Neural effects of natural behavior on renal blood flow in spontaneously hypertensive rats

Background In states of stress and exercise, renal blood flow is shown to be depressed, mainly through neural mechanisms. Little is known, however, about the effects of natural or spontaneous behaviors on renal blood flow and renal sympathetic nerve activity. Methods We simultaneously measured renal sympathetic nerve activity and renal blood flow as a Doppler shift during grooming and exploring behaviors in spontaneously hypertensive rats. We also tested the effects of vasodilating drugs on changes in renal blood flow. Results Grooming behavior (n=21) increased renal sympathetic nerve activity, mean arterial pressure, and decreased renal blood flow. Percentage changes in renal sympathetic nerve activity correlated negatively with percentage changes in renal blood flow. Exploring with rearing (n=14) induced similar but larger changes in these variables. Denervation of renal nerves suppressed a reduction in renal blood flow during these behaviors. After intravenous injection of manidipine (a calcium channel blocker) or CV-11974 (an angiotensin II receptor antagonist), the behavior-induced reduction in renal blood flow was significantly smaller than that found before treatment, despite similar increases in renal sympathetic nerve activity. Conclusion Natural behaviors decrease renal blood flow in relation to the enhancement of renal sympathetic nerve activity, which is similar to the responses of the animals to stressful psychologic stimuli. Vasodilating drugs can attenuate the reduction in renal blood flow.     

Hepatic blood flow and drug metabolism in glycerol-rechallenged rats

Summary To analyze the hepatic blood flow and drug metabolism during glycerol-induced acute renal failure, 24 male Wistar rats were randomly divided into three groups: Group I received an intra-muscular injection of 1 ml/100g body weight 50% glycerol, group II a second injection on day 14 and group III a second injection on day 42 after the first injection respectively. The inulin clearance, the aminopyrine N-demethylase activity, the NADPH-cytochrome P-450 activity and the cardiac output and blood flow to the organs were measured before and after glycerol injection. The total hepatic and renal blood flow decreased less significantly in group II compared to group I and III. Various P 450 activities were kept on a high level only in group II. This observation indicates that the maintenance not only of renal but also of hepatic blood flow plays an important role in preventing the development of glycerol-induced acute renal failure. The mechanism may be the induction of various P 450 activities resulting in an increased hepatic clearance of nephrotoxic substances.Part of this paper was presented at the 9th Symposium of the Association for Experimental Urology of the German Urological Society, June 17–18, 1988, Aachen, Federal Republic of Germany     

Methods of renal blood flow measurement

Variations in regional renal blood flow have been implicated in a variety of disease states. Many techniques have been developed in an attempt to accurately assess these changes. The microsphere technique is the most widely used method at the present time. This technique allows focal measurements to be performed, but there is a conflict between the resolution of the method and the number of microspheres necessary in each sample. New imaging techniques such as tomography and autoradiography enable visual assessment of renal blood flow. Though there is no ideal method, these techniques have opended up new possibilities in the quantification of regional renal blood flow.     

An ontogenic study of renal tissue kallikrein in Okamoto spontaneously hypertensive rats: comparisons with human hypertensive nephropathy.

Urinary excretion of tissue kallikrein is reduced in essential hypertension. Although a similar finding has been reported in spontaneously hypertensive rats (SHR), only a few studies have been concerned with the amount of enzyme within the kidney both at the time of onset and during progression of the hypertension. We have performed an ontogenic study on the renal parenchymal values and immunoreactivity of tissue kallikrein in Okamoto SHR aged 4-78 weeks. Additionally, these two parameters were analysed in human biopsies taken from patients with hypertensive nephropathy. The enzymatic activity of renal tissue kallikrein (active and total; specifically antagonized by anti-tissue kallikrein antibodies), increased from 4 to 52 weeks in SHR when compared to normotensive Wistar Kyoto (WKY) rats; this increase was associated with a significant increase in blood pressure. In contrast, 78 weeks SHR and human biopsy tissue showed a substantial reduction in tissue kallikrein values. Also, both renal tissues showed a reduction in immunoreactivity in the cells of the connecting tubules that specifically store the enzyme. In advanced hypertension the observed reduction in tissue kallikrein was probably secondary to a loss of distal tubular mass, as a result of tubular atrophy and fibrosis. The greater values for renal tissue kallikrein in the kidney and reported reduced urinary excretion during the early phases of spontaneous hypertension may be explained by a primary defect in the mechanisms that regulate release of tissue kallikrein from the connecting tubule cells.     

Equality of the left and right renal venous flow predicts the severity of variceal bleeding in portal hypertensive children

Portasystemic collaterals develop as a result of portal hypertension. The collaterals in the cardioesophageal region is the leading cause of bleeding from esophageal varices. Some of the portal hypertensive patients present with bleeding episodes but the others do not, and some of the bleeders do not respond to endoscopic sclerotherapy procedure, although the underlying pathology is the same. The capacity of the natural collateral vessels might be a determining factor about the hemorrhagic events. Since the first step of portasystemic collateralization takes place in the naturally existent vascular channels, the present study, with its anatomic and clinical parts, was focused on these venous structures.     

Losartan increases renal blood flow during isoflurane anesthesia in sheep

BACKGROUND: Inhaled anesthetics cause a transient reversible depression of renal function by direct renal effects or indirectly by changes in neurohumoral systems or cardiovascular performance. When the sympathetic nervous activity is decreased during anesthesia, other vasoactive systems like vasopressin (AVP) and particularly the renin angiotensin system (RAS) are of importance for blood pressure maintenance. Little is known about how the renal circulation is affected by angiotensin receptor blockade during isoflurane anesthesia. METHODS: The study was performed on isoflurane anesthetized sheep equipped with flow probes (placed around a femoral and a renal artery) and a pulmonary artery catheter. During stable conditions the sheep were given one or more of the following substances: isotonic saline (NaCl); losartan (LOS) 10 mg x kg(-1); prazosin (PRAZ) 0.2 mg x kg(-1) and a vasopressin V1-receptor antagonist (AVP-a) 10 microg x kg(-1). RESULTS: LOS and AVP-a did not affect mean arterial pressure (MAP), whereas PRAZ lowered MAP significantly (from 98+/-12 to 65+/-7 mmHg). Renal blood flow (RBF) increased after LOS treatment (148+/-34 to 222+/-33 ml x min(-1)). The other substances were without effect on RBF. Femoral blood flow remained unchanged after all treatments. CONCLUSION: We conclude that the sympathoadrenal system is still the major determinant for blood pressure maintenance during isoflurane anesthesia in sheep. The apparently increased activity of the renin angiotensin system in this situation causes a reduction in renal blood flow, which is counteracted by angiotensin II AT1-receptor blockade.     

Effects of parathyroidectomy on blood pressure in spontaneously hypertensive rats

The long-term effects of parathyroidectomy (PTX) on blood pressure, intravascular volume, pressor hormones, and on acute vascular effects of intravenous parathyroid hormone (PTH) were evaluated in spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WK) rats. PTX or sham operation (CO) were done at 4-5 weeks of age, and a high calcium diet was offered to PTX rats to study them at eucalcemic calcium levels. The cardiovascular effects of PTX, determined after 11-13 weeks, were qualitatively similar in SH and WK rats: mean arterial blood pressure (conscious unrestrained rats) was lower, intravascular volume was higher, total body sodium was slightly higher, and plasma angiotensin II or norepinephrine levels were not different from CO groups. The acute hypotensive and chronotrophic effect of intravenous PTH was unchanged in PTX groups. When parathyroid intact SH rats and PTX SH rats were both examined on an 1.6% Ca diet, blood pressure was significantly lower in PTX than in parathyroid-intact SH rats. The results are compatible with the hypothesis that PTH has a permissive action on blood pressure maintenance in eucalcemic SH and WK rats by mechanisms unrelated to volume status or circulating pressor hormone concentrations.     

颈交感神经干离断对应激大鼠NO及胃粘膜血流量的影响

目的研究颈交感神经干离断(TCST)对浸水大鼠胃粘膜血流量(GMBF)的影响。方法30只雄性SD大鼠随机分为三组,每组10只。Ⅰ组为正常对照组;Ⅱ组为浸水对照组;Ⅲ组为TCST后浸水组。Ⅰ组、Ⅱ组将大鼠颈交感神经干暴露、分离,不离断;Ⅲ组TCST并将断端结扎。将Ⅱ、Ⅲ组大鼠垂直浸水[水温(23±1)℃]至剑突水平,6 h后取出,测定各组GMBF,评价粘膜损伤程度。硝酸还原酶法测定血清及胃粘膜一氧化氮(NO)含量。结果Ⅱ组胃粘膜见出血及糜烂,Ⅲ组粘膜损伤程度显著轻于Ⅱ组;Ⅲ组与Ⅱ组比较,GMBF显著升高,两者分别为(130.0±14.5)和(68.9±12.7)pu(P<0.01);Ⅱ组和Ⅲ组的溃疡指数(UI)分别为50.1±12.3和26.6±9.4(P<0.01);Ⅱ组大鼠的血清及胃粘膜的NO值显著高于Ⅰ组(P<0.01);Ⅲ组的血清NO值与Ⅱ组比较显著减少(P<0.01)。结论TCST可增加浸水应激大鼠的GMBF,对胃粘膜损伤有保护作用;其机制可能有NO的参与。     

The role of the abdominal sympathetic nervous system in regulating portal venous flow and its functional distribution

The role of the abdominal sympathetic nervous system in regulating portal venous flow (PVF) was examined in anesthetized rats using an ultrasonic volume flowmeter. Electrical stimulation of the hepatic sympathetic branch, given at 10 Hz, 1 ms, 10 s and 12 V, caused approximately a 28 per cent reduction in PVF, which was equivalent to that produced by occlusion of the bilateral carotid arteries for 30 s, without causing any change in the systemic arterial pressure. Stimulation of the major splanchnic nerve decreased PVF, the response being greater by stimulation of the right nerve than by stimulation of the left (p<0.05). Bilateral adrenalectomy shortened the recovery time without changing the magnitude or lateral predominancy. Neither proper hepatic arterial occlusion nor partial hepatectomy affected the response. In the partially hepatectomized animals, stimulation of the hepatic branch did not decrease the splenic flow but decreased the superior mesenteric venous flow (SMVF) and induced a similar response in PVF even when the SMVF was interrupted. An intraportal injection of noradrenaline decreased PVF dose-dependently. These findings indicate that the sympathetic nerve regulates PVF directly, and that there is functional laterality of the regulatory mechanism in the abdominal cavity, which suggests that adrenal factors work together with the nerve that supplies the portal vein.     

Regional renal blood flow in normal and disease states

Renal function is intimately dependent on renal blood flow. Alterations in either total or regional renal blood flow have major consequences for renal function. Through homeostatic mechanisms the kidneys are able to maintain relatively stable rates of flow over a wide range of perfusion pressures. A combination of neural, endocrine, exocrine and autocrine signals serve to regulate renal blood flow at both local and systemic levels. Alterations in the balance of these systems occur in the presence of certain pathophysiological conditions and an understanding of the subsequent changes in regional renal blood flow distribution aids in the understanding of the associated changes in renal function. The regulation and distribution of regional blood flow and the effects of surgical and pathophysiological conditions on these factors are reviewed.     

Renal Ischemic Injury Affects Renal Hemodynamics and Excretory Functions in Sprague Dawley Rats: Involvement of Renal Sympathetic Tone

The role of renal sympathetic nerves in the pathogenesis of ischemic acute renal failure (ARF) and the immediate changes in the renal excretory functions following renal ischemia were investigated. Two groups of male Sprague Dawley (SD) rats were anesthetized (pentobarbitone sodium, 60 mg kg^?1 i.p.) and subjected to unilateral renal ischemia by clamping the left renal artery for 30 min followed by reperfusion. In group 1, the renal nerves were electrically stimulated and the responses in the renal blood flow (RBF) and renal vascular resistance (RVR) were recorded, while group 2 was used to study the early changes in the renal functions following renal ischemia. In post-ischemic animals, basal RBF and the renal vasoconstrictor reperfusion to renal nerve stimulation (RNS) were significantly lower (all p < 0.05 vs. control). Mean arterial pressure (MAP), basal RVR, urine flow rate (UFR), absolute and fractional excretions of sodium (U_NaV and FE_Na), and potassium (U_KV and FE_K) were higher in ARF rats (all p < 0.05 vs. control). Post-ischemic animals showed markedly lower glomerular filtration rate (GFR) (p < 0.05 vs. control). No appreciable differences were observed in urinary sodium to potassium ratio (U_Na/U_K) during the early reperfusion phase of renal ischemia (p > 0.05 vs. control). The data suggest an immediate involvement of renal sympathetic nerve action in the pathogenesis of ischemic ARF primarily through altered renal hemodynamics. Diuresis, natriuresis, and kaliuresis due to impaired renal tubular functions are typical responses to renal ischemia and of comparable magnitudes.     

The impact of in-situ balloon occlusion of the renal artery and hypothermic perfusion on renal blood flow

Summary Unilateral renal blood flow was evaluated in-situ in 13 dogs by cineangiodensitometry and microsphere distribution studies before and after intermittent balloon occlusion with and without hypothermic perfusion of one kidney. The contralateral kidney served as control. No significant difference in renal blood flow and vascular resistance was noted before, and 5, 30 and 60 minutes after unilateral intra-arterial manipulation. Compartmental flow distribution studies in 5 dogs revealed no evidence of alteration of intra-renal haemodynamics. In a clinical pilot study, unilateral renal blood flow measured by cineangiodensitometry showed no change of clinical significance 5 and 60 minutes after intraluminal balloon occlusion of the renal artery for 60 seconds.     

Effects of peritoneal insufflation on hepatic and renal blood flow

The effects of peritoneal insufflation with carbon dioxide on hepatic and renal blood flow have not been reported hitherto. We evaluated these effects in a porcine model of abdominal laparoscopic surgery. Seven anesthetized pigs underwent peritoneal insufflation in a step-wise manner to create intraabdominal pressures of 6, 12, 18 and 24 mmHg, and changes in the arterial and venous pressure, arterial blood gases, and hepatic and renal blood flow were monitored. Both the hepatic and renal blood flow decreased as the intraabdominal pressure increased. Therefore, in order to carry out laparoscopic abdominal surgery safely in patients with hepatic or renal impairment, low intraabdominal pressures or noninsufflating techniques are recommended.     

Local cerebral blood flow in spontaneously breathing rats subjected to graded isobaric hypoxia

Local cerebral blood flow (l-CBF) was measured with an autoradiographic technique in spontaneously breathing rats exposed to air or gas mixtures of O2 and N2, giving inspired oxygen fractions (FiO2) ranging from 0.21 to 0.07. The arterial O2 tension (PaO2) changed from 10.9 +/- 0.3 (FiO2 0.21) to 3.9 kPa (FiO2 0.07) (82 +/- 2 to 29 mmHg). Hypoxia caused hyperventilation, and the arterial CO2 tension (PaCO2) fell from 5.21 +/- 0.05 kPa (FiO2 0.21) to 3.27 kPa (FiO2 0.07) (39.1 +/- 0.4 to 24.5 mmHg). The hyperventilatory response was markedly augmented when changing FiO2 from 0.13 to 0.11, causing a fall in PaCO2 of 0.75 kPa and a shift in arterial pH from 7.45 +/- 0.01 (FiO2 0.13) to 7.54 +/- 0.01 (FiO2 0.11). The l-CBF response to hypoxia was found to be biphasic for all the observed regions. At FiO2 0.13, l-CBF was measured about 75% above control but at FiO2 0.11, only 30% above control. A further reduction in FiO2 to 0.07 caused a marked increase in l-CBF, at least 240% of control; however, the applied CBF technique did not admit quantitation. These results suggest that the mechanisms controlling the cerebrovascular response to hypoxia and changes in arterial CO2 tensions are different. The results also indicate that hyperventilation might be harmful to the patient suffering from acute hypoxia.     

Intravenous digital subtraction angiography for the evaluation of renal artery blood flow following the removal of a neuroblastoma

There have been several reports of acute renal failure following the resection of an abdominal neuroblastoma combined with ipsilateral nephrectomy as well as the atrophy or disappearance of an unresected kidney after tumor resection. Spasms or thrombosis of the renal artery during tumor excision are considered to be the major cause. Since 1989, intravenous digital subtraction angiography (IVDSA) has been used to evaluate the renal artery blood flow immediately following surgery in seven patients with abdominal neuroblastomas. IVDSA was performed using a central venous catheter inserted prior to surgery. In all seven patients, IVDSA provided clear images for the evaluation of renal artery blood flow. In one of the two patients whose kidneys briefly became cyanosed during tumor excision, IVDSA demonstrated an occlusion of the renal artery and prompt measures could be taken to reestablish the blood flow. No complications of IVDSA occurred in any of the seven patients. IVDSA using a central venous catheter was thus considered to be useful for evaluating the renal artery blood flow in patients with a suspected renal artery blood flow disturbance without any risk of complications, and this modality obviated the need for intraarterial angiography.     

On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine

To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n =10). Cerebral blood flow was estimated during arterial normo-, hyper-and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 ± 7.8, 90.9 ± 13.3, and 33.6 ± 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 ±10.3,139.9 ± 19.9, and 55.2 ± 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 ± 15.2,144.7 ± 15.0, and 43.8 ± 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 ± 29.1, 143.0 ± 42.1, and 75.5 ± 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study.     

神经生长因子在自发性高血压大鼠前列腺组织中的表达意义

目的:探讨不同时期自发性高血压大鼠(SHR)前列腺组织中神经生长因子(NGF)及其mRNA的表达变化及其意义。方法:1月龄(幼年期)、6月龄(成年期)和12月龄(老年期)SHR组和血压正常WKY组各5只,分别计算腹侧前列腺指数;并采用免疫组化和RT-PCR方法,分别检测各组腹侧前列腺组织中NGF及其mRNA表达情况。结果:1月龄时,SHR和WKY前列腺指数分别为:1.16±0.06、1.03±0.09;6月龄时,SHR和WKY前列腺指数分别为:1.12±0.14、0.93±0.07;12月龄时,SHR和WKY前列腺指数分别为:1.11±0.05、0.96±0.09;SHR组腹侧前列腺指数无论成年期还是老年期均高于WKY组(P<0.05),在幼年期则差别不明显(P>0.05)。NGF及其mRNA在SHR组和WKY组的不同时期的腹侧前列腺组织中均有表达,随着月龄增长,NGF及其mRNA在SHR组和WKY组的表达逐渐增强(P<0.05);在同一个月龄期,SHR组表达强度高于WKY组(P<0.05)。结论:在发生BPH的SHR中,其交感神经兴奋性增强可能是BPH和高血压发病的共同机制之一,NGF在这一环节中发挥重要作用。     

偶测血压与动态血压在肾性高血压诊治中的临床价值

目的 探讨偶测血压与动态血压评价肾性高血压的临床价值.方法 选择97例肾性高血压患者,服用盐酸贝拉普利联合缬沙坦治疗4个月,观察治疗前、后采用偶测血压和24 h动态血压监测,并检测24 h尿蛋白、血清肌酐及肝功能进行分析.结果 9r7例患者用偶测血压与24 h动态血压监测诊断肾性高血压的符合率为73.2%;因低血压(26例)与高血钾(3例)等不同原因提前退出试验34例.余63例患者经治疗后与治疗前偶测血压和24 h动态血压监测值比较均降低;治疗前、后24 h平均收缩压、24 h平均舒张压值与动态血压值比较差异有统计学意义(P<0.01);治疗后24 h动态血压的总有效率与偶测血压比较差异也有统计学意义(P<0.05);昼夜节律比与治疗前比较明显恢复(P<0.01).结论 24 h动态血压监测与偶测血压比较更能敏感的、客观的、全面的评价肾性高血压的诊疗价值与安全性.