术前扩容对预防妇科腹腔镜致缺血再灌注肝损害的研究

目的 探讨腹腔镜术前扩容与预防经妇科腹腔镜手术所致肝功能损害的相关性.方法 将我院80例妇科腹腔镜手术患者随机分为术前扩容治疗组(Ⅰ组)和非术前扩容治疗组(Ⅱ组),每组40例;检测并对比各组患者术后肝脏缺血再灌注各个时点(T=1h、3h、6h、12h)肝功能(丙谷氨酸转氨酶ALT、天门冬氨酸转氨酶AST)及缺血再灌注损伤标记物脂质过氧化物丙二醛(MDA)在缺血再灌注期内的水平变化情况.结果 Ⅱ组肝脏缺血再灌注各个时点( T=1 h、3h、6h、12h)的肝功能血清ALT、AST水平及缺血再灌注损伤标记物MDA均明显高于Ⅰ组(P＜0.05);各组血清ALT、AST及MDA水平在缺血再灌注期均呈增高趋势,且在再灌注6h时达高峰,但在12h时有显著回落趋势(P＜0.05);与Ⅱ组相比,Ⅰ组在缺血再灌注期内的ALT、AST及MDA水平等实验室检查指标波动相对平稳,两组结果差异具有统计学意义(P＜0.05).结论 术前扩容可有效保护腹腔镜手术患者术后肝脏缺血再灌注期的肝功能,是行之有效的预防妇科腹腔镜手术肝功能损伤的治疗措施.     

Renal response to blood volume expansion in Brattleboro rats after acute treatment with vasopressin

Summary The renal response to iso-oncotic blood volume expansion with bovine serum albumin was studied in anaesthetized homozygous Brattleboro (DI) rats after acute (1 day) pretreatment with 1 U arginine-vasopressin (AVP) compared to heterozygous controls. In AVP-treated DI (DI+AVP) rats, basal urine flow as well as urinary sodium, chloride, and potassium excretion, were not different from controls.Diuresis and kaliuresis induced by volume expansion were blunted in DI+AVP rats. However, natriuresis and chloruresis were exaggerated in DI+AVP rats. They increased faster, reached a higher maximum, but declined earlier, compared to controls. The blunted diuresis resulted in a positive volume balance by the end of the experiment in DI+AVP rats, whereas the controls showed restoration of normal balance. Significant retention of sodium and chloride was observed in controls, but not in DI+AVP rats, over the time of the experiment.DI+AVP rats lost significantly less potassium than controls during the experiment. As judged from the lithium clearance method, the exaggerated saluresis in DI+AVP rats was mainly due to a reduced proximal sodium reabsorption. Plasma immunoreactivity of atrial natriuretic peptide (ANP) rose during blood volume expansion and fell in the recovery period. It was not different between AVP-treated DI rats and controls at any time of the experiment. Inulin clearance was slightly, but not significantly, lower in DI+AVP rats and increased after blood volume expansion in DI+AVP rats only.The results indicate that acute AVP substitution may abolish the exaggerated volume loss, but not the increased saluresis known to occur in DI rats after blood volume expansion. Send offprint requests to R. Palluk at the above address     

Involvement of the renal kallikrein-kinin system in K(+)-induced diuresis and natriuresis in anesthetized rats

Intravenous infusion of a high-K(+) solution (67.5 mM KCl, 67.5 mM NaCl) to anesthetized rats increased urine volume by 47.6% after 60 min, compared with infusion of a Na(+) solution (135 mM NaCl). This treatment also increased urinary excretion of Na(+) by 32.2%, in parallel with an increase in excretion of K(+) or Cl(-). Urinary excretion of kallikrein increased within 60 min after the start of K(+) infusion. A bradykinin B(2) receptor antagonist, 8-[3-[N-[(E)-3-(6-acetamidopyridin-3-yl)acryloylglycyl]-N-me thylamino ]-2,6-dichlorobenzyloxy]-2-methylquinoline (FR173657; 1.0 mg/kg, i.v. ), inhibited the K(+)-induced diuresis and natriuresis by 41.0% and 26.7%, respectively. These results indicate that K(+) load induces diuresis and natriuresis through the renal kallikrein-kinin system in rats.     

Supranormal natriuretic response to volume expansion in vagotomized and renal-denervated rats

1. To investigate the participation of both vagal cardiopulmonary baroreceptor activity and efferent renal sympathetic nerve activity (ERSNA) in the natriuretic response to saline volume expansion (SVE), three series of experiments were undertaken in anaesthetized rats. 2. In the first two series of experiments, the natriuretic (series A) and ERSNA (series B) responses to SVE were evaluated in both sham operated and cervical bilateral vagotomized rats. The acute experiment consisted of two baseline (BL) periods, treatment (sham control (CTR) or real cervical bilateral vagotomy), a volume expansion phase (Ringer's solution, 10% bodyweight) and a postexpansion phase. The results of these two series indicate that vagotomy significantly enhances basal ERSNA (37 +/- 8%; P < 0.05 vs BL) and significantly attenuates the renal sympathoinhibitory response (by approximately 50%; P < 0.05 vs CTR) but not the natriuretic response to SVE, suggesting the potential expression of a vagotomy induced compensatory natriuretic mechanism. 3. To assess this, the natriuretic response to SVE was evaluated in chronic sham operated or renal denervated groups of rats in which vagotomy was or was not performed (series C). There were no differences among groups in either systemic haemodynamics or plasma protein concentration. Vagotomy plus chronic renal denervation induced a supranormal natriuretic and diuretic response (approximately 30%; P < 0.01) to SVE when compared with similar natriuretic and diuretic responses of the remaining groups. 4. These data support the idea that, in intact rats on a normal sodium diet, neither cardiopulmonary baroreceptors nor renal nerves are necessary for the elimination of an acute intravenous isotonic sodium load and indicate that during SVE the activation of vagal cardiopulmonary baroreceptors exerts an inhibitory effect on both ERSNA and the expression of a natriuretic mechanism. Such a natriuretic mechanism is expressed only when SVE is induced in vagotomized rats (compensating for the vagotomy mediated antinatriuretic effects of an enhanced ERSNA), but is unmasked only when, in addition, renal nerves are chronically transected. All of this offers an efficient element of safety in eliminating an acute isotonic sodium load when cardiopulmonary baroreceptors are severed.     

Pravastatin inhibits arrhythmias induced by coronary artery ischemia in anesthetized rats

We have reported that chronically administered pravastatin prevented coronary artery reperfusion-induced lethal ventricular fibrillation (VF) in anesthetized rats without lowering the serum cholesterol level. The present study was undertaken to evaluate whether pravastatin prevents ischemia-induced lethal VF, simultaneously examining myeloperoxidase (MPO) activity in ischemic myocardial tissues. Anesthetized rats were subjected to 30-min ischemia and 60-min reperfusion after chronic administration of pravastatin (0.02, 0.2, and 2 mg/kg), fluvastatin (2 and 4 mg/kg), or vehicle for 22 days, orally, once daily. ECG and blood pressure were continually recorded, and MPO was measured by a spectrophotometer. Pravastatin and fluvastatin significantly (P<0.05) decreased MPO activities, but only pravastatin decreased the incidence of ischemia-induced lethal VF. Both statins had no significant effects on body weight, blood pressure, heart rate, and QT interval as we reported earlier. Our results prove further that pravastatin has benefits to decrease cardiovascular mortality beyond its cholesterol-lowering effect. Pravastatin is more potent than fluvastatin in prevention of arrhythmias. A decrease in the neutrophil infiltration may be partly involved in the inhibitory effect of pravastatin on the ischemia-induced VF.     

Urotensin Ⅱ inhibits carotid sinus baroreflex in anesthetized male rats

AIM: To study the effects of urotensin II (UII) on the carotid sinus baroreflex (CSB). METHODS: The functional curve of carotid sinus baroreflex was measured by recording changes in arterial pressure in anesthetized male rats with perfused isolated carotid sinus. RESULTS: UII at the concentration of 3 nmol/L had no effect on the CSB, while at the concentration of 30, 300 and 3000 nmol/L inhibited the CSB, shifting the functional curve of the baroreflex upward and to the right. There was a marked decrease in peak slope and reflex decrease in blood pressure. These effects of UII were concentration-dependent. Pretreatment with verapamil (an antagonist of the L-type calcium channel, 10 micromol/L) partially eliminated the above effects of UII (300 nmol/L) on the CSB. Pretreatment with BIM-23127 (3 micromol/L), an antagonist of human and rat UII receptors, abolished the actions of UII on the CSB. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) 100 micromol/L did not affect the inhibitory effects of UII (300 nmol/L) on the CSB. CONCLUSION: These data suggest that UII exerts an inhibitory action on the isolated CSB. Such an action of UII is predominantly mediated by the UII receptors in vascular smooth muscles, resulting in the opening of L-type calcium channels.     

The 2-oxopyrrolidinacetamide piracetam reduces infarct brain volume induced by permanent middle cerebral artery occlusion in male rats

In this study, the temporal development of focal cerebral infarction induced by permanent middle cerebral artery occlusion (pMCAO) and the effects of piracetam, a derivative of gamma-aminobutyric acid widely used in clinical practice as a nootropic agent, on infarct area and volume were investigated. pMCAO caused a cerebral infarct whose size progressively increased after 3, 6, 9, and 24 h. Piracetam (125 mg/kg i.p.), administered 6, 9, and 22 h after pMCAO, did not reduce pMCAO-induced brain infarct area size detected at the 24th hour. By contrast, when this agent was administered at the doses of 250 and 500 mg/kg, it caused a marked reduction of the infarct area size. This reduction was observed in almost every brain slice affected by pMCAO, although statistical differences (p <0.05) were detected in slices located at 3-5.5 mm posterior to the anterior pole in animals treated with 250 mg/kg piracetam and in slices located at 3.5-5 mm in those receiving 500 mg/kg. When the mean total volumes of brain infarct resulting from pMCAO were calculated, it was observed that in animals which had received piracetam (250 or 500 mg/kg) infarction volume was markedly ( approximately 50%) and significantly (p <0.05) reduced in comparison with saline injected rats. Finally, piracetam (250 mg/kg administered i.p. 6, 9, and 22 h after the ischemic insult) significantly reduced brain infarct area evaluated 48 h and 7 days after pMCAO.     

Adrenomedullin inhibits the pressor effects and decrease in renal blood flow induced by norepinephrine or angiotensin II in anesthetized rats.

Adrenomedullin (AM), a hypotensive peptide originally isolated from human pheochromocytoma, has been reported to regulate renal functions. In patients with glomerulonephritis, the serum levels of AM are elevated as well as hypertensive agents norepinephrine (NE) and angiotensin II (AII). The effects of AM on the NE- or AII-induced pressor effects and renal blood flow responses, however, are not well clarified. We examined the effects of AM on blood pressure and renal blood flow induced by NE or AII in anesthetized rats. Arterial blood pressure and renal blood flow were measured using a calibrated pressure transducer and a laser Doppler flowmeter, respectively. Drugs were injected into the tail vein with a syringe. Intravenous administration of AM (1-3 nmol/kg) decreased the arterial blood pressure in anesthetized rats in a dose-dependent manner, whereas it did not affect the renal blood flow. NE or AII administration in anesthetized rats caused both increases in blood pressure and decreases in renal blood flow. Simultaneous administration of AM with NE or All prevented the increasing effects of blood pressure and inhibited the decreases in renal blood flow caused by NE or AII. These findings suggest that AM may have a protective role against the pressor effects and decrease in renal blood flow caused by NE or AII.     

Significance of endothelin on volume homeostasis in obese Zucker rats

1. The present study explored the impact of endothelin (ET) and its interaction with renal sympathetic nerves in the control of volume homeostasis in obesity. 2. Groups of lean and obese Zucker rats with innervated and denervated kidneys were subjected to an acute isotonic saline volume expansion (VE), 10% bodyweight and renal haemodynamics and excretory function were evaluated following administration of SB209670 (a non-selective ET antagonist) or UK 350 926 (a selective ETA receptor antagonist). 3. Volume expansion in untreated obese rats resulted in a blunted cumulative urine sodium excretion (CuUNaV) after 40 min, VE compared with untreated lean rats being 36 and 51% in the denervated and innervated kidneys, respectively (both P < 0.001). 4. In lean rats, both SB209670 and UK 350 926 caused a depressed ability to excrete the saline load and CuUNaV after 40 min, VE compared with untreated being decreased by 51 and 60% in the denervated and innervated kidneys, respectively (both P < 0.001). 5. SB209670 and UK 350 926 given to obese rats reduced (both P < 0.001) CuUNaV after VE by 43% in denervated kidneys compared with untreated obese rats, whereas they were without effect on the magnitude of the excretory response in innervated kidneys. 6. These findings show that the blunted renal excretory responses to VE present in obese rats were not mediated by ET. Conversely, ET, acting through ETA receptors, plays a role as a diuretic and natriuretic factor in maintaining volume homeostasis by, at least in lean rats, renal nerve-independent mechanisms.     

Liver blood flow and blood volume following chronic phenobarbitone administration.

Mlae rats were ra&ndomly divided into 2 groups one of which received 30 mg/kh phenobarbitone for 4 days i.p. and the other sodium chloride. Liver blood flow was measured 24 hr following the last injection of phenobarbitone or sodium chloride using the radioactive colloidal gold clearance technique. In addition, blood volume, liver weight and extraction of radioactive gold were estimated. Following 4 daily infections of phenobarbitone the body weight and the blood volume of both groups were not significantly different. The liver weight in the phenobarbitone treated groups was 27% higher than that found in the control group. Liver blood flow increased from 22.7 ml/min (92,8 ml/min/kg body weight) to 30.1 ml/min (123.7 ml/min/kg body weight). This increase of 33% was highly significant (p less than 0.005). In contrast, the extraction of radioactive gold was 11% lower in the phenobarbitone treated groups than in the controls. The earlier, semiquanititative finding of increased blood flow using a chronic implanted thermocouple could thus be quantified by the present study.     

排石(金车)颗粒解热、利尿、排石、抗炎和镇痛作用的实验评价

目的:研究排石(金车)颗粒的解热、利尿、排石、抗炎和镇痛作用。方法:采用角叉菜胶致热法、利尿试验、二甲苯致小鼠耳肿胀法、角叉菜胶致大鼠足跖肿胀法、扭体法、热板法等多种动物模型和方法;并给予大鼠乙二醇和氯化铵,连续30 d,以形成结石模型进行排石试验。结果:排石颗粒在3和6 g·kg~(-1)剂量灌胃给药对实验大鼠和小鼠有显著的解热、利尿、排石、抗炎、镇痛作用。结论:排石颗粒对泌尿系统结石具有一定的治疗作用。     

Effect of extracellular volume expansion and surgical stress on splanchnic blood flow and cardiac output in anesthetized rats: role of nitric oxide

In a normal volume state, surgical stress decreases rather than increases nitric oxide (NO) production in the vascular system. In our studies, the effect of minor and major surgical stress and three different degrees of volume expansion on systemic and splanchnic circulatory parameters and on the NO dependence of the circulation have been investigated. When the degree of volume expansion was increased, cardiac output and organ blood flow increased without significant change in vascular resistances. Major surgical stress reduced the increase in cardiac output and organ blood flow elicited by the volume expansion. NO synthase (NOS) inhibition significantly increased blood pressure and total peripheral resistance (TPR) and decreased cardiac output in all groups of animals. As the degree of volume expansion was increased, the NO dependence of the circulation in the surgically less- and more-stressed animals was inversely influenced in some cases. With the three degrees of volume expansion (20, 40, and 60 ml/kg), the NOS inhibition increased the TPR from 30.7 R/kg +/- 1.90 to 73.6 R/kg +/- 5.00, from 20.7 R/kg +/- 1.43 to 66.7 R/kg +/- 3.88, and from 19.9 R/kg +/- 1.25 to 49.1 R/kg +/- 3.84 in the surgically less-stressed animals and from 38.6 R/kg +/- 2.14 to 59.8 R/kg +/- 5.62, from 31.9 R/kg +/- 2.70 to 81.7 R/kg +/- 9.89, and from 29.1 R/kg +/- 2.49 to 91.1 R/kg +/- 6.36 in the surgically more-stressed animals. Volume expansion increases the NO dependence of the vascular resistance in the surgically more-stressed animals but decreases it in the surgically less-stressed animals.     

Effects of dopamine and nitric oxide on arterial pressure and renal function in volume expansion

1. The aim of the present study was to investigate the role of dopamine (DA) in the hypotensive and renal effects of L-arginine during extracellular fluid volume expansion (10% bodyweight). 2. Animals were randomized to non-expanded and expanded groups. Both groups received different treatments: L-arginine (250 mg/kg, i.v.), N(G)-nitro-L-arginine methyl ester (L-NAME; 1 mg/kg, i.v.), haloperidol (3 mg/kg, i.p.) and L-arginine + haloperidol (n = 8). Mean arterial pressure (MAP), diuresis, natriuresis, kaliuresis, glomerular filtration rate, renal plasma flow (RPF) and nitrite and nitrate (NO(x)) excretion were determined. 3. The increase in MAP induced by L-NAME was greater in expanded than in non-expanded rats (42 +/- 3 vs 32 +/- 3 mmHg, respectively; P < 0.01). Administration of haloperidol did not modify the L-arginine hypotensive effect. 4. Blockade of nitric oxide synthase diminished urine flow in non-expanded (4.15 +/- 0.56 vs 0.55 +/- 0.11 microL/min per 100 g; P < 0.01) and expanded animals (24.42 +/- 3.67 vs 17.85 +/- 2.16 microL/min per 100 g; P < 0.01). Diuresis induced by L-arginine was reduced by DA blockade in both non-expanded (17.15 +/- 2.11 vs 6.82 +/- 0.61 microL/min per 100 g; P < 0.01) and expanded animals (44.26 +/- 8.45 vs 25.43 +/- 5.12 microL/min per 100 g; P < 0.01). 5. Sodium excretion decreased with L-NAME treatment in non-expanded (0.22 +/- 0.03 vs 0.06 +/- 0.01 microEq/min per 100 g; P < 0.01) and expanded animals (3.72 +/- 0.70 vs 1.89 +/- 0.23 microEq/min per 100 g; P < 0.01). Natriuresis induced by L-arginine was diminished by haloperidol both in non-expanded (0.94 +/- 0.13 vs 0.43 +/- 0.04 microEq/min per 100 g; P < 0.01) and expanded rats (12.77 +/- 0.05 vs 3.53 +/- 0.75 microEq/min per 100 g; P < 0.01). Changes in kaliuresis changes seen following treatment with L-arginine, L-NAME and L-arginine + haloperidol followed a pattern similar to that observed for sodium excretion in both groups of rats. 6. L-arginine enhanced RPF in non-expanded animals (11.96 +/- 0.81 vs 14.52 +/- 1.05 mL/min per 100 g; P < 0.01). Glomerular filtration rate was increased by extracellular volume expansion (3.08 +/- 0.28 vs 5.42 +/- 0.46 mL/min per 100 g; P < 0.01). 7. The increase in NOx induced by acute volume expansion (0.18 +/- 0.03 vs 0.52 +/- 0.08 nmol/min per 100 g; P < 0.01) was diminished following the administration of haloperidol (0.52 +/- 0.08 vs 0.26 +/- 0.06 nmol/min per 100 g; P < 0.01). 8. Although DA does not participate in the actions of nitric oxide on vascular tone, both systems would play an important role in renal function adaptation during extracellular fluid volume expansion.     

Indomethacin and diclofenac sodium increase sodium and water excretion after extracellular volume expansion in the rabbit

The renal effects of an acute extracellular fluid volume expansion (50 ml Ringer/kg body weight/60 min) were studied in aldosterone-treated (100 μg/kg), anesthetized rabbits with and without pretreatment with either indomethacin (3.0 mg/kg) or diclofenac sodium (3.0 mg/kg), two different inhibitors of renal prostaglandin (PG) biosynthesis. In controls (n = 7), the volume expansion increased urine flow from 1.5 ± 0.24 to 6.1 ± 0.5 (S.E.) ml/min/100 g kidney weight and sodium excretion from 0.15 ± 0.03 to 0.99 ± 0.10 mmol/min/100 g. PAH and insulin clearance increased by 42 and 58%, respectively, while plasma renin activity and urinary excretion of PGF_2α-like immunoreactivity were reduced (P < 0.05). In aninals pretreated with indomethacin (n = 6) or diclofenac sodium (n = 6), the diuresis and the natriuresis following volume expansion were significantly increased about two-fold over controls, whereas PAH and inulin clearance, plasma renin activity and hematocrit did not differ from controls. Both drugs were found to reduce urinary excretion of PGF_2α-like immunoreactivity by 75–95% throughout the experiment. The results indicate that diclofenac sodium, indomethacin and extracellular volume expansion enhance sodium and water excretion partly by suppression of a PG sensitive reabsorption process in the kidney.     

扩容和麻黄碱对老年病人全麻诱导期循环功能的影响

目的 讨论使用预先扩容或麻黄碱对老年手术病人全麻诱导期对低血压和低心输出量的预防作用.方法 将90位ASAⅠ～Ⅱ级65岁以上老年患者随机分为三组:对照组(n=30),诱导时不给麻黄碱或扩容;麻黄碱组(n=30):麻醉诱导前给予麻黄碱;扩容组(n=30):诱导前给予羟乙基淀粉扩容.观察患者入室时(T1)、诱导后1 min...     

Intracerebral administration of naloxone and drinking in water-deprived rats

In 24-hr water-deprived rats, naloxone, at various doses (0, 12.5, 25, 50 μg/rat), was administered prior to a 15-min drinking period. Infusions were made bilaterally into each lateral ventricle, frontal cortex, lateral preoptic area, lateral hypothalamus, and caudate nucleus. Naloxone reliably reduced water consumption at 50 μg/rat when infused into the lateral ventricles and lateral hypothalamic areas. When comparable doses of naloxone were given by peripheral injection, no effect on drinking was observed. There appeared to be a trend developing for greater sensitivity to naloxone when infusions were made into a particular part of the hypothalamus. These data support the idea that naloxone reduces drinking by acting at central opiate receptors.     

利尿肾图在肾积水诊断及肾盂成形术疗效评价中临床意义的研究

目的:探讨利尿肾图在鉴别梗阻性与非梗阻性肾积水中的临床意义。方法:选择门诊及住院患者56例,涉及56侧肾输尿管。记录入选者一般情况和既往史,做普通肾图。对普通肾图呈梗阻型患者,按一次法做利尿性肾图,观察排泄曲线及速率。根据相关指标计算使用利尿剂后的排泄指数(DEI)。参与的病例最终均经B型超声检查,静脉肾盂造影或手术确诊。计算利尿肾图的确诊率。选取利尿肾图呈部分和完全梗阻的病例行肾盂成形术,术后随访6⁸个月,根据利尿肾图曲线及排泄率的变化对术侧肾脏做手术前后对比并对结果作秩转换的非参数检验。结果:如果利尿性肾图呈梗阻样,肾盂出口与输尿管梗阻可能性非常大。如果利尿性肾图是阴性的,说明肾盂输尿管是通畅的,可能肾盂扩张或张力下降,为动力性肾盂积水。利尿肾图检查显示手术(肾盂成形术)前后,肾盂积水改善明显。结论:利尿性肾图是诊断梗阻性与非梗阻性肾盂扩张的首选检查方法。利尿性肾图可作为手术(肾盂成形手术)后功能恢复的监测手段。     

分消走泄治疗法应用于肾病患者的临床分析

目的探讨分消走泄法中医治疗在IgA肾病患者治疗中的临床疗效。方法选取笔者所在医院2009年1月～2010年12月收治的IgA肾病患者62例,将患者随机分为两组,治疗组进行分消走泄法中医疗法联合西药常规治疗,对照组进行常规西药治疗。结果治疗后,两组患者尿蛋白、尿红细胞数与血肌酐含量、中医症候积分均显著改善(P<0.01),治疗组尿红细胞含量、24小时尿蛋白、中医症候积分与对照组相比均显著改善(P<0.01)。结论分消走泄法联合西药治疗能够改善肾病中医症候,改善西医的治疗效果,针对施治在肾病治疗中具有较高的临床价值。     

Central mechanisms of the isoprenaline-induced hypotension in anesthetized and conscious rats

Isoprenaline was microinjected into the cerebroventricular spaces of anesthetized or unanesthetized rats and the blood pressor effects recorded prior to or after intraventricular administration of pharmacologic antagonists. Injection of 1-20 micrograms of isoprenaline produced only depressor responses in both groups of animals. Pretreatment with 400-200 micrograms of propranolol partially antagonized the depressor effect of isoprenaline, whereas pretreatment with 40 micrograms of phenoxybenzamine or 100 micrograms phentolamine potentiated the depressor response to isoprenaline. The involvement of central beta-adrenoceptors and a propranolol-insensitive mechanism in the depressor response to intracerebroventricular isoprenaline is proposed. Indirect evidence of a central alpha-adrenoceptor mediation of pressor mechanisms counteracting the depressor responses elicited by beta-adrenoceptor stimulation is presented.