摘要:

Voltage‐sensitive glass micro‐electrodes were used to determine the electrical characteristics ofNecturusproximal duodenal epithelium. Some comparative experiments with amiloride were performed with gastric antrum. The apical and the basolateral cell membrane potential differences in duodenum averaged ‐32 mV and ‐34 mV (cell negative) respectively. The transepithelial potential difference was ‐2 mV (lumen negative). The EMF across the apical cell membrane was ‐29 mV and that across the basolateral cell membrane ‐39 mV. The transepithelial resistance (R1) of 63 Ω cm2and the paracellular pathway resistance (Rs) of 8oΩ cm2are of magnitudes similar to that previously reported for more distal amphibian small intestine. The apical and basolateral cell membrane resistances, however, were lower than those reported for distal small intestine. Ion permeabilities for Na+, K+and Cl‐across the apical cell membrane were calculated from ion substitution experiments. The permeability sequence across the apical cell membrane was PK:Pcl:PNa3.02:1.31:1.00. Luminal amiloride (10‐4M) was without significant effect, further indicating a low duodenal membrane conductance for Na+. The low conductances for K+, Na+and Cl‐suggest that the major ion transport modes across the apical duodenal cell membrane are electroneutral in nature. In contrast, amiloride caused a marked increase in the transmembrane pot

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08783.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Proximal duodenum from the amphibianNecturuswas stripped of muscle layers and the mucosa was mounted as a tube for studies of alkali transport or as a flat sheet for intracellular impalement by voltage‐sensitive glass micro‐electrodes. The mucosa alkalinized the unbuffered luminal perfusate at a high rate (34 μequiv. Cm‐1h‐1) and developed a transepithelial electric potential difference of 5.7 mV (lumen negative). Transport was inhibited by 2,4‐dinitrophenol (10‐4M) and by furosemide (10‐3M) and SITS (10‐3M) on the serosal but not on the mucosal side, indicating dependence on tissue metabolism and on serosal membrane Cl‐/HCO3‐exchange. Prostaglandin E2(107‐105M) and dibutyryl cyclic AMP (10‐6‐10‐4M) had no effects on the secretion or transepithelial electrical potential difference. Removal of serosal HCO‐3decreased luminal alkalinization by 75%, indicating a contribution by passive migration of HCO‐3, and/or a dependence of transcellular transport on the nutrient supply of this ion. Administration of HCO‐3(17.8 mM) to the luminal perfusate affected neither the transepithelial nor transmembrane electrical potential differences nor the resistance ratio. It is thus unlikely that the luminal membrane po

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08784.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

The guinea‐pig ileum longitudinal muscle‐myenteric plexus preparation, pre‐incubated with [3H]choline, was mounted in an organ bath and superfused with Tyrode's solution. [3H]Acetylcholine secretion was evoked by 150 electrical shocks at 0.5 Hz.>N6,2′‐0‐Dibutyryladenosine 3′,5′‐cyclic monophosphate (dibutyryl cyclic AMP) enhanced the [3H]acetylcholine secretion in the presence of eserine and the adenosine receptor antagonist 8‐phenyltheophylline (10 μmol 1‐1). Conversely, in the absence of 8‐phenyltheophylline the [3H]acetylcholine secretion was reduced by dibutyryl cyclic AMP. In the absence and presence of 8‐phenyltheophylline(apparent KD= 12 μ.mol 1‐1), adenosine reduced the [3H]acetylcholine secretion to 33% of control (IC50= 8, μmol l‐1) and to 48% of control (IC50= 14 μmol l‐1) respectively. Neither butyrate, dibutyryl cyclic GMP nor guanosine altered the [3H]acetylcholine secretion.Interaction experiments with 3‐isobutyl‐1‐methylxanthine and oxotremorine were done in the absence of eserine, i.e. when oxotremorine is effective. Oxotremorine depressed the fractional secretion of [3H]acetylcholine with a ‘maximal inhibition’ of 13% of control (IC50= 10 nmol l‐1). In the presence of 3‐isobutyl‐1‐methylxanthine (5 mmol l‐1) oxotremorine depressed the secretion to 2% of control with an apparent IC50) value of 0.9 μmol l‐13‐Isobutyl‐I‐methylxanthine (0.01–4 mmol l‐1) enhanced the fractional secretion of [3H]acetylcholine with a ‘maximal enhancement’ value of 232% of control (EC50= 0.19 mmol l‐1). The presence of oxotremorine (30 nmol l‐1) counteracted, and higher concentrations reversed, the enhancement caused by 3–isobutyl‐I‐methylxanthine.The results are consistent with the suggestion that the presynaptic muscarinic acetylcholine receptor‐mediated control of the secretion of [3H]acetylcholine in the g

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08785.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Botulinum neurotoxin (BoTx) serotype E blocks spontaneous and evoked quanta! release of acetylcholine at the rat neuromuscular junction. Increasing extracellular Ca2+to 8 mmol l‐1or substituting Ca2+with La3+(0.1 and 1.0 mmol l‐1) or depolarizing the nerve terminals by 20 mmol l‐1K+markedly increases miniature end‐plate potential frequency in normal muscle, but in BoTx‐E poisoned preparations none of these ions, with the exception of 1 mmol l‐1La3+, was able to restore spontaneous quantal transmitter release to levels recorded at unpoisoned junctions. In absolute values the enhancement with La3+was much less than that reported at normal junctions.Nerve stimulation in the presence of 3,4–diaminopyridine (10–20 μmol l‐1) and high calcium (8 mmol l‐1) evoked multiquantal end‐plate potentials and muscle twitches. We conclude that the neuromuscular block produced by BoTx serotype E is similar to that previously described for BoTx serotype A but differs from that produced by BoTx serotypes B, D and F in not causing desynchronization of nerve impulse‐evoked transmitter release. 3,4–Diaminopyridine might be useful in the treatment of poisoning by BoTx serotype E since it markedly enhanced synchronous transmitter release from pois

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08786.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

A previous field potential study has indicated a monosynaptic projection of fibres from the central lateral nucleus (CL) to the mid‐suprasylvian gyrus (MSSG). The present study, which is based on an analysis of current source density (CSD), aims to investigate further the sites of major localized synaptic activities in different layers of the MSSG after electrical stimulation in the CL. An initial positive surface potential was evoked in the MSSG with a latency of 3–5 ms and followed by a large negative potential with a peak latency of 8–15 μs. The initial positivity was only found in the rostral part of the MSSG, which corresponds to area 5. The positivity reversed in deeper layers. The CSD analysis showed a sink at a depth from 650 to 1050 μ. A corresponding source was found more superficially at 400–600 μ. This indicates that CL fibres have an excitatory synaptic termination on the soma or proximal dendrites of neurons in layers III and IV. The surface negative potential reversed at the border between layers II and III, suggesting a superficial CL projection. The CSD analysis of potentials in superficial layers showed a sink appearing between the pial surface and a depth of 350 μm, and a source lying in layers below. This indicates a depolarization of apical dendrites of cells in layers II and III. The superficial sink appeared in a large part of the MSSG. Application of a solution of 0.5% gamma‐aminobutyric acid (GABA) on the surface of the cortex blocked the superficial sink and source and revealed a prominent sink current in layers III and IV in agreement with a deep termination of CL fibres. Application of a solution of 25 mM DL‐2–amino‐5–phosphono‐valeric acid (APV) abolished CL‐evoked cortical responses indicating that N‐methyl‐D‐aspartate (NMDA) receptors are involved in the cortical activation. The CSD analysis confirms that CL has a wide superficial projection to the MSSG. It also confirms a deeper monosynapt

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08787.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

Compensatory absorption of extravascular fluid from skeletal muscle and skin into the circulation in response to experimental hypovolaemia was studied by plethysmographic technique in the upper arm of man. Lower body negative pressure (LBNP) of 90 cmH2O, applied for 10 min, served to produce rapid and prominent hypovolaemic stress as indicated by prompt decrease in central blood volume (external recording of [99Tcm]erythrocyte activity) followed by marked tachycardia. The arm concomitantly showed an initial mobilization of regional blood, an increased vascular resistance, and a continuous net transcapillary fluid absorption, i.e. similar responses as reported in animals upon haemorrhage. The absorption of extravascular fluid, validated by simultaneous analyses of changes in tissue volume and in regional blood volume [99Tcm]erythrocyte activity), was rapid and averaged 0.13 ml min‐1100 ml‐1soft tissue during the 10 min of LBNP exposure. In some subjects with symptoms and signs of pronounced circulatory stress fluid was transferred twice as fast. Separate experiments indicated that the rapid fluid flux was causally linked to the existence in the studied tissue of a large transcapillary hydraulic conductance. It is concluded that man possesses a surprisingly great capacity for compensatory circulatory refill via fluid transfer from tissue to blood. The data in fact suggest that in true states of hypovolaemia as much as 500 ml might be gained into the circulation in only 10

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08788.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

The renal medulla harbours powerful humoral antihypertensive mechanisms, as earlier explored in unclipping experiments on renal hypertensive rats or in normotensive isolated kidneys cross‐circulated at increased perfusion pressures from ‘donor rats’, in which renal function also seemed to be affected. Injection of the renomedullary factor medullipin I (Med I; formerly ANRL) mimics these haemodynamic responses, and Med I seems to be one of the most important mediators of the depressor effects.The present study was performed to analyse further the haemodynamic and, particularly, the renal effects of Med I, using anaesthetized intact WKY rats and constant‐pressure perfused (90 mmHg) isolated WKY kidneys, cross‐circulated by these intact ‘donor’ rats. Mean arterial pressure (MAP), heart rate (HR) and renal function were followed for one 30‐min period before and two 30‐min periods after injection of 1 mg Med I (M; n = 7) or an equal volume of saline as control (C;n= 13).In the intact ‘donor’ WKY, MAP and HR remained largely constant in C during the three periods, being 126 ± 5, 125 ± 5, and 120 ± 5 mmHg, while MAP fell in the M group after Med I, from 121 ± 5 to 107 ± 7 and 107 ± 5 mmHg(P<0.05), and also HR tended to decrease in M. Renal resistance (RR) fell while renal plasma flow (RPF) and glomerular filtration rate (GFR) increased significantly (P<0.05) after Med I in the M donor rats despite their MAP reduction. However, in the constant‐pressure perfused, cross‐circulated kidneys the RR, RPF and GFR changes were clearly more pronounced (P<0.01) and also diuresis, natriuresis, osmolar excretion and osmolar clearance increased significantly after Med I (P<0.01). In conclusion, the present results support the view that Med I not only has important and long‐lasting depressor effects but also affects renal function in important ways, inducing vasodilatation and increasing GFR, RPF, diur

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08789.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

摘要:

The possible relationship between peptic ulcer and the occurrence of auto‐antibodies was investigated by means of an enzyme‐linked immunosorbent assay (ELISA). Sera from 24 patients with active duodenal ulcer were analysed using cells and subcellular fractions from pig gastric and duodenal mucosa for binding of immunoglobulins. Four sera (17%) reacted with a homogenate from duodenal mucosa. Nine sera (38%) were found to contain auto‐antibodies against gastric mucosal cells. The cell‐reactive autoantibodies were shown to bind preferentially to parietal cells and chief cells. In these cells the antigens were identified as H, K‐ATPase and pepsinogen respectively. Six sera were positive against purified H,K‐ATPase; 12 sera were positive against pepsinogen, and only one of these sera reacted with both H,K‐ATPase and pepsinogen. The results show that auto‐antibodies are formed in a large fraction of patients (18/24; 75%) with peptic ulcer disease. The present study further demonstrates that enrichment of antigenic structures is required for obtaining a satisfactory sensitivi

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08790.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08791.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1989.tb08792.x

出版商:Blackwell Publishing Ltd    

年代:1989

数据来源: WILEY