摘要:

We examined the effect of opioid receptor antagonists on the seizure phenomena induced by specific delta opioid receptor agonist [D-Ser2, Leu5] enkephalyl-Thr (DSLET). The experiments have been performed in the anesthetized rats, and the DSLET-induced seizure phenomena were registered by electrocorticogram and electromyogram. It was demonstrated that two selective delta opioid receptor antagonists, ICI 152,129 and ICI 174,864 inhibitied DSLET-induced epileptiform ECoG pattern and myoclonic contractions in a dose-related manner. An equimolar concentration of naloxone failed to antagonize the epileptiform effects of DSLET. It is concluded that delta opioid receptor agonist-induced seizure is mediated by delta receptors, since it can be blocked by delta opioid receptor antagonists. Evidently, delta opioid antagonists can be used as a good tool, in order to demonstrate a delta component in the seizure phenomena induced by other endogenous opioid peptides or their derivatives.

ISSN:0031-7012    

DOI:10.1159/000138253

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In this study, male Sprague-Dawley rats maintained under controlled environmental conditions were used. Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with morphine (10 mg/kg) for 1 or 2 days. Repeated administration of morphine was associated with a decline in the degree of analgesia produced. Significant increase (p < 0.01) in AChE activity of the medulla oblongata was observed following morphine administration for 1 or 2 days. A single injection of morphine resulted in a significant decline (p < 0.01) in ChAT activity of hypothalamus, cerebellum and medulla oblongata. However, no such decline could be observed after 2 consecutive daily injections of morphine. In the cerebral cortex there was a significant decline (p < 0.01) in ChAT activity after the second administration of morphine. These findings indicate that the changes in the responsiveness of the brain cholinergic enzymes following repeated morphine administration may in part explain the rapid development of tolerance to the analgesic effect of morphine.

ISSN:0031-7012    

DOI:10.1159/000138254

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Cholinesterase inhibitors induce changes in plasma hormones in the rat. Since these compounds induce hypothermia the question has been raised as to whether the endocrine responses are secondary to the fall in core temperature. The time course of the changes in temperature and plasma levels of corticosterone, growth hormone and prolactin have been examined following injection of diisopropylphosphofluoridate (DFP), soman or physostigmine. All three cholinesterase inhibitors caused an initial rise in corticosterone; DFP decreased growth hormone; physostigmine reduced prolactin. The time course of the hypothermia after DFP and soman did not correlate with that of the rise in corticosterone. The data do not suggest that the hormone changes are secondary to the temperature change.

ISSN:0031-7012    

DOI:10.1159/000138255

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

When guinea pig isolated trachea is contracted with either carbachol or methacholine, relaxant concentration-response curves to isoprenaline, salmefamol and fenoterol were shifted to the right, compared with curves obtained with either spontaneous or histamine-induced tone. Carbachol and methacholine also reduced the maximal relaxation to fenoterol and abolished relaxations to the partial agonist pindolol. It is concluded that the processes linking receptor to contractile response in trachea are different for histamine receptors and muscarinic cholinoceptors.

ISSN:0031-7012    

DOI:10.1159/000138256

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In order to investigate effects of khat chewing on uteroplacental blood flow (+) norpseudoephedrine (NPE) infusions were given to 11 anesthetized guinea pigs in late pregnancy (62–66 days) after unilateral uterine artery ligation at days 30–32. Regional blood flows were determined with radioactive microspheres. Mean arterial blood pressure increased with 25% and heart rate with 9% during NPE infusion. Myoendometrial blood flow was reduced by 31 %. Placental vascular resistance (PVR) increased by 56% in the control horn (17 fetuses) and by 82% in the ligated horn (17 fetuses). This vasoconstriction was counteracted by the systemic vasopressor response since placental blood flow remained unchanged. When considering only the 13 growth-retarded fetuses, however, PVR increased by 98% and a 19% reduction of placental blood flow could be demonstrated. These results suggest that the placenta of the growth-retarded fetus may be more sensitive to adrenergic stimulation than the normal placenta. Furthermore, since one of the active constituents of khat, (+)norpseudoephedrine, causes vasoconstriction in the uteroplacental vascular bed it is possible that khat chewing could reduce placental blood flow and, as a consequence, impair fetal gro

ISSN:0031-7012    

DOI:10.1159/000138257

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Acetylsalicylic acid (ASA; 0.1–10 mg/kg), indomethacin (IND; 0.1–1.0 mg/kg), and tartrazine (TZ; 0.1–2.0 mg/kg), given intravenously induced dose-dependent increases in carotid-sinus nerve (CSN) activity, accompanied by increases in mean arterial blood pressure (MABP), but only the IND-induced MABP increases were dose-dependent. The MABP and CSN activity responses to all three drugs were not correlated, suggesting a direct action on CSN afferents that is unrelated to the pressor effects of the drugs. Sodium cromoglycate (10 mg/kg) selectively reduced the increases in CSN response to ASA and IND. Phentolamine (0.2 mg/kg) inhibited the increased CSN activity induced by ASA, IND, and TZ. These findings indicate that ASA, IND, and TZ act directly on carotid baroreceptors to increase their act

ISSN:0031-7012    

DOI:10.1159/000138258

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

This study investigated the effect of sodium pump activity on vascular smooth muscle responsiveness to norepinephrine (NE) in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Dose-response curves to NE were generated in normal (5.9 mM), high (10 mM) or 0 mM potassium (K) Krebs physiological solution. Inhibition of the sodium pump (0 mM K) in femoral arterial smooth muscle from control rats resulted in an increased response to NE which was similar to the DOCA-salt rat, while increasing sodium pump activity (10 mM K) in femoral arterial smooth muscle from DOCA-salt rats resulted in a decreased response which was similar to controls. These results show that altering sodium pump activity in vitro by changing extracellular K concentration can affect femoral arterial smooth muscle responsiveness to NE in both control and DOCA-salt rats. Alterations in sodium pump activity observed in vascular smooth muscle from DOCA-salt hypertensive rats may contribute to the increased NE responsiveness and increased vascular resistance seen in this model of hypertension.

ISSN:0031-7012    

DOI:10.1159/000138259

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

We compared the abilities of three different calcium (Ca2+) entry blockers, verapamil, diltiazem and felodipine to abolish ouabain-induced ventricular ectopy (100 × ectopic/total beats, VE) in anesthetized, closed-chest dogs. Ventricular tachycardia (VT) was produced in anesthetized, bilaterally vagotomized, closed-chest dogs by an average dose of 65 ± 19 μg/kg ouabain. 30 min after establishing VT, either verapamil (25–50 μg/kg + 5–10 μg/kg/min), diltiazem (50–100 μg/kg + 20–50 μg/kg/min), felodipine (3 μg/kg + 0.3 μg/kg/min) or saline was administered for another 30 min. Verapamil, at the higher dose utilized, practically abolished ouabain-induced VT (97 ± 3 to 8 ± 19% VE); diltiazem was moderately effective (96 ± 4 to 50 ± 8% ectopy) at 100 μg/kg, and felodipine exerted no antiarrhythmic effects in this model. All three Ca2+ entry blockers lowered mean aortic pressure, felodipine lowering this parameter most prominently. Thus, these structurally and electrophysiologically dissimilar Ca2+ entry blockers differed in their abilities to abolish the digitalis glycoside-induced arrhythmias in vivo. The superiority of verapamil may be related to its multiple, additional elect

ISSN:0031-7012    

DOI:10.1159/000138260

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In anesthetized dogs, the cumulative intravenous administration of 1.0–40.0 mg/kg sulphinpyrazone failed to alter the ventricular excitation threshold, ventricular refractory period and ventricular fibrillation threshold determined during nonobstructed coronary blood flow. Sulphinpyrazone, however, did attenuate the reduction in the ventricular fibrillation threshold occuring during transient myocardial ischemia. G25671, the sulfide metabolite of sulphinpyrazone, failed to alter ventricular refractoriness and ‘nonischemic’ ventricular fibrillation thresholds, and was minimally effective in reducing the decrease in ‘ischemic’ fibrillation thresholds when administered in cumulative intravenous doses of 5.0–20.0 mg/kg. In conscious dogs in the subacute phase of anterior myocardial infarction, the administration of a cumulative 10.0–40.0 mg/kg sulphinpyrazone failed to alter the mode of induction, rate or morphology of ventricular tachyarrhythmias initiated by programmed ventricular stimulation. These data suggest that neither sulphinpyrazone nor its sulfide metabolite possess primary electrophysiologic properties which might contribute directly to significant antiarrhythmic or antifibrilla

ISSN:0031-7012    

DOI:10.1159/000138261

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Increased dietary salt intake alters renal function which often leads to deleterious cardiovascular consequences. Studies were carried out to characterize the effects of high-salt diets on renal catecholamines and α2-adrenergic receptors. These parameters were evaluated in both genetic and acquired forms of hypertension and also in normotensive rats on high-salt diets. Renal catecholamine content was determined by high-performance liquid chromatography with electrochemical detection. Renal α2-adrenergic receptor-binding studies were performed on whole kidney homogenates using 3H-p-aminoclonidine to label both high- (0.5 nM) and low-affinity (5.0 nM) renal α2-adrenergic receptors. Increased salt intake elevated blood pressure, decreased renal norepinephrine stores and resulted in renal α2-adrenergic receptor up-regulation in deoxycorticosterone acetate salt hypertensive rats, Dahl-S rats and COX-SHR. The decreased renal stores of norepinephrine (NE) appeared to reflect increased renal NE utilization. In contrast, SHR (Charles River) had elevated NE stores and α2-adrenergic receptors while on normal salt diets. Short-term (10–14 days) exposure to high-salt diets had modest effects in normotensive rats or COX-SHR, although it was sufficient to increase low affinity renal α1-adrenergic receptor number. Renal dopamine metabolism was also altered by high-salt diets. These studies demonstrated a relationship between renal NE content and renal α2-adrenergic receptors. The implications of this relationship and other salt-related changes in renal catecholamine metabolism were discussed as they pertained to hypertension and renal

ISSN:0031-7012    

DOI:10.1159/000138262

出版商:S. Karger AG    

年代:1987

数据来源: Karger