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PubMed1983

Influence of circulating NE and Epi on adipose tissue vascular resistance and lipolysis in humans.

The effects of circulating norepinephrine (NE) and epinephrine (Epi) on vascular resistance in subcutaneous adipose tissue and the calf as well as on plasma glycerol, an indicator of lipolysis, were studied in healthy volunteers. Adipose tissue blood flow was determined by the local clearance of 99mTcO-4 or 133Xe. The two isotopes gave similar results. Calf blood flow was determined by venous occlusion plethysmography. Intravenous infusion of NE caused increases in systolic and diastolic blood pressures, adipose tissue and calf vascular resistances, and plasma glycerol and a decrease in plasma insulin and heart rate, all of which were significant when arterial plasma NE was elevated from 1.17 +/- 0.14 to 8.38 +/- 0.30 nM (n = 16). Epi reduced diastolic and mean arterial pressures and adipose tissue and calf vascular resistances and increased plasma glycerol without affecting systolic blood pressure or plasma insulin. An increase of arterial plasma Epi from 0.20 +/- 0.03 to 1.15 +/- 0.05 nM (n = 6) was sufficient to induce vasodilatation in adipose tissue and lipolysis. Human adipose tissue differs from canine adipose tissue inasmuch as Epi causes vasodilatation in humans (present results) but vasoconstriction in the dog (previous results), presumably due to a predominance of vascular beta 2-adrenoceptors in human and beta 1-adrenoceptors in canine adipose tissue. Furthermore, Epi is a considerably more potent lipolytic hormone than NE in humans but not in the dog. Our results indicate that both NE and Epi may influence human adipose tissue blood flow and lipolysis as circulating hormones.

Adipose Tissue↗

PubMedDate not supplied

Effects of vasoactive stimuli on coronary vascular resistance in isolated perfused rabbit hearts: no vasospastic response to ergonovine with or without atherogenic diet.

The mechanism of ergonovine-provoked coronary vasospasm is poorly understood. We tested the effect of ergonovine in perfused hearts from normal and cholesterol-fed (18 weeks, 2% cholesterol diet) rabbits in a constant-flow Langendorff perfusion. Aortic perfusion pressure was monitored to measure coronary vascular resistance, and left ventricular pressure was measured with an isovolumetric balloon in the left ventricle. Control coronary vascular resistance was 1.12 +/- 0.11 mm Hg/ml/min in hearts from normal rabbits and 1.53 +/- 0.16 mm Hg/ml/min in hearts from cholesterol-fed rabbits (n = 9 each, mean +/- SEM, p less than 0.05). The cholesterol content of aortae from cholesterol-fed rabbits was markedly increased (432 +/- 85 mg/g protein vs. 14.9 +/- 8.2 in controls, p less than 0.001; for coronaries: 396 +/- 136 mg/g protein vs. 125 +/- 25, p less than 0.05). In both groups, increases in coronary vascular resistance were observed with vasopressin (40 IU/l) and phenylephrine (30 microM) and decreases with adenosine (10 microM), isoprenaline (0.1 microM) and 30 sec stop-flow (all p less than 0.05). Ergonovine maleate (10 microM) and serotonin (10 microM) did not increase coronary vascular resistance. Although in whole heart perfusion small changes in the caliber of epicardial vessels may not be detectable, changes severe enough to produce measurable changes in total coronary resistance were not found. Therefore the absence in our model of an increase in coronary vascular resistance after ergonovine is not compatible with a local direct mechanism in epicardial arterial wall, even when sensitized by a high cholesterol diet.

Animals↗

PubMed1996

Role of nitric oxide in the local regulation of pulmonary vascular resistance in humans.

BACKGROUND: Endothelium-derived nitric oxide (NO) may be an important mediator of vascular resistance in the pulmonary circulation. We tested the hypotheses that in conscious adults the endothelium, through NO production, is important in maintaining basal pulmonary vascular resistance and that it can increase NO production further in response to receptor-mediated stimulation, leading to further vasodilation. METHODS AND RESULTS: Pulmonary arterial resistance vessel function was studied within the distribution of a segmental lower lobe pulmonary artery in eight conscious adults 37 to 76 years old who were undergoing cardiac catheterization. Segmental blood flow was determined with use of a Doppler-tip guide wire and quantitative angiography. Drugs were administered locally within the segmental artery through an infusion catheter. NG-Monomethyl-L-arginine (L-NMMA) was used as a specific inhibitor of NO production, whereas acetylcholine (ACh) was used to test receptor-mediated vasodilation. To demonstrate that vasodilation to ACh was NO dependent, ACh response was tested alone, in the presence of L-NMMA, and in the presence of a control constrictor phenylephrine. Basal pulmonary vascular resistance was NO dependent because L-NMMA infusion resulted in a dose-dependent decrease in local flow velocity (P < .005), with flow decreasing 33% at the highest dose of L-NMMA. ACh infusion resulted in a dose-dependent increase in flow velocity (P = .001). The ACh response was at least in part NO dependent because it was diminished by the presence of L-NMMA (P < .05). The effect of L-NMMA on the ACh response was not due to nonspecific preconstriction because L-NMMA diminished the ACh response significantly more than did the endothelium-independent constrictor phenylephrine (P < .05) despite comparable preconstriction. CONCLUSIONS: In healthy conscious adults, (1) normal basal pulmonary resistance is maintained in part by continuous local production of NO and (2) the local NO production is responsive to receptor-mediated stimulation, leading to further vasodilation, and can be tested with ACh.

Acetylcholine↗

PubMed1992

Adrenergic receptors and the regulation of vascular resistance in bullfrog tadpoles (Rana catesbeiana).

Vascular adrenergic sensitivity to exogenous catecholamines was examined in tadpoles of the American bullfrog (Rana catesbeiana), ranging from stage III to XIV. Central arterial blood pressure was measured in decerebrate bullfrog tadpoles to determine a reasonable initial infusion pressure. Solutions of epinephrine and phenylephrine were infused into the vasculature of pithed tadpoles, and the resulting changes in vascular resistance (Rv) were used to construct log dose-response relationships. Epinephrine infusion produced a dose-dependent increase in Rv (EC50 = 5.3 x 10(-7) M), which could be reversed by sodium nitroprusside (a smooth muscle relaxant) and blocked by phenoxybenzamine (an alpha-adrenergic antagonist). Larval Rv also increased with infusion of the alpha-agonist phenylephrine (EC50 = 7.4 x 10(-8) M). Infusion of 10(-6) M isoproterenol (a beta-agonist) largely reversed the phenylephrine-induced increase in Rv. These results indicate that the capacity exists for both alpha-mediated vasoconstriction and beta-mediated vasodilation early in bullfrog ontogeny. Neither initial Rv nor the responses to infused epinephrine or phenylephrine were significantly correlated to development over the range of larval stages used in this study.

Animals↗

PubMed2004

Noninvasive measurement of systemic vascular resistance using Doppler echocardiography.

BACKGROUND: Systemic vascular resistance (SVR) is an integral therapeutic component of patients with heart failure and shock. We hypothesized that the ratio of the peak mitral regurgitant velocity (MRV) (m/s) to left ventricular outflow time-velocity integral (TVI(LVOT)) (cm) by Doppler would provide a noninvasive correlate of SVR. METHODS: SVR was correlated to MRV/TVI(LVOT) in 33 patients undergoing right heart catheterization. Receiver operating characteristic curves were generated to determine the best-balanced sensitivity and specificity to identify SVR > 14 Wood units (WU) and <10 WU. RESULTS: MRV/TVI(LVOT) correlated well with SVR (r = 0.842, 95% confidence interval 0.7-0.92, P <.001, Y = 0.459 + 49.397*X). By receiver operating characteristics, MRV/TVI(LVOT) > 0.27 had a 70% sensitivity and a 77% specificity to identify SVR > 14 WU. MRV/TVI(LVOT) < 0.2 had a 92% sensitivity and a 88% specificity to identify SVR < 10 WU. CONCLUSION: Doppler echocardiography provides a reliable noninvasive assessment of SVR.

Aged↗

PubMed1992

Neural, humoral, and metabolic control of coronary vascular resistance during exercise.

Neural, humoral, and metabolic effects on coronary vascular resistance were examined during exercise in conscious dogs, chronically instrumented for the measurement of aortic pressure, heart rate, and left circumflex coronary blood flow. Exercise significantly decreased coronary vascular resistance (CVR) in intact (INT) group, in which CVR was controlled by neural, humoral, and metabolic factors. In cardiac denervated (CD) group with pretreatment of alpha blocker (phentolamine, 2 mg/kg), in which CVR was controlled only by metabolic factor, exercise significantly decreased CVR. To eliminate metabolic effect on CVR, CVR was normalized by the product of CVR and double product (DP = mean aortic pressure x heart rate). CVR.DP did not change throughout the exercise in dogs with CD with alpha blocker. Thus, metabolic effect on CVR during exercise can be excluded by the product of CVR and DP. This calculation was applied to INT group with alpha blocker and CD group without blockers. The 12 km/h exercise significantly increased CVR.DP from 4.1 +/- 0.3 x 10(4) to 6.4 +/- 0.9 x 10(4) in INT group with alpha blocker, in which CVR was controlled only by neural factor, and from 2.8 +/- 0.2 x 10(4) to 4.5 +/- 0.5 x 10(4) in CD group, in which CVR was controlled only by humoral factor. These data suggest that 1) neural and humoral coronary vasoconstriction occurs during exercise, 2) neural and humoral vasoconstriction is overwhelmed by metabolic vasodilation, and 3) CVR.DP is a beneficial calculation for excluding metabolic effect on CVR during exercise.

Animals↗

PubMedDate not supplied

Right ventricular assist and prostacyclin infusion for allograft failure in the presence of high pulmonary vascular resistance.

The presence of high pulmonary vascular resistance (PVR) greater than 4 Wood units contributes to significant early posttransplant mortality, and remains a negative predictor of long-term survival. Current trends have been toward exclusion of the recipient with high PVR from the orthotopic procedure; elective heterotopic allograft placement is increasingly advocated. A patient with a PVR of 6 Wood units underwent orthotopic transplantation; the cardiac allograft from a 12 kg heavier donor was implanted after an ischemic time of 115 minutes. Early graft failure at 4 hours and subsequent cardiac arrest were followed by reinstitution of cardiopulmonary bypass, during which time optimal pharmacologic manipulation of the pulmonary vasculature was undertaken, including the use of high-dose prostacyclin. Refractory right heart failure indicated the requirement for right ventricular assistance (RVA) for patient survival. RVA with a Bio-Medicus pump was instituted in association with high-dose prostacyclin; an intraaortic balloon pump was inserted 12 hours later. Maintenance immunosuppression consisted of cyclosporine and azathioprine alone. RVA was maintained for 3 days; during this time the patient was totally pump dependent. Over an 18-hour period the patient was weaned and successfully withdrawn from RVA. Intraaortic balloon pump counterpulsation and the prostacyclin infusion were continued for 6 and 10 days, respectively. The clinical implications of the various interventions that resulted in the patient's survival are discussed.

Cardiac Output, Low↗

PubMed2005

The effect of the K+ agonist nicorandil on peripheral vascular resistance.

BACKGROUND: The vasoactive effect of nicorandil on coronary arteries is well known. Nicorandil exerts its vasodilatory effect through a dual mechanism of action: involving on the one hand cyclic guanosine monophosphate (c GMP) as a nitrovasodilatator, and on the other hand, acting as a potassium channel opener. OBJECTIVE: To address the question if nicorandil works in peripheral arteries, its effect on peripheral vascular resistance was evaluated in isolated perfused guinea pig hind limbs. METHODS: A catheter was inserted via the distal aorta and common iliac artery. Perfusion pressure was monitored under constant perfusion with Tyrode's solution, therefore changes in perfusion pressure represent changes in vascular resistance. After stabilization precontraction of the peripheral vascular bed was achieved with noradrenaline 3 microM and nicorandil was added in concentrations of 1, 10 and 100 microM. The effect of nicorandil (1, 10 and 100 microM) was tested in the presence of L-NAME and glybenclamide. RESULTS: A significant reduction of vascular peripheral resistance was already achieved at a concentration of 1 microM nicorandil (30.3+/-6.1%, mean S.E.M., p < 0.001). At a concentration of 100 microM nicorandil the reduction of peripheral vascular resistance was 94.4+/-16.4%. Peripheral vascular resistance was less but nearly comparable reduced by nicorandil (100 microM) if the endothelial NO effect was inhibited by L-NAME (58.6+/-18.6%) or if the ATP-dependent potassium channels were blocked by glybenclamide (56.4+/-14.6%). CONCLUSIONS: In peripheral arteries the nitrovasodilator effect of nicorandil is nearly comparable to the potassium agonistic effect, and the concentration, which is necessary to reduce peripheral vascular resistance significantly, is comparable with dosages necessary for reduction of coronary resistance.

Animals↗

PubMed2003

[Study on the relationship between changes of adrenomedulin in plasma and vascular resistance during traumatic shock in rats].

OBJECTIVE: To observe the changes of adrenomedulin in plasma and vascular resistance during traumatic shock in rats. METHODS: The concentration of adrenomedulin in plasma of rats after traumatic shock was detected by radio immunization. Mean arterial pressure, total peripheral vascular resistance (TPVR) and cardiac index (CI) were estimated by electrical conductance method. RESULTS: The concentration of adrenomedulin in plasma of traumatic shock without resuscitation group (68.34+/-3.71)ng/L and traumatic shock with resuscitation group (146.27+/-9.83)ng/L were higher than that of control group(32.63+/-7.55)ng/L (P<0.01 and P<0.05). TPVR of traumatic shock with resuscitation group (10.57+/-0.35) kPa.s.L-1 was lower than that of traumatic shock without resuscitation group (16.75+/-0.23) kPa.s.L-1(P<0.01) and its CI (215.59+/-1.29) ml.min-1.kg-1 was higher than that of traumatic shock without resuscitation group (143.11+/-0.86) ml.min-1.kg-1 (P<0.01). CONCLUSION: Adrenomedulin is closely correlated with changes of vascular resistance and plays an important role during pathophysiological processes in rats after traumatic shock.

Adrenomedullin↗

PubMed1994

Aortic baroreceptors play a predominant role in the regulation of hindlimb vascular resistance in rats.

In previous studies using bilateral carotid occlusion in conscious freely moving rats we suggested that aortic baroreceptors may play a more important role in the regulation of hindlimb than in renal and mesenteric vascular resistances. In the present study we performed electrical stimulation of the aortic baroreceptor nerve and analyzed the changes in mean arterial pressure and in hindlimb, renal, and mesenteric vascular resistances. All the experiments were performed under urethan anesthesia. Unilateral electrical stimulation (3 V, 2 ms, 50 Hz) of the aortic baroreceptor nerve produced a fall in arterial pressure (-27 +/- 3 mmHg) and an important reduction in hindlimb vascular resistance (-43 +/- 5%), with an increase in renal (+3 +/- 14%) and mesenteric (+48 +/- 12%) vascular resistances. Similar changes in arterial pressure as well as in the resistance of the three vascular beds studied were also observed during electrical stimulation of the aortic baroreceptor nerve in rats with bilateral carotid baroreceptor denervation or in rats treated with methylatropine. The data obtained with electrical stimulation indicated that aortic baroreceptors play a more important role in the regulation of blood flow in hindlimb than in renal and mesenteric vascular beds.

Animals↗

PubMed1982

The effect of renal perfusion pressure on renal vascular resistance in the spontaneously hypertensive rat.

Renal hemodynamics and renal vascular resistance (RVR) were measured in the spontaneously hypertensive rat (SHR) and in the normotensive Wistar-Kyoto rat (WKY). In addition, the autoregulatory response and segmental RVR in the SHR were studied after aortic constriction. Mean arterial pressure (MAP) and RVR were higher in the SHR than in the WKY, but renal blood flow (RBF) and glomerular filtration rate were similar in both groups. Measurement of mean afferent arteriolar diameter (AAD) by a microsphere method showed a significantly smaller AAD in SHR (17.7 +/- 0.35 micrometers) than in the WKY (19.5 +/- 0.20 micrometers). This decrease in AAD could account for a 47% increase in preglomerular resistance. Aortic constriction in the SHR, sufficient to reduce renal perfusion pressure from 152 to 115 mmHg, did not alter the AAD. Since RBF and glomerular filtration were also well maintained following aortic constriction, these autoregulatory responses suggest that vessels proximal to the afferent arteriole rather than postglomerular vasculature are primarily involved in the changes on intrarenal vascular resistance in SHR.

Animals↗

PubMed1995

Simultaneous measurement of plasma protein extravasation and carotid vascular resistance in the rat.

Stimulation of the right trigeminal ganglion in pentobarbital anaesthetised rats increased mean arterial blood pressure and decreased right carotid vascular resistance but had no effect on left carotid vascular resistance. Sumatriptan (0.3 mg/kg i.v.) pretreatment did not significantly affect basal levels or stimulation induced changes in blood pressure or carotid vascular resistance. Trigeminal stimulation produced plasma protein extravasation (measured using a fluorescent marker) into the dura mater on the ipsilateral side which was significantly reduced by sumatriptan. These studies show that sumatriptan can reduce plasma protein extravasation while having no measurable effect on total carotid blood flow.

Animals↗

PubMed1993

Influence of hydrogen ion concentration versus carbon dioxide tension on pulmonary vascular resistance after cardiac operation.

Disturbances of respiratory acid-base status are common in patients supported with mechanical ventilation of the lungs after cardiac operations. This study was conducted with two protocols. The purpose was to determine whether respiratory acid-base status influences pulmonary vascular resistance in adults after cardiac operations and whether the influence is mediated by hydrogen ion concentration or carbon dioxide tension. Patients were studied while under general anesthesia immediately after aorta-coronary bypass. In the first protocol, with seven patients, arterial carbon dioxide tension was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Pulmonary vascular resistance index was determined as arterial carbon dioxide tension rose from 30 mm Hg to 50 mm Hg and back to 30 mm Hg. In the second protocol, with 10 different patients, hydrogen ion concentration was manipulated by the addition of 0.2N hydrochloric acid, sodium bicarbonate, or both as arterial carbon dioxide tension was held constant. We used analysis of variance for statistical data. The results of the first protocol showed that pulmonary vascular resistance index rose by 44% (p < 0.05) as arterial carbon dioxide tension rose from 30 to 50 mm Hg. The results of the second protocol showed that changes in pulmonary vascular resistance index were parallel to changes in hydrogen ion concentration as arterial carbon dioxide tension was held constant (p < 0.05). These data demonstrate that respiratory acid-base status is an important determinant of pulmonary vascular resistance in the adult after cardiac operations. Furthermore, these data suggest the effect is mediated by hydrogen ion concentration, not carbon dioxide tension.

Acid-Base Equilibrium↗

PubMed1990

Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT).

Endotoxemia is responsible for many of the pathophysiologic alterations that occur with Gram-negative sepsis. We utilized a chronic ovine model to determine the hemodynamic disturbances in the gastrointestinal tract during endotoxemia. Sheep with indwelling arterial, venous, and pulmonary arterial catheters were used. An ultrasonic flow probe was placed on the cephalic mesenteric artery. The animals were subjected to: 1) Ringer's lactate infusion (sham n = 6); or 2) 1.5 mcg/kg E. coli endotoxin (n = 6) over over a period of one half hour and were monitored for 48 hours. They were then sacrificed and specimens of mesenteric lymph node, liver, spleen, kidney, and lung obtained for bacteriologic cultures and histologic analysis. Sheep receiving endotoxin showed more than 50% reduction in the mesenteric blood flow. Mesenteric vascular resistance increased while non-mesenteric systemic vascular resistance decreased. The increase in the total systemic vascular resistance, noted during endotoxemia, was thus likely due to the increase in the mesenteric vascular resistance. At autopsy there were positive cultures for microorganism in the mesenteric lymph nodes in six out of six sheep with endotoxemia as compared to one out of six of control. Thus the vasoconstriction in the mesenteric areas may have resulted in bacterial translocation from the GI tract.

Animals↗

PubMed1984

Congenital diaphragmatic hernia: association between pulmonary vascular resistance and plasma thromboxane concentrations.

After repair of a Bochdalek diaphragmatic hernia, shunting of blood away from the lungs produced progressive hypoxaemia in a neonate. Changes in plasma concentrations of the vasoconstrictor prostanoid thromboxane were associated with changes in pulmonary vascular resistance in this infant. Plasma concentrations of the vasodilator prostanoid prostacyclin were also monitored during acute changes in pulmonary vascular resistance. Tolazoline administration was followed by reductions in pulmonary vascular resistance and in plasma thromboxane and prostacyclin values. Further studies indicated that tolazoline inhibits platelet thromboxane synthesis and vascular prostacyclin synthesis. These data suggest that thromboxane plays a part in the increased pulmonary vascular resistance that occurs after repair of congenital diaphragmatic hernia and that tolazoline may reverse pulmonary hypertension by a mechanism additional to its known action as an alpha adrenergic blocking agent and its effect on histamine release.

6-Ketoprostaglandin F1 alpha↗

PubMed1977

Coronary vascular resistance during halothane anesthesia.

To study the effect of halothane on the coronary circulation, the circumflex diastolic coronary vascular resistance was measured in the working heart and total mean coronary resistance (TCR) in the isolated nonworking heart of the dog during administration of 100 per cent oxygen and during administration of 2--3 per cent halothane in oxygen. In the working heart, when the diastolic aortic pressure was kept at a nearly control level, halothane induced decreases of 12 per cent in circumflex diastolic coronary vascular resistance and 18 per cent in left ventricular arteriovenous oxygen content difference and no significant change in diastolic coronary blood flow. This effect occurred in spite of the absence of any significant change of myocardial oxygen consumption. In the nonworking beating, arrested or fibrillating heart, halothane induced a decrease of 24 per cent in total mean coronary resistance. Since the decrease in circumflex diastolic coronary vascular resistance in the working heart connot be attributed to myocardial hypoxia and since the results in the isolated nonworking heart eliminate the influences of mechanical and neurohumoral factors on coronary resistance, it is concluded that the observed decrease in resistance is probably due to vasodilation produced by a direct action of halothane on the coronary vessels. This effect was not modified by beta-adrenergic blockade.

Animals↗

PubMed1988

Effects of forskolin on placental vascular resistance in rabbits.

Forskolin is a direct stimulant of adenylate cyclase and increases cAMP production. It also acts as a vasodilator. To study the effect of forskolin infusion on rabbit maternal vascular resistance, we instrumented 11 pregnant rabbits with catheters in the left ventricle, jugular vein, and left and right femoral arteries. After a 2-day recovery period, one of two protocols was performed. In the control period of the first protocol (N = 6), 50% ethanol in saline was infused at 0.103 ml.min-1 for 5-min. Forskolin (10(-3) M) in 50% ethanol was then infused for 5 min at 0.103 ml.min-1. After each infusion period, regional blood flows were measured by microsphere injection. Data are expressed as means +/- SEM. Blood pressure decreased from 81 +/- 3 to 79 +/- 3 mm Hg, (P less than 0.05, N = 10) during forskolin infusion. Total placental resistance fell from 180.3 +/- 10.7 to 133.8 +/- 12.0 mm Hg.min.ml-1 per gram, P less than 0.05. Cerebral, coronary, and renal vascular resistance fell significantly. During the second protocol (N = 5), angiotensin II (0.05 microgram.min-1) was infused for 5 min followed by the addition of forskolin (10(-3) M at 0.103 ml.min-1) to the infusate. Regional blood flows, vascular resistances and blood pressures were determined. Blood pressure fell from 99 +/- 6 to 92 +/- 7 mm Hg (P less than 0.05) when forskolin was added to the infusate. Placental resistance fell from 202.5 +/- 21.6 to 158.0 +/- 29.0 mm Hg.min.ml-1 per gram (P less than 0.05). While cerebral vascular resistance did not change, renal and coronary resistances fell in response to forskolin. This study demonstrates that forskolin is able to dilate rabbit placental vessels alone and in the presence of the vasoconstrictive agent angiotensin II.

Angiotensin II↗

PubMedDate not supplied

Atrial natriuretic peptide, plasma renin activity, plasma volume, systemic vascular resistance and cardiac output in patients with cirrhosis.

The present study aimed to assess relationships between plasma levels of atrial natriuretic peptide (ANP) and plasma volume, systemic vascular resistances, cardiac output and plasma renin activity in patients with cirrhosis. Thirty patients were included: eight with no history of liver disease were used as controls; 22 patients had biopsy-proven alcoholic cirrhosis without ascites (n = 11) and with ascites (n = 11). Mean ANP plasma level was significantly higher in both groups of cirrhotic patients than in controls (P less than 0.05). In the control group, ANP and plasma renin activity were inversely correlated (P less than 0.05) but no correlation was found in cirrhotic patients. In the group of patients with ascites, ANP plasma levels were inversely correlated to plasma volume (P less than 0.05) and to cardiac output (P less than 0.01) and directly correlated to systemic vascular resistances (P less than 0.01). Using multiple regression analysis, ANP remained correlated only with systemic vascular resistances (P less than 0.05). These results suggest that cirrhotic patients have high plasma levels of ANP whether or not they have ascites. In the light of current knowledge of ANP actions, the relationships between ANP plasma levels and plasma volume, cardiac output, and systemic vascular resistances are paradoxical in cirrhotic patients with ascites. ANP does not seem to play a critical role in the pathogenesis of sodium and water retention observed in these patients.

Ascites↗