Elevated plasma levels of neuropeptide Y upon electrical stimulation of the sympathetic chain in humans

Neuropeptide Y (NPY) a potent vasoconstrictor peptide, is co-stored with the classic neurotransmitter noradrenaline (NA) in certain peripheral sympathetic neurons and has been suggested to be a co-transmitter in vascular control. Surgical interruption of the sympathetic nerve supply of the upper extremity was performed to treat palmar hyperhidrosis in five patients. Intraoperative electrical stimulation (10 Hz; 0.5 ms; 0.5-3.0 mA) of the right and left sympathetic chains for 1 min was employed to determine the correct level for surgical excision. Blood pressure and heart rate were recorded continuously. Blood was sampled from the antecubital vein on the side subjected to stimulation for the determination of NPY-like immunoreactivity (LI) and plasma catecholamines. Blood samples were collected before and during stimulation, as well as 30 s and 2, 5, and 10 min after stimulation. A maximal blood pressure response was observed during the stimulation, but the magnitude varied markedly and was independent of the side on which the sympathetic chain was stimulated. During 3 of the 10 stimulations, the mean arterial blood pressure (MABP) increased 5-10 mm Hg, while in the other 7 an increase of 30-75 mm Hg was seen. No significant changes in heart rate or plasma adrenaline were found. The peak increase in NPY-LI plasma levels was noted 2 or 5 min after stimulation, while the corresponding peak for NA occurred during or 30 s after the stimulation. The maximal changes in plasma NPY-LI and NA were significantly correlated with the changes in blood pressure (NPY-LI, r = 0.80, p <0.01; NA, r = 0.84, p <0.01) as well as with each other (r = 0.95; p <0.001). It is concluded that, after electrical stimulation of the sympathetic chain in humans, plasma levels of both NPY-LI and NA rise, indicating release of these substances from sympathetic neurons. It is therefore possible that the vasoconstrictor peptide NPY is involved, together with NA, in the blood pressure response elicited by the stimulation.     

Changes in the levels of neuropeptide Y-LI in the external jugular vein in connection with vasoconstriction following subarachnoid haemorrhage in man

Summary NPY is a putative neurotransmitter mainly co-localized with noradrenaline in sympathetic fibers which innervate the cerebral vasculature. The origin of most of the perivascular NPY fibers seems to be in the superior cervical ganglion. To investigate involvement of Neuropeptide Y (NPY) mechanisms in subarachnoid haemorrhage (SAH), twenty patients with SAH were investigated. NPY-LI (-like immunoreactivity) levels in the external jugular vein were assessed using radioimmunoassay in blood samples collected postoperatively (or after SAH in non-surgical patients) on days 1, 2, 3, 5, 7 and 9. These levels were compared with the clinical course and blood flow velocity changes monitored with ultrasonic Doppler equipment from both middle cerebral arteries (MCA) and both internal carotid arteries (ICA).Compared to NPY-LI levels in 14 controls (mean 116±3 pmol/ l), increased levels (up to 253 pmol/l) and a close relationship between velocities and NPY-LI levels were found in a subpopulation of the SAH patients. When comparing the mean haemodynamic index (V MCA/ipsilateral V ICA) and mean NPY-LI levels in each of the 20 patients, a correlation of r=0.75, p=0.0001 was found. Increased NPY-LI were found (131±8 pmol/l) when simultaneous Doppler velocity recordings showed vasoconstriction (Haemodynamic index >5) compared with samples taken when the haemodynamic index was <5, p<0.05. When MCA velocity exceeded 120 cm/sec, increased levels were found (129±9 pmol/l) compared with the conditions when MCA velocity was less than 120 cm/sec (113±5 pmol/ l), p=0.06. The results indicate a possible NPY involvement in cerebral vasoconstriction after SAH.     

Is neuropeptide Y a contributor to volume-induced hypertension?

Hypertension often occurs with fluid overload. The most common mechanism is considered to be mediated by increased cardiac output. Hemodialysis (HD) patients frequently have large amounts of fluid overload. Neuropeptide Y (NPY) is activated by stress and contributes to hypertension and heart failure. We speculated that NPY may be released by the stress of fluid overload and, by its vasoconstrictor effect, may contribute to hypertension and heart failure. Plasma levels of NPY and other vasoconstrictors were studied in 20 HD patients with varying degrees of fluid overload, and the relationship of NPY plasma levels to blood pressure was analyzed. The plasma concentrations of NPY correlated with the degree of fluid overload (r = 0.89; P < 0.0001) and the mean arterial blood pressure (r = 0.85; P < 0.0001). Seven patients had fluid overload of greater than 6% of body weight. They had higher blood pressures and higher plasma concentrations of NPY than 13 HD patients with less than 5% of fluid retention (systolic blood pressure, 179+/-8.2 v 145+/-3.7 mm Hg, P = 0.007; NPY, 61+/-4.6 v 26.8+/-2.7 pmol/L, P < 0.001). In stepwise multiple regression analysis, NPY alone explained blood pressure elevation when analyzed with fluid overload and angiotensin II, renin, noradrenaline, and adrenaline levels. We hypothesized that fluid overload in dialysis patients is a stress-inducing state that activates the sympathetic nervous system and releases the vasoconstrictor NPY. The resulting inappropriate vasoconstriction may contribute to volume-induced hypertension and heart failure in a vicious cycle. We conclude that determination of plasma NPY levels may be useful as a marker of the clinical threat of overhydration.     

Changes in cardiac metabolism, perfusion, ECG and plasma catecholamines during increased intracranial pressure in the pig

The effects of graded elevations of intracranial pressure (ICP) on cardiac metabolism, blood flow and electrophysiology, and plasma catecholamines were studied in eight open-chest pigs. ICP was consecutively elevated from 15 +/- 3 mmHg in the control state to 40 +/- 4, 84 +/- 4 and 152 +/- 11 mmHg. Mean arterial blood pressure and heart rate were significantly increased at the two highest ICP levels. Cardiac oxygen uptake was also increased from 2.9 +/- 0.4 ml X min-1 to a maximum of 7.1 +/- 2.0 ml X min-1, and coronary sinus blood flow increased from 49 +/- 7 to 131 +/- 35 ml X min-1 at the highest ICP level. The transmyocardial blood flow distribution was unchanged, as determined by the microspheres technique. Arterial plasma catecholamine concentrations were significantly elevated at the two highest ICP levels, but noradrenaline overflow from the heart did not increase. The high arterial adrenaline concentrations (51 +/- 25 nmol X 1(-1) at the highest ICP level) may be responsible for the cardiac stimulation seen in these experiments. No signs of ischaemia, as judged by myocardial lactate production or the relative flow distribution to the endocardium were observed. Changes in the T-wave morphology appeared in the subendocardial ECG at all ICP levels, the changes being more prominent with increasing ICP levels. It is concluded that the increase in circulating catecholamine levels, adrenaline in particular, together with an elevation of afterload cause an increase of myocardial work, which may explain the T-wave changes in the ECG which are observed upon rapid elevation of intracranial pressure.     

Plasma neuropeptide Y concentrations in patients on hemodialysis

BACKGROUND: Neuropeptide Y (NPY) is a 36-amino-acid peptide that was originally isolated from the porcine brain. NPY, in contrast to leptin, is one of the most potent appetite stimulants. In some previous studies, NPY was found to be correlated with mean blood pressure (MBP) and fluid volume in patients on hemodialysis (HD), contributing to volume-induced hypertension. However, it is still unclear which NPY-sensitive neuronal pathways are responsible for the various changes seen in response to central NPY administration. In this study we analyzed the correlation of circulating levels of NPY with parameters of nutritional conditions, and we investigated the relationships between NPY concentrations and clinical markers of fluid volume in patients on HD. We also evaluated the effects of high-flux dialysis membranes on plasma NPY levels as compared with those of low-flux membrane. METHODS: Plasma NPY concentrations in patients on regular HD were measured using commercially available radioimmunoassay (RIA) kits. We examined the relationship between plasma NPY concentration and other clinical indices in patients on HD. RESULTS: Plasma NPY concentrations were inversely correlated with the serum urea nitrogen levels (r = -0.32) as well as protein catabolic rate (PCR) (r = -0.28). Plasma NPY was also correlated with the increase in body weight between HD sessions (r = 0.29). On the other hand, plasma NPY concentrations were not correlated with MBP, atrial natriuretic peptide (ANP), or adrenomedullin (AM). The reduction rate of plasma NPY with a high-flux dialysis membrane was significantly higher than that with a low-flux dialysis membrane. CONCLUSIONS: The secretion of NPY may be enhanced in a poor state of nourishment and stress induced by fluid volume overload in patients on HD, and plasma NPY is removed by a high-flux dialyzer.     

Effects of ischaemia and reperfusion on vasoactive neuropeptide levels in the canine infrarenal aortic revascularization model

Infrarenal aortic cross-clamping is associated with remote vascular events, including myocardial infarction and renal insufficiency. The purpose of this study was to determine whether hindlimb ischaemia and reperfusion associated with infrarenal aortic cross-clamping results in the production of vasoactive regulatory neuropeptides. A canine model of infrarenal aortic cross-clamping was used for the study. Serial blood samples were drawn, prior to, at the time of, and serially following placement of the clamp and subsequent release of the clamp and reperfusion. Ischaemia resulted in increased mean (s.e.m.) plasma levels of neuropeptide Y (NPY) (initial 10.0(1.8) pmol/l versus ischaemia 24.7(2.3) pmol/l, P<0.001) and vasoactive intestinal polypeptide (VIP) (initial 2.53(0.5) pmol/l versus ischaemia, 7.3(1.3) pmol/l, P<0.05). Reperfusion produced three-fold elevation of VIP (initial 2.5(0.5) pmol/l versus reperfusion 9.6(1.5) pmol/l, P<0.001), two-fold elevation in the plasma levels of endothelin-1 (initial 1.3(0.1) pmol/l versus reperfusion maximum 2.5(0.3) pmol/l, P<0.01) and NPY (initial 10.0(0.8) pmol/l versus reperfusion maximum 23.9(2.3) pmol/l, P<0.001). Ischaemia and reperfusion did not alter calcitonin gene-related peptide (CGRP) (a potent vasodilator) levels. Endothelin-1 (ET-1) plasma levels were also increased following haemorrhagic shock (initial 1.3(0.1) pmol/l versus exsanguination 3.4(0.4) pmol/l, P<0.001), but not during ischaemia (initial 1.3(0.1) pmol/l versus ischaemia maximum 1.7(0.2) pmol/l, P=0.7). It was concluded that vasoactive regulatory peptides are released following ischaemia, reperfusion and shock in the canine infrarenal aortic revascularization model and, therefore could contribute to remote vascular events observed with infrarenal aortic cross-clamping. Copyright © 1996 The International Society for Cardiovascular Surgery.     

Thoracolumbar epidural anaesthesia and isoflurane to prevent hypertension and tachycardia in patients undergoing abdominal aortic surgery.

Cardiovascular and hormonal responses to reconstructive abdominal aortic surgery were studied in 20 patients anaesthetized either with moderate-dose fentanyl (20 micrograms kg-1) combined with isoflurane, nitrous oxide and oxygen (n = 10), or with thoracolumbar epidural bupivacaine combined with isoflurane, nitrous oxide and oxygen (n = 10). After the start of operation, hypotension occurred in four patients in the epidural group. In both groups, the aortic cross-clamping caused slight increases both in mean arterial pressure and in calculated systemic vascular resistance, and a significant decrease in cardiac index. At the same time, a marked increase in plasma vasopressin was seen in the fentanyl group. Plasma catecholamines were low in both groups. After aortic declamping, the cardiac index improved in both groups, although two patients in the fentanyl group and four patients in the epidural group were hypotensive. Post-operatively, eight patients in the fentanyl group were hypertensive, versus none in the epidural group, in which bupivacaine-fentanyl was administered epidurally. At the same time, plasma vasopressin and adrenaline increased significantly in both groups, whereas plasma noradrenaline did so only in the fentanyl group. The results suggest that thoracolumbar epidural bupivacaine combined with low-dose isoflurane in nitrous-oxide-oxygen prevents intra-operative hypertension and tachycardia, but it may cause hypotension. Post-operative hypertension and tachycardia as well as the increase in plasma noradrenaline are prevented by epidural administration of bupivacaine-fentanyl.     

Prospective study of neuropeptide y as an adverse cardiovascular risk factor in end-stage renal disease

Chronic renal insufficiency is a situation characterized by high plasma concentration of neuropeptide Y (NPY). Because this neuropeptide interferes with cardiovascular (CV) function, it is possible that it is involved in the high CV-related morbidity and mortality of these patients. To test this hypothesis, a follow-up study was performed (average duration, 34 mo; range 0.2 to 52.0 mo) in a cohort of 277 patients with end-stage renal disease receiving chronic dialysis. Univariate analysis revealed that plasma NPY was directly related to plasma norepinephrine (r = 0.37, P < 0.001) and epinephrine (r = 0.17, P = 0.005), exceeding the upper limit of the normal range in the majority of patients with end-stage renal disease (170 of 277, 61%). One hundred thirteen patients had one or more fatal and nonfatal CV events; 112 patients died, 66 of them (59%) of CV causes. Plasma NPY failed to predict all-cause mortality but was an independent predictor of adverse CV outcomes (hazard ratio [10 pmol/L increase in plasma NPY], 1.32; 95% confidence interval, 1.09 to 1.60; P = 0.004) in a Cox proportional-hazard model that included a series of traditional and nontraditional CV risk factors. Plasma NPY maintained its predictive power for CV events in statistical model including plasma norepinephrine. Plasma NPY predicts incident CV complications in end-stage renal disease. Controlled trials are needed to establish whether interference with the sympathetic system, NPY, or both may reduce the high CV morbidity and mortality of dialysis patients.     

Succinylcholine-induced increases in plasma catecholamine levels in humans

Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 min after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3-4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5-1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mg/kg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = +/- 19 pg/ml, P less than 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 +/- 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.     

Neuropeptide Y levels in central and peripheral cerebrospinal fluid in patients with intracranial disorders

Summary Neuropeptide Y (NPY) was measured in central and peripheral cerebrospinal fluid (CSF) in patients suffering from various intracranial disorders. The central NPY-like immunoreactivity (LI) level showed a concentration of 129±19 pmol·l^–1 and was significantly increased (p<0.05) compared to peripheral CSF (73±9 pmol·l^–1). From five patients with subarachnoid haemorrhage the CSF NPY-LI levels reached 154±47 pmol·l^–1. In five patients peripheral and central CSF was collected at the same occasion and the CSF NPY-LI concentration was 76±17 pmol·l^–1 in peripheral and 142±23 pmol·l^–1 in central CSF (p<0.01), respectively. In a reference group of 9 patients, who were examined by lumbar myelography because of suspected intervertebral herniated discs, the peripheral CSF NPY-LI concentration was 59±5 pmol·l^–1 a value which was also significantly lower compared to NPY-LI levels in central CSF.Thus it is obvious that NPY is present in human CSF with a relatively higher concentration in central than in peripheral CSF at least in patients with disorders of the central nervous system, suggesting a central origin of the NPY.     

Cardiovascular and metabolic responses to submaximal exercise in hemodialysis patients

Eight chronic hemodialysis (cHD) patients and six healthy sedentary controls (C) were exercised for 60 minutes at 52 +/- 8% (cHD patients) and 48 +/- 4% (C) of their maximal oxygen consumption levels. Plasma lactate levels at rest and during exercise were comparable in both groups. Respiratory exchange ratios were lower in cHD patients, but they increased during exercise to levels comparable to those of the C group. Despite comparable heart rates at rest, exercise of similar intensity led to lower heart rates at 30 and 60 minutes in cHD patients compared to C (P less than 0.05). The cHD patients had higher systolic and mean arterial pressures at rest than did C (P less than 0.05), but during exercise the increments in systolic and mean blood pressures were lower in cHD patients than they were in C (P less than 0.05). In spite of these blunted cardiovascular responses, plasma catecholamines increased during exercise in both groups. Plasma glucose levels were similar in both groups during exercise in spite of significantly higher plasma levels of insulin and glucagon in cHD patients throughout the exercise session (P less than 0.01). These data demonstrate that chronic cHD patients can exercise at a modest intensity for a prolonged period of time without untoward cardiovascular or metabolic responses. Their poor exercise response does not appear to be related to an inadequate activation of the sympathoadrenal system.     

Sympathetic nervous system sensitivity to hemorrhagic hypotension in the subhuman primate

The endogenous catecholamine response to hemorrhagic hypotension is poorly defined since most data have been derived from experiments in lower animal species. To clarify this situation we studied the plasma norepinephrine (NE) and epinephrine (Epi) responses to hemorrhagic hypotension in ten healthy male baboons (Papio anubis). After an overnight fast, animals were tranquilized with 100 mg of ketamine hydrochloride after which femoral artery and vein catheters were inserted. The animals then underwent phlebotomy of 20 ml/kg over 60 minutes with retransfusion of the autologous blood over the next 30 minutes. Plasma specimens for catecholamines were collected at 5, 15, 30, and 60 minutes during phlebotomy and again at 15 and 30 minutes during retransfusion. Plasma NE and Epi concentrations were measured by a radioenzymatic technique. Mean arterial blood pressure (MAP) decreased (p less than 0.01) and heart rate (HR) increased (p less than 0.01) within 15 minutes of phlebotomy, and these variables returned to baseline with retransfusion. Plasma NE and Epi levels increased (p less than 0.025) within 5 minutes of the onset of 'hemorrhage' and within 15 minutes plasma NE concentrations were 56% above baseline, whereas plasma Epi levels were six times greater than baseline. With retransfusion, plasma NE and Epi levels returned to baseline concentrations. We conclude: 1) in a primate species, the sympathetic nervous system responds rapidly to hemorrhage; 2) contrary to prior studies in rats, plasma NE increases as rapidly as Epi but not to the same degree; 3) plasma NE and Epi concentrations rapidly return to baseline levels with fluid resuscitation; and 4) there is little justification for the use of exogenous synthetic catecholamines in hemorrhagic hypotension where fluid resuscitation remains the treatment of choice.     

Atrial natriuretic peptide and other vasoactive hormones in nephrotic syndrome

Plasma levels of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), renin activity (PRA), aldosterone (PA), catecholamines and urinary prostaglandins (PG), as well as renal function were measured in children in the edematous state of the nephrotic syndrome before and after infusion of human serum albumin. Before albumin infusion, plasma levels of AVP, PRA, PA and noradrenaline (NA) and urinary excretion of PGE2, PGE-Met, PGF2 alpha were elevated. The mean value of plasma ANP was in the normal range. Albumin infusion produced a 36% increase in the calculated plasma volume. It was associated with a fivefold rise in the plasma level of ANP (31.6 +/- 22.6 vs. 151.4 +/- 52 fmol/ml mean, SD), and a significant fall in the levels of PRA, AVP, PA, and NA. Similarly, urinary concentration of PGE2, PGE-Met and PGF2 alpha fell. Urine flow, GFR, UNaV, FENa, and COsm increased significantly, while CH2O remained unchanged. The diuresis, natriuresis and GFR correlated with the level of plasma ANP, while urinary sodium excretion did not correlate with PA or NA levels. These findings suggest that ANP plays an important role in albumin induced natriuresis in children with nephrotic syndrome.     

Neuropeptide Y (NPY) in human penile corpus cavernosum tissue and circumflex veins--occurrence and in vitro effects

The concentration and distribution of neuropeptide Y (NPY) within the penile corpus cavernosum (CC) and in penile circumflex veins (CV) from healthy potent males was investigated by immunochemistry and immunohistochemistry. The concentrations were assessed to 28.6 pmol/gm. (CC) and 15.8 pmol/gm. (CV) respectively. Gel filtration on CC tissue extracts demonstrated a single peak of NPY-immunoreactivity (NPY-IR) similar to synthetic human NPY. The NPY-IR was confined to nerve fibers seemingly innervating smooth muscle cells. In vitro myographic examinations demonstrated contractile activation by NPY in 2/8 CC strips and in 5/8 CV strips. The mean contractile force was 1.17 +/- 0.62 mN (18.3 +/- 15.8% of the K(+)-induced contraction) and 2.42 +/- 0.42 mN (31 +/- 12%) respectively. NPY 10(-7) and 10(-6) M displayed a potentiating effect on the response to NA 10(-9) in one of six CC and four of six CV preparations. It is suggested that NPY could add to the contractile effect of NA in detumescence and in maintenance of the resting state; contribution of NPY to the veno-occlusive mechanism at initiation of erection is another putative physiological function.     

Systemic and cavernous plasma levels of neuropeptide Y during sexual arousal in healthy males

Neuropeptide Y (NPY) has been shown to induce contraction of isolated human penile erectile tissue and potentiate the response to noradrenaline. The purpose of our study was to measure in the cavernous and systemic blood of healthy male volunteers the course of NPY through different stages of sexual arousal. Whole blood was drawn simultaneously from the corpus cavernosum and the cubital vein of 16 healthy male volunteers during penile flaccidity, tumescence, rigidity and detumescence. Tumescence and erection were induced by applying audiovisual and tactile stimulation. Plasma levels of NPY (given in pmol l(-1)) were determined by means of an enzyme-linked immunoassay. NPY significantly decreased in the cavernous blood on sexual arousal, when the flaccid penis became tumescent and, finally, rigid (F: 88.8 ± 35.8, T: 62.4 ± 22.7, R: 62.3 ± 19.7), and only slightly rose in the phase of detumescence (64.8 ± 23). In the systemic circulation, no pronounced alterations in the concentration of NPY were registered (F: 64.4 ± 27, T: 65.8 ± 19, R: 59.6 ± 25, D: 67.6 ± 29.3). Our findings are in favour of the hypothesis that NPY could contribute to the maintenance of the resting state of cavernous smooth muscle.     

纳洛酮对创伤性休克家兔血管活性物质动态变化的影响

目的探讨家兔创伤性休克过程中血管活性物质的变化、意义及纳洛酮的抗休克作用.方法采用Lamson's法建立家兔创伤性休克模型.随机分为对照组和治疗组.观察两组家兔创伤性休克前、休克末及复苏后1h、3h、5h、12h血浆的一氧化氮(NO)、内皮素(ET)、神经肽Y(NPY)和心钠素(ANP)动态变化,并监测各时间点平均动脉压(MAP)变化.结果两组血浆一氧化氮、内皮素、神经肽Y、心钠素休克末、复苏后较休克前比较具有显著性差异(P＜0.001),治疗组与对照组比较差异显著,治疗组明显低于对照组.复苏后治疗组MAP明显高于对照组(P＜0.01).结论休克时血浆一氧化氮、内皮素、神经肽Y、心钠素表达上调,纳洛酮可降低一氧化氮、内皮素、神经肽Y、心钠素浓度.     

A comparison of the endocrine effects of hypotension induced by nicardipine with those by sodium nitroprusside in dogs

Plasma catecholamines, plasma renin activity, plasma aldosterone and plasma cortisol during hypotension induced by sodium nitroprusside and nicardipine were studied in 27 mongrel dogs under 0.87% halothane in oxygen. They were randomly divided into three groups: sodium nitroprusside (group S: n = 8), nicardipine (group N: n = 8) and controls (group C: n = 9). Group C received no vasodilator therapy and served as a control. Mean arterial pressure was reduced and maintained at 60 mmHg for 60 minutes in hypotensive groups. No changes were noted in plasma catecholamines and plasma cortisol in group C throughout the experiment, but plasma renin activity and plasma aldosterone decreased progressively. During hypotension induced by sodium nitroprusside and nicardipine, plasma epinephrine was significantly higher than the control value. However, after the hypotensive drugs were discontinued, plasma epinephrine decreased slightly. During and after induced hypotension, plasma renin activity of group N and group S were significantly higher than the control values. The highest levels of plasma renin activity 36.7 ng.ml-1.hr-1 in group N and 23.2 ng.ml-1.hr-1 in group S were observed. Plasma aldosterone concentration was significantly higher than the control value in group N. The maximum increase occurred 30 minutes after discontinuation of the nicardipine and the highest concentration of plasma aldosterone was three times control value. In contrast, in group S, plasma aldosterone was unchanged from the control value. Plasma cortisol concentration of group N was significantly increased than the control value. However, in group S, plasma cortisol concentration showed a slight but not significant increase.(ABSTRACT TRUNCATED AT 250 WORDS)     

尿毒症患者在肾移植围手术期血浆神经肽Y含量变化及其意义

目的 探讨血浆神经肽Y(NPY)在成功肾移植围术期的变化及其与肾功能的关系.方法 采集45例行同种异体肾移植术的尿毒症患者术前、术后24 h、出院前1 d外周静脉血标本5 ml,测定血浆NPY、血清尿素氮(BUN)、肌酐(Cr)水平.对照组为20例健康志愿者.结果手术前的血浆NPY平均值(400.8±105.6)ng/L较对照组20例健康志愿者的血浆NPY水平(77.2±16.6)ng/L显著升高(P<0.01).术后24 h血浆NPY较术前略有降低(P>0.05).出院前1 d血浆NPY较术前显著降低(P<0.05),但明显高于健康志愿者血浆NPY水平(P<0.05).结论 肾移植术后尿毒症患者的血浆NPY水平在肾功恢复正常后明显下降,血浆NPY浓度在一定程度上可以作为肾移植围术期肾功能的评估指标之一.     

Effects of atrial natriuretic peptide (99-126) in chronic renal disease in man

Plasma concentrations of human atrial natriuretic peptide (99-126) are elevated in patients with end-stage chronic renal failure and on haemodialysis. Plasma atrial natriuretic peptide (ANP) concentrations change with extracellular fluid volume, suggesting that ANP continues to have a role in chronic renal failure. We have studied the effects of an infusion (5 pmol/kg per min) in subjects with chronic renal failure (CCr) less than 30 ml/min per 1.73 m2). Glomerular filtration rate and effective renal plasma flow increased by 23% (P less than 0.01) and 27% (P less than 0.01) respectively and sodium excretion more than doubled. Systolic and diastolic blood pressures decreased by 14 (SD 1.6) and 6 (SD 0.8) mmHg respectively (P less than 0.001), and plasma renin activity declined (P less than 0.01). Plasma ANP concentrations were elevated compared to normal subjects and reached a peak of 224 (SD 87) pmol/l at the end of the infusion. Plasma half-life was 4.8 (SD 2.7) min. Plasma concentrations are elevated in chronic renal failure and ANP may play a physiological role in controlling extracellular fluid volume and blood pressure.     

Endocrine effects of induced hypotension by ketanserin in anesthetized dogs]

Plasma levels of catecholamines, aldosterone and cortisol as well as plasma renin activity during hypotension by ketanserin were studied in 9 mongrel dogs under 0.87% halothane in oxygen (1MAC). Mean arterial pressure was reduced and maintained at 60 mmHg for 60 minutes by the infusion of 0.1% ketanserin solution. Plasma norepinephrine decreased progressively during hypotension to 35% of the control value after induced hypotension. In contrast, plasma epinephrine increased three-four folds compared with the control value during and after induced hypotension, but this change was not statistically significant. Plasma renin activity and plasma aldosterone showed a slight increase during hypotension but returned toward the control value after discontinuing the infusion of ketanserin. Plasma cortisol remained unchanged throughout the experiment. In conclusion, our data show that hypotension by ketanserin is not accompanied by the activation of the renin-angiotensin-sympathetic system or adrenocortical system.