ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08050.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08051.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The primary aim of the study was to evaluate the potential value of intravenous (i. v.) infusion of angiotensin II (AII) for phonocardiographic differential diagnosis of equine valvular insufficiency. Ten‐minute AII infusions at 4.5–33 pmol kg‐1min‐1induced clear‐cut dose‐dependent rises in systemic arterial blood pressure (aBP), whereas the pulmonary aBP remained largely unaffected. It implies that i. v.infusion of All at about 10 pmol kg‐1min‐1could be a valuable tool for the acoustic differentiation between mitral and tricuspid valvular dysfunction in the horse. The infusion at, and above 9 pmol kg‐1min‐1caused increased heart rate. This chronotrophic effect was not strictly dose‐dependent and exhibited significant tachyphylaxis. Angiotensin II administration at, or above 9 pmol kg‐1min‐1was needed to induce an urge to drink, suggesting that angiotensin‐induced thirst does not appear in the euhydrated horse until the octapeptide reaches supraphysiological blood concentration. Determinations of plasma aldosterone concentration (PA) revealed comparatively high morning control values (269 ± 46 pmol‐1).Three consecutive AII infusions with 10‐min intervals and at increasing dosages caused a cumulative, almost fourfold elevation of PA.The PA pattern indicated that AII‐induced hypersecretion of aldosterone continued for several minutes after the end of the infusions, but also showed that the metabolic clearance of the hormone took precedency of the secretion within 20 min post‐infusion. In two of the horses a fall in PA occurred during a fourth, final infusion, indicating that in these instances the previous AII administration had impoverished the store of aldosterone available

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08052.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

In order to assess the possible role of atrial natriuretic peptide (ANP) in the development of deoxycorticosterone (DOCA)‐NaCl‐induced hypertension, plasma immunoreactive ANP concentration was compared with sodium balance and blood pressure in NaCl‐ or DOCA‐NaCI‐treated rats. Both NaCl‐and DOCA‐NaCl‐loading increased plasma ANP levels (to 86 ± 8.1 and 105 ± 12 pg ml‐1respectively; 47±6.7–60±4.6 pg ml‐1in controls), which were correlated to sodium intake and excretion. In DOCA‐NaCI‐treated rats, the highest ANP levels (105 ± 12 pg ml‐1) were found 4 weeks after the beginning of DOCA‐NaCl treatments. Along with the development of DOCA‐NaCl hypertension in 1‐kidney‐DOCA‐NaCl‐treated rats, however, plasma ANP concentration did not rise further. We conclude that secretion of ANP into the circulation is increased during DOCA‐NaCl treatment. Elevated blood pressure does not stimulate

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08053.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The effect of moderate hypoxia on cerebral blood flow (CBF) in man has not been well described, and little is known about the interaction of changes in arterialPO2andPCO2as regards CBF.Using a non‐invasive doppler ultrasound method we have measured the instantaneous mean blood velocity (which is proportional to CBF as long as the cross‐section of the vessel is constant) in the carotid artery in four healthy unanaesthe‐ tized subjects. We found in all subjects that a reduction in alveolarPO2from about 13 to about 8.7 kPa with maintained constant alveolarPCO2(PACO2) caused CBF to increase gradually over 10 min (half‐time about 4 min) to about 125% of control. The CBF decreased quickly (half‐time about 45s) towards control when alveolarPO2was reset to 13 kPa. As measured 5 min after a step‐change inPA,O2, the change in CBF was independent ofPA, CO2within the range 3.3–6.7 kPa. An increase inPA, O2to about 33 kPa reduced CBF only ifPA,CO2was in the hypercapnic range. Unexpectedly we found that the CBF response showed ‘adaptation’ during both maintained increase and decrease inPA, CO2.The CBF started to return towards control level within 10 min after induction of hypo‐ or hypercapnia. We conclude that also moderate hypoxia causes increased CBF in unanaesthetized man within a

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08054.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The present study was designed to investigate if the immunoreactivity of insulin‐like growth factor I (IGF‐I, somatomedin C) in blood vessels was changed in relation to the vascular load in adult rats. Occlusion of the right femoral artery resulted within 24 h in a strongly increased IGF‐I immunoreactivity in the media of the contralateral, left, femoral artery and a significant decrease in the IGF‐I expression in the right femoral artery distal to the occlusion. The increased labelling of the smooth muscle cells persisted for at least 21 days. Inactivity of the right hind limb, secondarily to an ischaemic insult, likewise induced a significant increase in IGF‐I immunoreactivity, within 24 h, in the femoral vessels of the undamaged, contralateral left hind limb. It is concluded that IGF‐I immunoreactivity varies with the dynamic load in the vascular walls. It is proposed that IGF‐I may serve as a parahormone exerting its effect by paracrine and/or autocrine mechanisms, taking part in regulating the structural adaption of blood vessels in respo

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08055.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

A search was made for a model tissue of NaCl absorption which would be sensitive to inhibition by diuretics of the thiazide type. A lack of such a model through the years has hampered the analysis of the cellular mechanism of action of this important class of drugs. Using the short‐circuit current technique, the urinary bladders of the toadsBufo spinosusandBufo marinus, and the frogRana temporariawere investigated regarding the effects of various thiazides. These bladders have NaCl absorptive properties similar to those of the distal renal tubules, and are claimed to be sensitive to the inhibitory effect of thiazides on sodium transport. The short‐circuit current (SCC), which is representative of the sodium transport across the epithelium, was reduced by cyclopenthiazide and polythiazide, but only at high concentrations (above 0.1 mM).To rule out the possibility that this was an unspecific effect, attempts were made to block the effect by the ‘thiazide blocker’ Ex 4877, but without success. This finding, together with the fact that dose‐response curves were difficult to obtain, would indicate that these epithelia are not suitable for the stated purpose. Preliminary studies were also conducted on the urinary bladder of the plaice,Pleuronectes platessa, which has a different system of NaCl absorption that is claimed to be rapidly and reversibly inhibited by thiazides. Polythiazide, added to both sides of the bladder, had no effe

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08056.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The effect of free oxygen radicals on the electrical resistance of brain venular endothelium was studied in anaesthetized frogs. The technique allowed continuous recording of the electrical resistance of the vascular wall reflecting its ionic permeability. The oxygen radicals were generated by an enzymatic reaction between xanthine oxidase and hypoxanthine supplied to the surface of the exposed brain. Electrical resistance of the venular endothelium decreased within 1–2 s after the reaction was initiated. Hypoxanthine (1 mM) and xanthine oxidase at a concentration of 10, 25, 50, 100, and 250 mU ml‐1lowered resistance to 1.0, 0.9, 0.8, 0.5 and 0.2 × control value, respectively, within a 3 min period of administration. The effect induced by 25 and 50 mU ml‐1of xanthine oxidase was readily reversible, whereas that induced by the two highest concentrations was irreversible within the observation time. The response was totally blocked by allopurinol as well as by superoxide dismutase plus catalase. Pretreatment with methylprednisolone or BW755C (an inhibitor of cyclo‐ and lipoxygenase) did not inhibit the response, nor did removal of calcium or magnesium from the extracellular medium. Free oxygen radicals are powerful agents that rapidly induce dynamic changes in the electrical resistance of brain vessels, supporting the notion that they may be important mediators of vascular endothelial damage in t

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08057.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Adenosine exerts anti‐aggregatory effects on human plateletsin vitro, probably by increasing intraplatelet levels of cyclic AMP.In addition, adenosine prevents platelet lossin vivo.We have studied the relationship between the concentration of adenosine in the platelet media and the level of cAMP.In PRP, exogenous adenosine (2–16 μM) was eliminated with a half‐life close to 5 min. Approximately half of the added adenosine was deaminated (blocked by 1–2 μM EHNA), and half was eliminated by uptake into platelets (blocked by 2 μM dipyridamole).In whole blood the half‐life for adenosine was much shorter, about 155.Addition of adenosine deaminase (0.3 μg ml‐1) to PRP resulted in a measured half‐life for adenosine approximating that of whole blood. In PRP where adenosine was eliminated as quickly as in whole blood, the adenosine‐mediated stimulation of cAMP was 35% lower than in PRP, and the cAMP response lasted 2 min, versus 15 min in normal PRP.These results suggest that the magnitude and duration of adenosine's effect on platelets are markedly overestimated by studying platelet suspensions. In blood, the effect of adenosine is smaller in magnitude and very transient. The possibility is discussed that the action of adenosinein vivoon blood platelets can there

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08058.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Ventilation increases when the concentration of CO2in the inspired gas is increased, thereby limiting the increase in alveolar and arterialPCO2The extent of this compensation at low levels of inspired CO2has been debated. In five healthy humans, we have measured arterialPCO2, arterial pH and ventilation during exposure to 1 and 2% CO2in the inspired gas. Each exposure lasted at least 7 min and arterial blood was sampled over at least 30 s during the last minute of each period. The ventilation was measured in the sixth and seventh min. The protocol included the sequences: control test‐control and test‐control‐test with ‘test’ representing CO2loading and ‘control’ 0% CO2, respectively. We found that arterialPCO2increased and pH decreased at both levels of inspired CO2.The mean increase in arterialPCO2was 0.09 and 0.25 kPa, at CO21 and 2%, respectively. Three subjects were exposed to 1 % CO2in the inspired gas for 28 min flanked by similar control periods. In each period arterial blood samples were taken at 2‐or 3‐min intervals. ArterialPCO2.remained elevated for at least 20 min during the CO2loading. The sensitivity to CO2(ratio of increase in ventilation to increase in arterialPCO2) was within the range described by others at higher levels of inspired CO2.ArterialPCO2increased by about 10% of the imposed load. We conclude that the increase in ventilation provides only incomplete compensation for exposure to CO2: arterial CO2is increased and arterial pH decreased also at very low level

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08059.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY