) and venous pressure, and the rate of net transcapillary fluid flux were continuously recorded in sympathectomized muscle during 30 min of graded exercise and for 30 min in the post‐exercise period. Regional changes in colloid osmotic pressure (±p1) and total osmolality in plasma, the latter reflecting work‐induced interstitial hyperosmolality, were measured at intervals. In the control state at rest with a Starling fluid equilibrium,Pcv, averaged 17.6±40.8 mmHg. Exercise caused a rapid transcapillary plasma fluid loss, the net driving pressure for which in the initial phase of heavy work was 58 mmHg (transcapillary fluid flux divided by the capillary filtration coefficient). This comprised an increase inPcvof 16 mmHg, a nonprotein osmotic force (Posm) related to exercise‐induced tissue hyperosmolality corresponding to 46 mmHg and an opposing force established by a raised ±p1of 4 mmHg. A theoretical analysis indicated that the main fraction of the osmotic fluid loss passed through transcellular ultrapores and only a minor part through conventional small pores. In spite of the fact thatPcremained high throughout the exercise period, the outward fluid flux gradually declined and a Starling equilibrium was re‐established 23 min after the commencement of heavy exercise. This was explained by a gradual declineof Posmand apparently also by a secondary increase in tissue pressure (Pu) and/or a decrease in interstitial colloid osmotic pressure (±if). Net fluid absorption occurred in the post‐exercise period as a result of a gradual decrease inPe, reversed transcapillaryPosmand also maintained highPifand/or low ±if. Exercise (even light) abolished normalPcautoregulation, implying that the filtration component of net transcapillary fluid flux becomes distinctly modulated

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08994.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Non‐myelinated C‐fibre responses during sympathetic trunk stimulation were studied in rabbit common peroneal nerve 2 weeks after the nerve had been subjected to compression at 400 mmHg for 30 min. Our previous studies have demonstrated that during sympathetic trunk stimulation the compound action potential of uninjured somatic C‐fibres is characterized by a reduced amplitude and an increased latency. In the present study, nerve compression changed the C‐fibre response to sympathetic stimulation. Three out of eight nerves reacted to nerve compression by increased C‐fibre compound action potential amplitude in response to sympathetic stimulation. In three other rabbits with compressed nerves the C‐fibre action potential amplitude was unchanged, and in the remaining two rabbits the action potential amplitude was decreased during sympathetic stimulation. The action potential latency increased in all tested compressed C‐fibres. The phenomenon of increased C‐fibre amplitude during sympathetic activation has not been observed in uninjured nerves. As in uninjured nerves, noradrenaline infusion produced an increased C‐fibre action potential amplitude and latency in six animals. Sympathetic stimulation did not affect the A‐fibre response. These results indicate that sympathetic activity influences the conduction properties in C‐fibres of somatic origin and that the response can be changed after a nerve injury. The findings may be of importance for the understanding of pain aggravation in different types of nerve injuries during increased

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1990.tb08995.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY