摘要:

Renal function was measured by clearance technique before and after acute myocardial infarction (MI) induced by left coronary artery ligation in male Sprague–Dawley rats. The animals were anaesthetized with halothane‐nitrous oxide, paralysed with pancuronium and artificially ventilated. All parameters were stable throughout the experiment in sham‐operated time control animals (n = 8). After MI, rats developed left ventricular dysfunction with increased left ventricular end‐diastolic pressure and decreased mean arterial pressure. MI produced antidiuresis and antinatriuresis without changes in glomerular filtration rate (GFR), lithium clearance or renal albumin excretion (n = 8). The antidiuretic and antinatriuretic responses to MI were similar in rats with chronic bilateral renal denervation (n = 5). Three additional rats with chronic bilateral renal denervation had cardiac arrest and were resuscitated with cardiac massage, i.v. lidocaine and intracardiac adrenaline administration. These animals showed a transient increase in urine flow rate, sodium and albumin excretion with maximum 30–60 min after resuscitation, while GFR and lithium clearance were normal. Since cardiac ischaemia and sympathetic stimulation are strong stimuli for the release of atrial natriuretic peptide (ANP), we examined if ANP (0.25, 0.50, and 1.00 μg kg−1 min−1,n = 8 per dose) affects urinary albumin excretion. ANP increased dose‐dependently the urine/plasma concentration ratio of albumin relative to inulin, which suggests that ANP increases the glomerular permeability for albumin. We conclude that MI causes stimulation of renal tubular sodium and water reabsorption by a mechanism which is independent of intact renal innervation. MI does not produce any change in renal albumin excretion in rats, but transient albuminuria may be observed in rats following cardiac arrest and/or manoeuvres used in cardiac resuscitation. Since ANP produces albuminuria, we speculate that ANP may be an important mediator of albuminuria in states wi

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00162.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Dopamine produced in the kidney acts as a natriuretic hormone by inhibiting tubular Na+, K+‐ATPase activity. Previousin vitrostudies have shown that Na+, K+‐ATPase activity in the proximal tubule is inhibited by a synergistic action of dopamine 1 (DA1) and dopamine 2 (DA2) receptors. Thisin vivostudy, performed on rats, investigates whether the natriuretic response to DA requires a synergistic action of DA1and DA2receptors. The DA1agonist, fenoldopam, significantly increased urinary sodium excretion, but there was no increase in sodium excretion when a DA1agonist was given together with a DA2antagonist. Neither DA1nor DA2antagonists had any influence on sodium excretion. The natriuretic response to fenoldopam was also significantly attenuated after the administration of benserazide, which inhibits aromatic acid decarboxylase and thereby suppresses the endogenous production of dopamine. In conclusion, the natriuretic effect of dopamine depends on the activation of both DA1and DA2receptors. The DA2receptor appears to be constitutively activated by endogenous dopam

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00166.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Solute flux per unit surface area and concentration gradient, (JS/SΔC), was quantified in arterioles isolated from hearts of sedentary (SED) and exercise‐trained (EX) female Yucatan Miniature Swine. Apparent permeability (PS) was assessed from measures ofJS/SΔCfor two proteins, α‐lactalbumin (α‐lact) and porcine serum albumin (PSA), under basal conditions and following 5 min suffusion with 10−5Madenosine (ADO). Both proteins were labelled with the fluorescent dye tetramethyl rhodamine isothiocyanate. Basal Psto α‐lact differed with exercise training ((Pα‐lacts)SED=5.2±1.8 (median±median absolute deviation (MAD),n=9 pigs) versus (Pα‐lacts)EX=7.4±1.1×10−7cm s−1,n=9,P<0.05). For the larger protein PSA, basal Psdid not change with training ((PPSAs)SED=5.0±1.6,N=11 vs. (PPSAs)EX=4.1±1.2×10−7cm s−1,N=11). Suffusion of the arterioles (33±4 μm diameter,n=18 vessels) from SED hearts (n=14) with 10−5MADO decreased Pα‐lacts15±8% relative to control and was without effect on PPSAs. By contrast, in arterioles (39±4 μm diameter,n=22 vessels) from EX hearts (n=14), ADO increased Pα‐lactsand PPSAsby 32 and 65% respectively, indicating that receptor‐mediated changes in permeability were also sensitive to exercise training. These data demonstrate that, for coronary arterioles, permeability to macromolecules adapts to exercise training. The adaptive mechanisms may involve more than one structural component of the vessel wall

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.661369000.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

This study investigated the time course change of myoglobin concentration ([Mb]) in skeletal muscle during muscle hypertrophy in rats. Seven groups of Wistar rats (n = 7 per group) were examined. Compensatory hypertrophy of the plantaris muscle was induced by the bilateral ablation of the medial and lateral heads of the gastrocnemius muscle, and the effect of compensatory hypertrophy on the [Mb] of the plantaris muscle was examined at 7, 21 and 42 days post‐ablation. The [Mb]expressed as mg g−1wet muscle weight tended to decline at 7 days post‐ablation (−12.1%) and returned to the control level by 42 days post‐ablation, as did the muscle protein concentration. However, the [Mb] expressed as mg g−1protein weight was not significantly different between the ablation and control groups throughout the experimental period. The estimated value of absolute Mb content in the whole plantaris muscle was significantly increased by 28.4% (P < 0.01) at 42 days post‐ablation compared with the age‐matched controls. Therefore, the longer period of compensatory activity allowed the Mb to increase in its absolute content, although the [Mb] did not exceed the level of control muscle. The capacity of facilitated oxygen diffusion and oxygen storage by Mb in the muscle cells will not change even when muscle

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00170.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

We have recently shown thatin vivonatural cytotoxicity is enhanced after chronic exercise in spontaneously hypertensive rats (SHRs). In the present report, we have studied the duration of this augmentation and some possible mechanisms involved. Exercise consisted of voluntary running for 4–5 weeks, with the running distance ranging from 2.7–15.6 km day−1during the last week of running.In vivocytotoxicity was measured as clearance of injected51Cr‐labelled YAC‐1 lymphoma cells from the lungs. Thein vivonatural cytotoxicity was increased in running SHRs, and also in SHRs that had their running wheel locked for 24 and 48 h prior to the experiment, and was still present after 96 h. The enhancement ofin vivocytotoxicity after 5 weeks of exercise was abolished after an acute injection of theβ‐adrenergic receptor antagonist timolol (0.5 mg kg−1i.v.), indicating that catecholamines are involved in this augmentation. Interestingly, 24 h after the last exercise bout, the increased natural cytotoxicity could be blocked by timolol. The opioid receptor antagonist naloxone given subcutaneously for 7 days by osmotic pumps (6 mg kg−1h−1) could not reverse the increasedin vivocytotoxicity seen in the running SHRs, suggesting that opioid receptor mechanisms are not involved, or at least not the naloxone‐sensitiveμ‐receptor. Natural immunity was not influenced by the histamine H2receptor antagonist ranitidine, either in controls or in runners, indicating that the natural killer cell‐regulatory effect of histamine is not present in SHRs and does not seem to be involved in the exercise‐induced changes in natural immune function. We conclude that the augmentation ofin vivonatural cytotoxicity after voluntary chronic exercise in rats is long‐lasting and that the augmentation

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00185.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

This study investigated the relationship between muscle morphology and surface electromyographic parameters (mean frequency,fmean; and signal amplitude, RMS) during sustained static knee extension to exhaustion at 25% maximal voluntary contraction (MVC) and at 70% MVC. Twenty clinically healthy subjects participated. EMGs were registered from the quadriceps. Muscle forces during knee extension at a 90° joint angle were maintained at the respective levels throughout the measurement periods. A biopsy was obtained of the vastus lateralis muscle. The total time to exhaustion was normalized for each subject. By means of regression analysis, the intercept (i ) (i.e. the unfatigued state) and the regression coefficient (k ) were determined for each EMG parameter.The endurance time increased with decreasing force level. A significantly higher perception of fatigue was found at 25% MVC than at 70% MVC. From principal component analyses it was concluded that RMS‐kat 25% MVC mainly correlated with the type 2 muscle fibre proportions (%), and at 70% MVC mainly with the areas of type 2 muscle fibre. At 25% MVC,fmean‐kcorrelated with the areas of type 2A, 2B and 2C fibres, and at 70% MVC negatively with the proportion of type 2B and to some extent with areas of type 2A, 2B and 2C fibres.fmean‐iat 25% MVC correlated with fibre type proportions (%); fmean‐iat 70% MVC correlated with the areas of type 2A, 2B and 2C.The present study indicates relationships between surface EMG and muscle morphology, which is contrary to presented model

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00167.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

This study investigated changes in intramuscular pressure (IMP) and surface electromyographic (EMG) parameters (mean frequency of the power spectrum,fmean; and signal amplitude denoted as root mean square, RMS) during contractions to fatigue at 25 and 70% of maximal voluntary contraction (MVC). Parameters were recorded simultaneously from the vastus lateralis muscle during knee extension. A significant decrease infmeanoccurred with time at both contraction levels; however, the rate of decline (slope) was greater at 70% MVC. RMS increased throughout the contractions at both levels, with the relative increase being significantly greater for 25% MVC. IMP increased during 25% MVC but did not change during the 70% MVC contraction. IMP at rest was significantly higher post‐contractions than it was pre‐contractions at 25% MVC (21.1 vs. 8.0 mmHg,P < 0.01) and 70% MVC (13.7 vs. 8.6 mmHg,P < 0.01). Consequently, post‐contraction IMP was higher at 25% MVC than at 70% MVC (P < 0.01). IMP changes throughout the fatiguing contractions correlated negatively withfmeanand positively with RMS at both MVC levels; however, these correlations were better at 25% MVC. The extent of intramuscular water accumulation is discussed as a major cause of the difference in IMP changes between 25% and 70% MVC. Significant differences in the rate of change for all parameters between high vs. low contraction levels may suggest a common mechanism governing changes in IMP and E

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00168.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

The aim of the study was to determine if and by what mechanism(s) nitric oxide inhibition modulates the susceptibility of the duodenum to hydrochloric acid‐induced disturbances of mucosal integrity. A second aim was to investigate whether basal permeability is a determinant of epithelial acid barrier function. Using anin situduodenal perfusion model, mucosal permeability, alkaline secretion and morphology were investigated in anaesthetized rats. Luminal perfusion with 50 mmhydrochloric acid increased duodenal mucosal permeability in the control animals. In animals receiving the nitric oxide synthase inhibitorN‐nitro‐l‐arginine methyl ester (l‐NAME 3 mg kg−1and 1 mg kg−1h−1) and in those receiving vasopressin (1 IU kg−1h−1), however, the mean increase in permeability in response to acid was markedly higher. In rats treated with either hexamethonium (20 mg kg−1) or atropine (0.5 mg kg−1)l‐NAME failed to augment the acid‐induced increase in permeability. Perfusion with hypotonic saline (25 mm) increased basal permeability but did not influence the response to acid. Exposure of the duodenum to hydrochloric acid caused very subtle changes of duodenal morphology. It is concluded that both inhibition of endogenous nitric oxide synthesis and vasopressin treatment augment the acid‐induced increase in mucosal permeability. The mechanisms involved may be related to changes of Starling forces in the microcirculatory bed. Endogenous nitric oxide may protect the duodenal mucosa by regulating vascular per

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00171.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Several mechanisms involved in nervous secretory reflex(es) of the enteric nervous system may be dependent on the flux of calcium across the plasma membrane, which may be controlled by voltage‐gated calcium channels. In this study, we investigated the importance of plasma membrane calcium channels for intestinal fluid secretion. Two types of studies were performed, in which intestinal net fluid transport in anaesthetized rats was followed with a gravimetric method. First, the effects on intestinal fluid transport of placing A23187, a calcium ionophore, in the intestinal lumen was studied. A23187 induced in a dose‐dependent manner a net fluid secretion, which was abolished by giving hexamethonium (10 mg kg−1body wt) i.v. or placing lidocaine (1% solution) on the intestinal serosa. Nifedipine (5.75 μmol kg−1body wt i.v.) also abolished the fluid secretion caused by the ionophore. In the second study, the effects of various calcium channel blockers (gadolinium chloride, nifedipine, verapamil) were tested on the cholera toxin‐induced secretion. It was attenuated by luminal application of gadolinium chloride (1–10 mm) or nifedipine (10–200 μm). Intravenously administered nifedipine (2.5–5.75 μmol kg−1body wt) abolished cholera toxin‐evoked secretion dose‐dependently, whereas verapamil (0.05–1 μmol kg−1body wt) was without consistent effect. It is concluded that the fluid secretion evoked by placing A23187 in the intestinal lumenin vivowas induced via an activation of the enteric nervous system. Cholera secretion was attenuated or abolishe

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00174.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Most intestinal secretagogues, including cholera toxin, evoke fluid secretion in part by activating the enteric nervous system (ENS). The enterotoxins that, due to size, cannot pass the intestinal epithelial lining have been proposed to activate the ENS via the release of amines/peptides from the intestinal endocrine cells. It has been shown that calcium channel blockers of the L‐type attenuate intestinal fluid secretion. This study was performed on rat jejunal segments to elucidate where calcium channel antagonists interact with the secretory nervous reflex(es) of the ENS.In vivo, net fluid transport, transmural potential difference (PD) and luminal release of serotonin from the enterochromaffin cells were monitored before and after exposing the intestinal mucosa to cholera toxin (20 μg/mL) or the calcium ionophore A23187 (0.5 mm).In vitro, the effects of transmural electrical field stimulation (EFS) on short circuit current (SCC) was investigated using the Ussing chamber method. Cholera toxin and A23187 evoked a net fluid secretion, an increased PD and an augmented luminal release of 5‐HT. These effects were markedly attenuated by giving the calcium channel blocker nifedipine i.v. (5.75 μmol kg−1body wt). On the other hand, nifedipine (0.02 mm) had no significant effect on the increased SCC caused by EFSin vitro. The results obtained in thein vivoexperiments suggest that the nifedipine markedly attenuates the initial event in cholera toxin‐ and A23187‐induced secretion, the release of amines and probably also of peptides from the intestinal endocrine cells. Thein vitroexperiments seem to exclude an effect of the calcium channel blockade on the efferent part of the sec

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00173.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY