ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03012.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1Intrapericardial procaine, used to produce cardiac nerve blockade in both conscious and anaesthetized animals, has been reported to also produce changes in respiration. This study systematically investigated the effects of two doses of intrapericardial procaine on respiration in the conscious rabbit.2Rabbits were pre‐instrumented with a chronic diaphragm electromyogram (dEMG) recording electrode and intrapericardial catheter. Arterial pressure, heart rate, dEMG and respiratory excursions (recorded with a pneumograph) were monitored in the conscious rabbit before and after intrapericardial and intravenous infusion of 2 and 5% procaine. Efficacy of cardiac nerve blockade was tested by intravenous infusion of phenyl biguanide. Arterial blood gases were determined at rest and during changes in respiration.3Following a low dose of intrapericardial procaine (12 mg), dEMG and respiratory excursions increased (65 ± 13 and 65 ± 13%, respectively) with no change in breathing frequency or arterial blood gases. Following a high dose of intrapericardial procaine (30 mg), four of six animals exhibited a similar response. However, four of the six rabbits also exhibited a second type of response pattern characterized by a further increase in respiratory efforts (65 ± 13%), abolition of dEMG, and a mild hypoxaemia.4Intravenous infusion of a low dose of procaine was without effect, whereas intravenous infusion of a high dose of procaine produced minor behavioural responses.5In four additional anaesthetized rabbits, it was demonstrated that high doses of intrapericardial procaine anaesthetized the phrenic nerve to produce the observed alterations in respiration.6We conclude that if intrapericardial procaine is used to block cardiac nerves in conscious rabbits, it should be used in a low concentration and at the lowest possible total dose to avoid complications due to changes in respira

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03013.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1The hypothesis that high levels of NaCl in the diet aggravates hypertension‐associated renal vascular lesions was examined in unilaterally nephrectomized deoxycorticosterone acetate treated (DOCA) and two kidney one clip (2K1C) hypertensive rats, as well as normotensive controls.2High NaCl diet significantly increased systolic blood pressure (SBP) in DOCA rats, but had little effect on SBP in normal control rats, and did not affect the rise of SBP in 2K1C rats.3High NaCl diet was associated with a higher percentage of glomerular lesions and renal arterial and arteriolar lesions in DOCA and 2K1C rats (P<0.05).4Thus high NaCl intake exacerbated renal arterial and arteriolar and glomerular lesions in both DOCA and 2KlC hypertensive rats. In 2K1C rats this effect may be in part independent of blood pressur

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03014.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1Parathyroidectomy (PTX) lessens the development of hypertension in young spontaneously hypertensive rats (SHR) and the involved mechanisms remain to be elucidated. We have studied here the aortic vascular reactivity to both norepinephrine (NE) and acetylcholine in 10 week old male PTX SHR and Wistar‐Kyoto (WKY) rats.2Depolarized (KCl 100 mmol/L) and NE (1 μmol/L or cumulative 10‐9‐10‐‐5mol/L) precontracted intact aortic rings from PTX rats show a significant and unexpected increase of maximal contractile responses in normotensive and hypertensive animals. These results are also obtained with low extracellular ionized calcium levels (0.625 and 0.9 mmol/L) similar to PTX ionized plasma calcium. Nω‐Nitro‐L‐arginine methyl ester (l‐NAME, 20 μmol/L) potentiates the NE response in SHR and WKY rats, more significantly in control than in PTX animals.3In the presence of indomethacin (10 μmol/L) in SHR the potentiating effect of PTX on NE contraction is still observed, ruling out a specific production of vasoconstrictors from the arachidonic cascade by the PTX rat aortic endothelium.4After PTX a moderate impairment of acetylcholine relaxant responses is observed in SHR and WKY rat aortas and basal aortic cyclic guanosine 3′‐4′ monophosphate (cGMP) content is also decreased; nevertheless sodium nitroprusside causes a similar relaxation. Furthermore in l‐NAME‐treated aortas and in the presence of l‐arginine (100 μmol/L), acetylcholine (1 μmol/L) produces a significantly less pronounced relaxation in PTX rats.5In conclusion, the enhancement of NE contractile response in PTX rat aortas is not linked to the strain but probably related to a decrease in endothelial nitric oxide (NO) release or activity. Enhancement of force generation that we describe does not directly participate in the attenuated hypertension obse

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03015.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1We examined the regulatory actions of bradykinin on norepinephrine release in the hypo‐thalamus of rats.2Bradykinin increased the stimulation‐evoked [3H]‐norepinephrine release from hypothalamic slices of Sprague‐Dawley rats in a dose‐dependent manner (1 Hz: S2/S1 ratio, mean ± s.e.m., control 0.868±0.016,n= 6; bradykinin 1±10–6mol/L 1.039±0.018,n= 6, P<0.05;bradykinin3.3 ×10–6mol/L 1.130 ± 0.064,n= 6, P<0.05). The basal release of [3H]‐norepinephrine was not affected by the peptide.3Bay K 8644, a dihydropyridine‐sensitive calcium channel agonist, significantly potentiated the facilitatory effect of bradykinin on norepinephrine release, although Bay K 8644 by itself had no significant effect. By contrast, nicardipine, a dihydropyridine‐sensitive calcium channel blocker, reversed the increase in norepinephrine release induced by bradykinin and Bay K 8644.4These results indicate that bradykinin may increase norepinephrine release in rat hypo‐thalamus, partially mediated by interactions with dihydropyridine

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03016.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1The vasoconstrictor effects of noradrenaline applied to the intimal and adventitial surfaces of perfused segments of rat tail artery in the presence and absence of endothelium were studied.2Noradrenaline was about six times more potent as a vasoconstrictor when applied to the intimal than to the adventitial surface. Cocaine (25 μmol/L) enhanced responses to adventitial noradrenaline to a greater extent than those to intimal noradrenaline. A high concentration of propranolol (1 μmol/L) had a similar effect.3The vasoconstriction elicited by adventitial noradrenaline declined from a peak whereas that to intimal noradrenaline remained steady. A low concentration of propranolol (0.1 μmol/L) abolished the decline in the response to adventitial noradrenaline.4The α1‐ and α2‐adrenoceptor antagonists prazosin (1 nmol/L) and idazoxan (100 nmol/L) significantly reduced responses to intimal and adventitial noradrenaline in the presence or absence of endothelium.5Removal of endothelium enhanced responses to intimal but not adventitial noradrenaline. Idazoxan produced a significantly greater reduction of responses to noradrenaline in the absence than in the presence of endothelium, and was more effective against intimal than adventitial noradrenaline. Similar effects were produced by the nitric oxide synthase inhibitor l‐NAME (30 μmol/L).6It was concluded that noradrenaline acts on both α1‐ and α2‐adrenoceptors to produce vasoconstriction: the α1‐adrenoceptors appear to be uniformly distributed, whereas α2‐adrenoceptors are located nearer the intima. Intimal noradrenaline also acts on endothelial α2‐adrenoceptors to release EDRF which counteracts the vasoconstrictor action of noradrenaline. Adventitial noradrenaline also acts on β‐adrenoceptors located near the adventitia to counteract the vasoconstriction produced by activation of α‐adrenoceptors and its acti

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03017.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03018.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03020.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03021.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Modulation of Cardiac Calcium Sensitivity: A New Approach to Increasing the Strength of the Heart.

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb03022.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY