The differential effect of arginine vasopressin on skin blood flow in man

Physiological elevation of plasma vasopressin in man results in a small reduction in skeletal muscle blood flow but the action on skin blood flow has not been reported. We have studied eight male subjects during infusion of arginine vasopressin (AVP) at 2 units/h for 90 min. Plasma levels of AVP, measured by radioimmunoassay, rose to 68.5 (7.0) pg/ml, mean (SEM). Forearm and finger blood flow was measured with an electronic plethysmograph, hand interdigital skin-fold blood flow with a laser-Doppler blood flow meter and facial temperature with a thermocouple. All subjects developed marked facial pallor during infusion of AVP, facial temperature falling from 34.2 (0.2) to 32.7 (0.1) degrees C (P less than 0.001) then rising to 33.7 (0.1) degrees C (P less than 0.01) after AVP was stopped. Hand interdigital skin-fold blood flow also fell from 2.6 (0.02) to 2.3 (0.02) V (P less than 0.001) and rose sharply to 3.6 (0.2) V (P less than 0.001) on stopping the infusion. There were small changes in forearm and finger blood flow: both rose, from 6.3 (0.1) to 6.9 (0.1) (P less than 0.001) and 46.1 (1.0) to 54.3 (0.7) ml min-1 100 ml-1 (P less than 0.001) respectively. Neither fell when AVP was stopped. Heart rate remained unchanged throughout. These results indicate that high physiological levels of AVP, comparable with those attained during physical stress, produced a fall in blood flow in the face and interdigital skin-fold of the hand consistent with a fall in nutritional blood flow to skin.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of chronic hypokalaemia on renal concentrating ability and secretion of arginine vasopressin

Two patients with a Bartter-like syndrome, who had been hypokalaemic for 129 and 55 months, and 13 normokalaemic control subjects were investigated during 24 h of water deprivation. The hypokalaemic patients had urine volumes, urine osmolalities, osmolar clearances and tubular capacities for water reabsorption within the normal range. During thirst, plasma-arginine vasopressin increased much more markedly in the patients (3.4 to 11.1 pmol/l and 3.0 to 17.7 pmol/l) than in the control subjects (2.1 pmol/l (median), range 1.0-3.1, to 3.7 pmol/l, range 1.7-6.4). Plasma angiotensin II increased during water deprivation in the patients (33 to 53 pmol/l and 147 to 208 pmol/l) but not in the control subjects (9 pmol/l (median), range 3-15, to 11 pmol/l, range 3-15). Plasma aldosterone was the same in patients and control subjects and did not change in response to thirst. It is suggested that renal concentrating ability can be preserved in patients with chronic potassium depletion by means of a compensatory increase in the secretion of antidiuretic hormone.     

Metabolic clearance rate of arginine vasopressin in severe chronic renal failure.

1. The metabolic clearance rate of arginine vasopressin was determined using a constant infusion technique in normal subjects and patients with chronic renal failure immediately before commencing dialysis. Endogenous arginine vasopressin was suppressed in all subjects before the infusion with a water load. 2. Plasma arginine vasopressin concentrations were determined using a sensitive and specific radioimmunoassay after Florisil extraction. The detection limit of the assay was 0.3 pmol/l, and intra- and inter-assay coefficients of variation at 2 pmol/l were 9.7% and 15.3%, respectively. 3. In normal subjects, the metabolic clearance rate was determined at two infusion rates producing steady-state concentrations of arginine vasopressin of 1.3 and 4.4 pmol/l. In the patients with renal failure, a single infusion rate was used, producing a steady-state concentration of 1.5 pmol/l. 4. At comparable plasma arginine vasopressin concentrations, metabolic clearance rate was significantly reduced in patients with renal failure (normal 1168 +/- 235 ml/min versus renal failure 584 +/- 169 ml/min; means +/- SD; P < 0.001). 5. Free water clearance was significantly reduced in normal subjects during the arginine vasopressin infusion from 8.19 +/- 2.61 to -1.41 +/- 0.51 ml/min (P < 0.001), but was unchanged in the patients with renal failure after attaining comparable plasma arginine vasopressin concentrations. 6. In normal subjects there was a small but significant fall in metabolic clearance rate at the higher steady-state arginine vasopressin concentration (1168 +/- 235 ml/min at 1.3 pmol/l versus 1059 +/- 269 ml/min at 4.4 pmol/l; P = 0.016).(ABSTRACT TRUNCATED AT 250 WORDS)     

A heterologous radioimmunoassay for arginine vasopressin.

A sensitive and specific radioimmunoassay for arginine vasopressin (AVP) was developed utilizing the antisera against lysine vasopressin (LVP) in combination with a labeled AVP. The assay employs an acetone extraction procedure and detects as little as 0.8 pg. per milliliter of AVP in human plasma. In normal subjects the mean (+/- S.D.) plasma concentration of AVP was 4.9 +/- 1.2 pg. per mililiter after fluid deprivation and 1.2 +/- 0.4 pg. per milliliter after water loading. Plasma AVP levels correlated significantly with plasma osmolalities. In four patients with diabetes insipidus, plasma AVP concentrations ranged from less than 0.8 to 1.2 pg. per milliliter, whereas six patients with the syndrome of inappropriate ADH secretion showed plasma levels of AVP which correspond to those of the dehydrated state in normal subjects or greater, although plasma osmolalities were low in all cases. It was concluded that the present radioimmunoassay method for AVP provides a useful way of assessing neurohypophyseal function in man.     

The effect of arginine vasopressin on ureagenesis in isolated rat hepatocytes

The effect of arginine vasopressin (AVP) on ureagenesis was measured in isolated rat hepatocytes with ammonium chloride and L(+)-lactate as substrates. AVP was found to stimulate urea synthesis and the dose-response curve suggests that such an effect is present at concentrations of the hormone as low as 25-50 pmol/l. Both the dose-response curve and the concentrations of NH+4 employed suggest that the effect observed could be of physiological significance.     

Relationship between urinary concentrating ability, arginine vasopressin in plasma and blood pressure after renal transplantation

Arginine vasopressin (AVP) and serum osmolality (Sosm) were determined in plasma before and after a 24-h period of water deprivation in 19 patients with post-renal-transplant hypertension (group I), 14 patients with normal blood pressure after renal transplantation (group II), and 16 healthy control subjects (group III). Urine was collected in four periods of 6 h each for measurement of urine volume (V), urine osmolality (Uosm) and tubular capacity for reabsorption of water (Tc water). AVP and Sosm increased significantly in all groups. The AVP levels were the same in groups I and II, but higher in group I than III both before and after water deprivation. In group II, AVP was higher than in group III only after water deprivation; V was significantly reduced in all groups. In groups I and II, V, Tc water and Uosm were the same. In group III, V was significantly lower than in groups I and II in the last three 6-h periods, and in group III, Tc water was higher in the first 6-h period than in groups I and II. There was a significant positive correlation between AVP and Sosm in all groups. In conclusion, renal water excretion cannot be reduced as rapidly and to the same degree in renal transplant recipients as in control subjects because of a decreased renal capacity for reabsorption of water. The higher AVP level in the transplant recipients may be a compensatory phenomenon for the decreased responsiveness of the renal collecting ducts in the transplanted kidneys. The sensitivity of the osmoreceptors to changes in osmotic stimuli was normal.     

Acute renal failure with selective medullary injury in the rat.

Since human acute renal failure (ARF) is frequently the result of multiple rather than single insults, we used a combination of treatments to induce ARF in rats. Uninephrectomized, salt-depleted rats injected with indomethacin developed ARF after administration of radiocontrast. After 24 h, the plasma creatine rose from 103 +/- 3 to 211 +/- 22 mumol/liter (mean +/- SE) and the creatinine clearance dropped from 0.7 +/- 0.1 to 0.2 +/- 0.04 ml/min (P less than 0.001). Severe injury was confined to the outer medulla and comprised necrosis of medullary thick ascending limbs (mTALs), tubular collapse, and casts. Other nephron segments were free of damage except for the proximal convoluted tubules which showed vacuole formation originating from lateral limiting membranes that resembled changes reported in human contrast nephropathy. Cell damage to mTALs included mitochondrial swelling, nuclear pyknosis, and cytoplasmic disruption with superimposed calcification; these changes were most severe in the deepest areas of the outer medulla, away from vasa recta in zones remote from oxygen supply. The fraction of mTALs with severe damage was 30 +/- 7% (range 2-68) and the extent of injury was correlated with a rise in plasma creatinine (r = 0.8, P less than 0.001). Thus, the nature of mTAL injury was similar to the selective lesions observed in isolated kidneys perfused with cell-free medium and was shown to derive from an imbalance between high oxygen demand by actively transporting mTALs and the meager oxygen supply to the renal medulla. Combined multiple renal insults in the rat produce ARF that resembles the clinical syndrome of contrast nephropathy and is characterized by selective mTAL injury conditioned by medullary hypoxia.     

Effect of corticosteroids on arginine vasopressin after pediatric cardiac surgery

Introduction

Arginine vasopressin’s (AVP) efficacy in the treatment of refractory hypotension is, in part, dependent upon preinfusion endogenous AVP concentration. Corticosteroids, also commonly used to treat refractory hypotension, have been shown to suppress endogenous AVP release. We aimed to determine if corticosteroids affect endogenous AVP concentrations in children recovering from cardiac surgery.

Materials and methods

We reviewed the records of children who underwent cardiac surgery between January 2008 and January 2009 and had AVP concentrations available as part of a prior prospective study. Doses of hydrocortisone, methylprednisolone, and dexamethasone administered within the first 48 hours after cardiopulmonary bypass were quantitated. Multivariable linear regression was performed to determine if corticosteroids had a significant effect on 48-hour plasma AVP concentration.

Results

Sixty-nine children with plasma AVP concentrations available were reviewed, 34 (49%) of which received corticosteroids within 48 hours after cardiopulmonary bypass. On multivariable regression, greater number of corticosteroid doses but not cumulative corticosteroid dosage was significantly associated with low 48-hour AVP concentration (β = − 4.0; 95% confidence intervals, − 6.5 to − 1.4).

Conclusions

Children who receive multiple doses of corticosteroids after cardiac surgery, regardless of potency, are likely to have low endogenous AVP concentrations. Children who remain unstable despite corticosteroids may respond favorably to exogenous AVP therapy.     

Splanchnic and renal blood flow after cardiopulmonary resuscitation with epinephrine and vasopressin in pigs

In laboratory investigations, vasopressin given during CPR resulted in improved vital organ blood flow when compared with epinephrine. Given the profound and long lasting vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation period when compared with epinephrine. After 4 min of ventricular fibrillation, 16 pigs were randomly assigned to receive either 0.045 mg·kg⁻¹ epinephrine or 0.4 U·kg⁻¹ vasopressin before defibrillation. Splanchnic and renal blood flow were measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in the epinephrine and vasopressin groups and in a control group of eight pigs using radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90, and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group (300 [273–334] and 256 [170–284] ml·min⁻¹·100 g⁻¹) (median and 25th and 75th percentile) as compared with the epinephrine group (370 [346–429] and 360 [326–420] ml·min⁻¹·100 g⁻¹; P<0.05). Pancreatic, intestinal, and hepatic blood flow were not significantly different in animals after receiving epinephrine or vasopressin. In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion in the post-resuscitation phase.     

In vivo effect of indomethacin to potentiate the renal medullary cyclic AMP response to vasopressin.

In a previous study we demonstrated that indomethacin potentiated the hydro-osmotic action of vasopressin in vivo. It was hypothesized that this action of indomethacin was due to its ability to suppress renal medullary prostaglandin synthesis, since in vitro studies have suggested that prostaglandins interfere with the ability of vasopressin to stimulate production of its intracellular mediator, cyclic AMP. In the present study this hypothesis was tested in vivo. Anesthetized rats undergoing a water diuresis were studied. In a control group, bolus injections of 200 muU of vasopressin caused a rise in urinary osmolality (Uosm) from 124 +/- 6 to 253 +/- 20 mosmol/kg H2O (P less than 0.005). In a group treated with 2 mg/kg of indomethacin the same dose of vasopressin caused a significantly greater (P less than 0.001) rise in Uosm from 124 +/- 7 to 428 +/- 19 mosmol/kg H2O. Medullary tissue cyclic AMP rose from 9.4 +/- 0.9 to 13.4 +/- 1.7 (P less than 0.05) pmol/mg tissue protein after vasopressin administration in animals receiving no indomethacin, while in indomethacin-treated animals there was a significantly greater rise (P less than 0.001) in medullary cyclic AMP from 10.4 +/- 0.9 to 21.6 +/- 2.1 pmol/mg tissue protein in response to the vasopressin injections. In neither control animals nor indomethacin-treated animals were there significant changes in renal hemodynamics, as measured by clearance techniques. Indomethacin, when given alone, had no effect on Uosm or medullary tissue cyclic AMP. Indomethacin did, however, reduce medullary prostaglandin E content from 84.7 +/- 15.0 to 15.6 +/- 4.3 pg/mg tissue. This study has shown that indomethacin, in a dose which suppresses medullary prostaglandin content, potentiates the ability of vasopressin to increase the tissue content of its intracellular mediator, cyclic AMP. Indomethacin caused no demonstrable inhibition of cyclic AMP phosphodiesterase. Therefore, it seems likely that indomethacin enhanced the ability of vasopressin to increase medullary cyclic AMP levels by causing an increased production rather than decreased destruction of the nucleotide. We conclude that this action of indomethacin contributes to its ability to potentiate the hydro-osmotic action of vasopressin in vivo. A corollary to this conclusion is that endogenous medullary prostaglandin E's may be significant physiological modulators of the renal response to vasopressin.     

Regional blood flow changes in response to mildly pressor doses of triglycyl desamino lysine and arginine vasopressin in the conscious dog

Arginine vasopressin (AVP) is used to treat esophageal variceal hemorrhage but has the drawbacks of rebleeding and reported coronary insufficiencies. In conscious dogs (n = 23) we compared AVP and an analog, triglycyl desamino lysine vasopressin (TDLVP), for arterial pressor responses and changes in regional blood flow. Dogs were infused with saline (n = 5), AVP (n = 7) or TDLVP (n = 7), and blood flow was measured with microspheres during control, infusion and postinfusion in 46 tissue sections including pieces of the esophagus, stomach, liver, kidney, spleen, heart, skin, muscle and brain. TDLVP (1.0 micrograms/kg/min) and AVP (0.025 micrograms/kg/min) produced a similar mean arterial pressure increase of 23 mm Hg and a heart rate decrease of 38 beats/min. TDLVP sustained the increase in mean arterial pressure and reduction in heart rate at 30 min postinfusion whereas AVP did not. Neither AVP nor TDLVP showed a reduction in brain, kidney or liver flow; however, both produced reductions (73 and 61%, respectively, P less than .01) in mucosal-esophageal flow. Only TDLVP reduced mucosal-fundus blood flow (P less than .01). Endocardial flow was reduced (27%) in both TDLVP and AVP groups; however, heart rate also decreased during this time and a linear correlation between these two measurements yielded a value for r2 of 0.83. Thus, TDLVP offers a therapeutic alternative to AVP in treating gastroesophageal varices due to its longer duration of action as represented by the sustained reduction in esophageal and mucosal-fundus flow.     

Effect of adrenalectomy on transport in the rat medullary thick ascending limb.

Previous studies in adrenalectomized (Adx) rats suggest that aldosterone may regulate ion transport in the ascending portion of Helen's loop. In order to examine directly the effect of adrenalectomy on transport, medullary thick ascending limb (Mtal) segments were isolated from Adx, Adx replaced with aldosterone (Adx + Ald, 0.5 micrograms X 100 g X body wt X d), and control Sprague-Dawley rats. Both net sodium and net chloride fluxes were significantly less in the Mtal segments from Adx rats compared with those in the control or Adx + Ald group. Physiologic levels of exogenous aldosterone increased net sodium chloride flux toward control values in the Adx + Ald group. Net potassium flux was not different among the three groups. We conclude that adrenalectomy impairs reabsorptive NaCl but not K transport in the Mtal, and that aldosterone restores this process. This reabsorptive defect may contribute to the urinary concentrating and diluting abnormality associated with adrenal insufficiency.     

Aldosterone metabolism in cultures of rat renal cortical and medullary cells.

The metabolism of 4-(14)C-d-aldosterone (at 3 nM) was studied in the primary target organ of the hormone, in renal cortical and medullary cell cultures obtained from Wistar rats. Larger amounts of aldosterone were metabolized in medullary cells than in cortical cells, as measured by a decreased 4-(14)C-d-aldosterone radioactivity concentration (26+/-9% and 12+/-7% of the initial aldosterone added, respectively (n=5, p<0.05)). The 14C radiometabolites of aldosterone in both cultures co-chromatographed with 5alpha dihydro- (DHA) and 3alpha,3beta tetrahydroaldosterone (THA). Aldosterone metabolism was totally inhibited by a mineralocorticoid receptor antagonist canrenoat (Soldactone) (at 10(-5) to 10(-3) M), while the glucocorticoid receptor antagonist RU 38486 (Roussel UCLAF) (at 10(-5) to 10(-4) M) had no effect. Thus, the study confirmed that, in rat kidney, aldosterone can be converted to its reduced metabolites by a metabolism which is inhibited by a mineralocorticoid receptor antagonist. This indicated that the metabolism might play some role in modulation of the intracellular response to aldosterone in the kidney.     

Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits

OBJECTIVE: Arginine vasopressin is being used increasingly to treat vasodilatory hypotension, although little is known of its effects on regional perfusion. Arginine vasopressin hemodynamic effects in physiology are mainly mediated through the V1a receptor on blood vessels. To investigate this further, we studied the effect of arginine vasopressin on systemic and renal blood flow in anesthetized, ventilated rabbits given either intravenous saline or endotoxin, and the impact of blocking V1a receptors. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male White New Zealand rabbits. INTERVENTIONS: Measurement was made of mean arterial blood pressure, aortic and renal blood flow velocities (pulsed Doppler), and renal cortical and medullary flow (laser Doppler). MEASUREMENTS AND MAIN RESULTS: In a first series of animals, incremental intravenous boluses of arginine vasopressin ranging from 1 to 1000 ng were administered 90 mins postendotoxin or saline. In control rabbits (n = 9), increasing doses of arginine vasopressin elevated mean arterial blood pressure but reduced both aortic and renal blood flow velocity and renal cortical flow (p <.05). In endotoxic animals (n = 6), arginine vasopressin produced a similar increase in mean arterial blood pressure although aortic flow was maintained while renal blood flow velocity increased, mostly in its diastolic component (p <.05). Pretreatment with the V1a receptor antagonist in a second series of animals blunted all the effects observed in both control (n = 5) and endotoxic (n = 6) animals, suggesting that arginine vasopressin acted mainly through V1a subtype in this early phase of sepsis. CONCLUSIONS: Preservation of renal blood flow with arginine vasopressin during endotoxemia, in particular to the cortex, suggests it could be a promising agent for hemodynamic support during septic shock.     

Effect of N-substituted arginine compounds on blood pressure in anesthetized rats.

Inhibition of endothelium-dependent relaxation by NG-monomethyl L-arginine (L-NMMA) and its reversal by excess L- but not D-arginine is used to support the hypothesis that the endothelium-derived relaxing factor (EDRF) is generated exclusively from the metabolism of L-arginine. However, in freshly isolated vascular tissues, L-arginine is a poor vasodilator when compared to the N-substituted arginine compound, N alpha-benzoyl L-arginine ethyl ester (BAEE). Here, we show that such N-substituted compounds are potent hypotensive agents in anesthetized rats. In contrast, L-arginine elicits hypotensive effect only at higher concentrations (greater than 100 mg/kg). This effect of L-arginine is not antagonized by L-NMMA. Furthermore, D-arginine, L-homoarginine and L-lysine also have hypotensive effects at these concentrations. Indomethacin treatment partially attenuates the hypotensive effects of the basic amino acids. In contrast, the hypotensive effect of BAEE is antagonized by L-NMMA in a dose-dependent manner and by methylene blue, which is an inhibitor of soluble guanylate cyclase. In addition, substitution at the arginine moiety determines the hypotensive effect. When the amino acid glycine is inserted between the benzoyl group and arginine as in benzoyl-glycine-arginine, significant attenuation of the hypotensive effect is observed. These data demonstrate that compounds such as BAEE generate an EDRF-like agent in vivo and basic amino acids such as L-arginine elicit hypotension at concentrations above 100 mg/kg by mechanisms other than the generation of EDRF.     

Effect of exercise on plasma concentrations of arginine vasopressin, angiotensin II and aldosterone in hypertensive and normotensive renal transplant recipients

Plasma concentrations of angiotensin II (A II), aldosterone (Aldo) and arginine vasopressin (AVP), and serum osmolality (Sosm) were determined before and after gradually increasing exercise loads on a bicycle ergometer in 10 hypertensive (group I) and 10 normotensive renal transplant recipients (group II), and in 15 healthy control subjects (group III). Working capacity was reduced in groups I and II. The A II, Aldo, AVP, Sosm increased in all groups after exercise. The A II was higher in group I than II and the percentage changes were significantly lower in groups I and II than in group III. There were no significant differences in Aldo between the groups either before or after exercise. The AVP was the same in groups I and II, and AVP in these groups was higher than in group III. The Sosm and AVP were significantly correlated in all groups. Neither A II, Aldo nor AVP were significantly correlated to systolic blood pressure (BP). Alterations in AVP, but not in A II or Aldo, were correlated to the degree of exercise load. It can be concluded that the renin-angiotensin-aldosterone system and the osmoregulatory system are stimulated during exercise in renal transplant recipients. The A II is elevated in post-renal transplant hypertension, but the responsiveness is reduced in both hypertensive and normotensive recipients. The alterations in AVP are probably secondary to changes in Sosm, and the higher AVP levels in recipients could be due to a decreased responsiveness of the renal tubules to AVP. Our findings are in good agreement with the hypothesis that hypertension after renal transplantation is angiotensin II-dependent.     

Hormonal control of the renal immune response and antibacterial host defense by arginine vasopressin

Ascending urinary tract infection (UTI) and pyelonephritis caused by uropathogenic Escherichia coli (UPEC) are very common infections that can cause severe kidney damage. Collecting duct cells, the site of hormonally regulated ion transport and water absorption controlled by vasopressin, are the preferential intrarenal site of bacterial adhesion and initiation of inflammatory response. We investigated the effect of the potent V2 receptor (V2R) agonist deamino-8-D-arginine vasopressin (dDAVP) on the activation of the innate immune response using established and primary cultured collecting duct cells and an experimental model of ascending UTI. dDAVP inhibited Toll-like receptor 4–mediated nuclear factor κB activation and chemokine secretion in a V2R-specific manner. The dDAVP-mediated suppression involved activation of protein phosphatase 2A and required an intact cystic fibrosis transmembrane conductance regulator Cl⁻ channel. In vivo infusion of dDAVP induced a marked fall in proinflammatory mediators and neutrophil recruitment, and a dramatic rise in the renal bacterial burden in mice inoculated with UPECs. Conversely, administration of the V2R antagonist SR121463B to UPEC-infected mice stimulated both the local innate response and the antibacterial host defense. These findings evidenced a novel hormonal regulation of innate immune cellular activation and demonstrate that dDAVP is a potent modulator of microbial-induced inflammation in the kidney.     

去甲肾上腺素并多巴酚丁胺治疗脓毒性休克伴顽固性低血压28例临床分析

目的 评价应用去甲肾上腺素并多巴酚丁胺治疗脓毒性休克伴顽固性低血压的疗效。方法 应用去甲肾上腺素并多巴酚丁胺治疗28例脓毒性休克伴顽固性低血压，对照组18例应用大剂量多巴胺并多巴酚丁胺，评价治疗前及治疗12h后两组的血压、心率、尿量、CRT、乳酸水平及EF值。治疗72h后统计两组MODS发生率及死亡率。结果 治疗12h后，治疗组血压上升。心率下降，尿量增加，CRT缩短，乳酸下降，EF值增加，与治疗前及对照组比较，差异有统计学意义（P〈0．05）。治疗72h后两组MODS发生率及死亡率比较差异有统计学意义（P〈0．05）。结论 去甲肾上腺素并多巴酚丁胺用于脓毒性休克能有效地升高血压，改善循环与灌注，提高脓毒性休克伴顽固性低血压救治成功率。     

Regional renal blood flow in hypertensive patients.

Renal blood flow measurements in three regions of each kidney were carried out in eighteen hypertensive patients using the radioactive Xenon-133 washout technique in conjunction with renal angiography. It was found that the regional differences were generally small but differences existed in four patients significant in spite of normal angiographic findings. The reduction in blood flow in the two kidneys was generally of the same degree which implies a uniform response to the elevated blood pressure.