摘要:

The role of prostanoids in the feline intestinal vascular and central haemodynamic responses to i.v. infusion of liveE. coli. Acta Physiol Scand130, 359–366. Received 23 July 1986, accepted 11 February 1987. ISSN 0001–6772. Departments of Surgery, East Hospital, Göteborg, and General Hospital, Malmö, Sweden.Bacterial infusion in the cat, causing experimental septic shock, induces an early vascular response mainly characterized by pulmonary hypertension and intestinal vasocon‐striction. Prostanoids are held to be important mediators of the pulmonary vascular reaction. This study was performed to explore the involvement of prostanoids in the central haemodynamics and the small intestinal vascular reactions in experimental septic shock. Aortic blood pressure was continuously monitored, as were aortic blood flow, the pressure in a. pulmonalis and the small intestinal venous outflow. All cats (n= 24) were given liveE. coli(1010ml‐1) as a continuous intravenous infusion. One series was pretreated with indomethacin, another with UK‐38,485, a specific thromboxane A, synthetase inhibitor, and a third series served as untreated control. The pulmonary hypertensive response was clearly attenuated in the two pretreated series, in fact abolished in the one given UK‐38,485. The early intestinal vasoconstriction was eliminated in the two pretreated series. Later during bacteraemia, when untreated and indomethacin‐pretreated cats showed intestinal vasoconstriction, UK‐38–485‐pretreated animals kept intestinal blood flow within the preseptic range. These data suggest that in the cat, thromboxane A, is the prostanoid mediating the vascular reactions, not only in the lung but also i

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08149.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Prevention of ischaemic acute renal failure with superoxide dismutase and sucrose.Acta Physiol Scand130, 367–372. Received 24 September 1986, accepted 10 February 1987. Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.The preventive effects of intravenously administered superoxide dismutase (SOD) and of SOD combined with sucrose on acute renal failure were investigated in rat kidneys exposed to 45 min of warm ischaemia. Superoxide dismutase (20 mg) given just before primary ischaemia and in the early recirculation phase was found to ameliorate the red cell aggregation in the renal medulla, in particular, in the inner stripe of the outer zone the volume of trapped red cells decreased from 11.2 ± 1.6% in untreated animals to 0.02 ± 0.001%, thus allowing improved restoration of medullary blood flow. This was also accompanied by an expected restoration of the urine osmolality reaching almost 400 mOsmkg‐1after administration of SOD + sucrose. Superoxide dismutase also restored the capillary macromolecular permeability as evidenced by normalization of plasma to lymph transport of proteins. Micropuncture studies showed that in ischaemically damaged but untreated kidneys the tubules were obstructed and that the proximal tubular pressure rose to such a level that the net driving force for filtration approached zero. This explains the marked decrease in glomerular filtration rate (GFR) from a normal value of about 1 ml min‐1to 0.01 ± 0.02 ml min‐1. After treatment with SOD the tubules were still largely obstructed, resulting in a depression of the net driving force and a decrease in single nephron glomerular filtration rate (SNGFR) to about 11 nl min‐1, that is, to only 25% of the normal SNGFR. The total filtration was 0.09 ± 0.04 ml min‐1. When sucrose (2 ml of a 12% sucrose‐Ringer solution) was given in addition to SOD, with the aim of preventing cellular swelling, rapid wash‐out of rejected cells and cell debris into the urine was observed. The obstructions were eliminated and the free‐flow proximal tubular pressure was next to normal. The resulting SNGFR was about 30 nl min‐1and the total filtrati

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08150.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Depressor and pressor actions of purine nucleosides and nucleotides in the anaesthetized rat.Acta Physiol Scand130, 373–380. Received 12 May 1986, accepted 28 January 1986. ISSN 0001–6772. Departments of Physiology, University of Goteborg, Sweden and Anatomy&Embryology and Centre for Neuroscience, University College, London, UK.In pentobarbitone‐chloralose anaesthetized rats, the effects of aortic administration of various purine compounds on systemic arterial pressure were investigated. All animals were pretreated with atropine and guanethidine to (largely) eliminate reflex neurogenic cardiovascular adjustments, and drugs influencing purine receptors, prostaglandin synthesis, etc. were used for analytical purposes. The compounds used were adenosine (AD) and its slowly degradable analogue, 2‐chloroadenosine (2‐chloro), adenosine‐5′‐triphosphate (ATP) and its slowly degradable analogues β,γ‐methyleneATP (β,γ‐meATP) and α,β‐methyleneATP (α,β‐meATP). Control cardiac output measurements before, at and after the peak pressure changes in some experiments revealed that they were at least 80% due to changes in systemic resistance, i.e. dominated by shifts in resistance vascular tone. Adenosine, 2‐chloro, ATP and β,γ‐meATP all elicited depressor (vasodilator) responses. 2‐chloro was more potent than AD. Furthermore, the results suggest that the depressor action of ATP involves P1‐purinoceptors, following the rapid degradation of ATP to AD, and probably also other mechanisms. The stable ATP analogues caused prompt pressor (vasoconstrictor) responses, where α,β‐meATP was more potent than β,γ‐meATP. The latter compound also produced delayed (probably P1‐purinoceptormediated) depre

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08151.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Acute blockade of β1‐receptors in the asphyxiated sheep fetus.Acta Physiol Scand130, 381–385. Received 5 November 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Paediatrics, Landspitalinn, University Hospital, Reykjavik, Iceland and Department of Physiology and Department of Paediatrics I, University of Goteborg, Sweden.The effects of acute β1‐blockade on fetal cardiovascular reactions during asphyxia were evaluated in 11 exteriorized sheep fetuses. Gestational age was 110–142 days. Asphyxia was induced either by ventilating the mother with low oxygen gas mixture or by mechanical reduction of placental blood flow. During asphyxia all fetuses reacted to metoprolol injection with a decrease in heart rate, myocardial contractility, cardiac output and arterial blood pressure. Five experiments resulted in irreversible fetal cardiovascular collapse. Isoprenaline was given to the fetuses during hypoxia to test the ability to further increase heart rate and activate myocardial β‐adrenoceptors. In those experiments with fetal cardiovascular demise after metoprolol, the isoprenaline injection did not result in a significant tachycardia. The surviving fetuses could increase their heart rate as a sign of a capacity to further increase the sympatho‐

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08152.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Bleeding‐induced in duodenal HCO‐3secretion in the rat is mediated via α2‐adrenoceptors.Acta Physiol Scand130, 387–391. Received 23 January 1987, accepted 23 February 1987. ISSN 6001–6772. Department of Physiology, University of Göteborg, Sweden.This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO‐3secretion. The HCO‐3output was measured byin situtitration in a duodenal segment. Blood loss of 0.6 ml per 100 g body wt (approximately 10% of total blood volume) reduced duodenal HCO‐3secretion by about 30%. Pretreatment with guanethidine did not affect basal output of HCO‐3but markedly reduced the bleeding‐induced response. The α2‐adrenoceptor antagonist yohimbine did not affect the basal secretion but almost abolished the depression of duodenal HCO‐3secretion due to blood loss. Pretreatment with the a,‐adrenoceptor antagonist prazosine or the β‐adrenoceptor antagonist propranolol did neither change basal duodenal HCO‐3secretion nor the bleeding‐induced decrease in duodenal HCO‐3secretion. It is suggested that a small blood loss by means of a reflex activation of the sympathetic nervous system, and via the release of transmitter substances from adrenergic nerve endings, reduces the duodenal HCO‐3secretion. The inhibitory effect is mainl

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08153.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Effects of atrial natriuretic peptide (ANP) during converting enzyme inhibition.Acta Physiol Scand130, 393–399. Received 1 December 1986, accepted 10 February 1987. ISSN 0001–6772. Department of Physiology&Medical Biophysics, Biomedical Centre, University of Uppsala, Sweden.Studies were performed on anaesthetized adult Münich‐Wistar rats to investigate the role of angiotensin 11 in the natriuretic response to synthetic atrial natriuretic peptide (ANP, 28 amino acids). For this purpose the whole kidney glomerular filtration rate (GFR) and urinary excretion of electrolytes were measured in groups of animals pretreated with the converting enzyme inhibitor captopril (3 mg h‐1kg‐1body wt) or vehicle and then given a continuous intravenous infusion of ANP at 10 μg h‐1kg‐1body wt. In the vehicle‐pretreated animals, 45 min of ANP infusion did not change GFR (control value 1.17 ± 0.11, experimental value 1.17 ± 0.06 ml min‐1g‐1kidney wt). Sodium excretion (UNaV) increased more than three‐fold from 0.036 ± 0.010 to 0.134 ± 0.058 pmol min‐1g‐1kidney wt (p0.05) and potassium excretion (UKV) increased from 0.481 ± 0.055 to 0.946 ± 0.068 μmol min‐1g‐1kidney wt (P0.05). Urine osmolality (UOsm) remained unchanged, while the blood pressure (BP) decreased by 15%. In animals pretreated with captopril, ANP infusion led to a decrease in GFR from 1.27 ± 0.11 to 1.05 ± 0.09 ml min‐1g‐1kidney wt (P0.05). Despite this effect,UNaVincreased more than two‐fold from 0.076 ± 0.020 to 0.193 ± 0.087 μmol min‐1g‐1kidney wt (P0.05). TheUKVwas not statistically significantly elevated (change from 0.623 ± 0.156 to 0.859 ± 0.146 μmol min‐1g‐1kidney wt) andUOsmremained unaltered, while BP decreased by 15% (P0.05). The captopril‐pretreated animals had a higher UNaVvalue during the control period than vehicle‐pretreated ones, but there was no statistical difference in this variable between the groups after ANP infusion. The captopril treatment decreased BP by 6%. It is concluded that converting enzyme inhibition induced by captopril does not interfere with either the natriuretic or with the hypotensive response to ANP, which suggests that angiotensin II does not participate in the generation of the acute effects of ANP. Atrial natriuretic peptide increases sodium excretion predominantly by

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08154.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The dopamine receptor antagonist haloperidol blocks natriuretic but not hypotensive effects of the atrial natriuretic factor.Acta Physiol Scand130, 401–407. Received 11 December 1986, accepted 10 February 1987. ISSN 0001–6772. Department of Physiology&Medical Biophysics and Department of Pharmacology, Biomedical Centre, University of Uppsala, Sweden.Studies were performed on anaesthetized male Münich‐Wistar rats to investigate the influence of the dopamine (DA) receptor antagonist haloperidol on the natriuretic response to infusion of a synthetic atrial natriuretic factor. The whole kidney glomerular filtration rate (GFR), urinary excretion of electrolytes, and arterial blood pressure (BP) were therefore measured in groups of animals pretreated with haloperidol or vehicle and given a continuous intravenous infusion of atrial natriuretic peptide (ANP; 28 amino acids). Forty‐five minutes of ANP infusion at 10 μg h‐1kg‐1body wt did not increase GFR (change from 1.14 ± 0.08 to 1.15 ± 0.05 ml min‐1g‐1kidney wt). Sodium excretion (UNaV) increased more than four‐fold from 0.037 ± 0.008 to 0.165 ± 0.070 μmol min‐1g‐1kidney wt (P0.01). Potassium excretion (UKV) increased by 86% (P0.001) and the urine flow rate (V) increased transiently by 63% (P0.05) and did not differ from the control value during the last 15 min of ANP infusion. The urinary sodium concentration (UNa) increased almost three‐fold, while BP decreased by 14%. There was no change in urine osmolality. In animals pretreated with haloperidol (I mg kg‐1body wt), 45 min of ANP infusion did not significantly alter GFR (from 1.10 ± 0.08 to 0.98 ± o.09 ml min‐lg‐1kidney wt). TheUNaVdid not increase significantly (change from 0.026 ± 0.006 to 0.030 ± 0.009 μmolmin‐1g‐lkidney wt). TheUKVwas not elevated by ANF infusion. The urine flow rate was transiently elevated by 45% but was not different from the control during the last 15 min of infusion. BothUNaandUosmremained unchanged, but BP was reduced by 11%. In conclusion, the DA receptor blocking agent haloperidol blunts the natriuretic effect of ANP. This action is probably exerted by inhibiting the postulated tubular effects of ANP through an unknown mechanism, but not the vascular ones, since the hypotensive effect of ANP is unaltered. Atrial natriuretic peptide increases sodium excretion not, mainly, by increasing GFR

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08155.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Nervous control of tracheal blood flow in the cat measured by the laser Doppler technique.Acta Physiol Scand130, 409–417. Received 2 December 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Anaesthesia. Karolinska Hospital and Departments of Pharmacology and Endodontics, Karolinska Institute, Stockholm, Sweden.The tracheal blood flow as determined by the laser Doppler technique was continuously monitored in anaesthetized cats. Electrical stimulation of the right superior laryngeal nerve caused an atropine‐resistant increase in blood flow of the upper trachea. Unilateral vagal nerve stimulation at the cervical level in the presence of atropine induced a frequency‐dependent increase in blood flow of the lower trachea. Intermittent stimulation with bursts of impulses at a high frequency resulted in a considerably larger blood flow increase than a continuous low frequency stimulation giving the same total number of impulses. The ganglionic blocking agent chlorisondamine abolished most of the vagally induced increase in tracheal blood flow when using low threshold parameters (2 V, 0.2 ms) presumably activating preganglionic nerves. High threshold stimulation (10 V, 5 ms) however, still resulted in an increased blood flow suggesting antidromic activation of sensory C fibres. Local mechanical irritation or chemical irritation by capsaicin also increased tracheal blood flow. Furthermore, local application of calcitonin gene‐related peptide on to the mucosa caused a slowly developing, long‐lasting increase in blood flow. Electrical stimulation of the cervical sympathetic trunk and local application of adrenaline reduced tracheal blood flow. In conclusion, vagal nerve stimulation induces an atropine‐resistant increase in tracheal blood flow probably mainly by activating preganglionic parasympathetic nerves and possibly also by antidromic stimulation of C‐

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08156.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Comparative effects of some calcium‐channel blockers on human peripheral arteries and veins.Acta Physiol Scand130, 419–427. Received 5 December 1986, accepted 9 February 1987. ISSN 0001–6772. Departments of Surgery and Clinical Pharmacology, Lund University, Sweden.We investigated the effects of five different calcium‐channel blockers (CCBs), verapamil, nifedipine, diltiazem, flunarizine and lidoflazine, on contractions evokedan vitroby noradrenaline (NA) in small human arteries and veins from the epigastric region. Vessels were obtained from patients without obvious vascular diseases undergoing surgery because of inguinal hernias. The human superficial epigastric artery has previously been shown to contain mainly α1‐adrenoceptors, whereas in the vein α2‐adrenoceptors predominate. In experiments where NA (10‐5m) was added non‐cumulatively, it was found that nifedipine was the most potent relaxant agent in both arteries and veins, but that this drug showed no preference for any type of vessel. In contrast verapamil (10‐6m) and (10‐5m) diltiazem, flunarizine and lidoflazine inhibited the NA‐induced contractions to a significantly greater extent in the arteries than in the veins. Comparison between diltiazem and nifedipine on contractions induced by cumulative addition to NA showed that both drugs had significantly more depressive effects on arteries than on veins if the vessels were contracted by relatively high concentrations of NA (10‐‐6and 10‐‐5m). The results thus confirm the clinical finding that CCBs have more pronounced effects on the arterial than on the venous side of the circulation. They do not support the view that CCBs are more effective inhibitors of α2‐‐than α1‐adrenoceptor mediated cont

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08157.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Lack of casual relationship between medullary blood congestion and tubular necrosis in postischaemic kidney damage.Acta Physiol Scand130, 429–432. Received 29 December 1986, accepted 23 February 1987. ISSN 0001–4772. Department of Histology, Gothenburg University, Sweden.The effect of haemodilution on medullary blood congestion and tubular necrosis was investigated in the rat kidney. Male Sprague‐Dawley rats were subjected to 60 min of unilateral, kidney ischaemia and 24 h of reperfusion. Haemodilution was performed by replacing blood by homologous serum and was done either before induction of ischaemia or during the ischaemic period. Cellular necrosis was evaluated morphologically by a histochemical staining for calcium and a dyeexclusion test. Trapped erythrocytes were visualized by the DAB reaction. It was found that haemodilution could totally prevent medullary congestion. In spite of this, the extent and distribution of necrotic tubular cells in the outer stripe of the outer medulla were the same whether the animal was subjected to haemodilution or not. Our results strongly suggest that the cellular necrosis and the medullary congestion are two separate phenomena occurring at the same time, but without a causal relationship to each

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08158.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY