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PubMed1996

Randomized trial of oxytocin alone and with propranolol in the management of dysfunctional labor.

OBJECTIVE: To compare oxytocin infusion alone and with intravenous (i.v.) propranolol in the management of dysfunctional labor. METHODS: Ninety-six parturients with abnormalities of the active phase of labor were randomly assigned to either propranolol 2 mg IV or an identical placebo, in addition to continuous infusion of oxytocin. Administration of propranolol or placebo was repeated in 1 hour if there was no change in cervical dilation. Patients not responding to this second administration of propranolol or placebo were delivered by cesarean. RESULTS: Among 96 subjects enrolled, 49 were allocated to the propranolol group and 47 to the placebo group; 13 (26.5%) of the former were delivered by cesarean, compared with 24 (51.1%) of the latter (relative risk 0.58, 95% confidence interval 0.35-0.93; P = .02). Between the two groups, no differences were observed in low Apgar scores, cord arterial pH, or incidence of admissions to the neonatal intensive care nursery. Maternal morbidity was similar in both groups. After logistic regression analysis controlling for nulliparity, birth weight, and epidural anesthetic use, the significant reduction in the cesarean rate associated with use of propranolol persisted. Propranolol administration was associated with a markedly reduced cesarean rate among patients with inadequate uterine contractility. CONCLUSION: Low-dose administration of IV propranolol in patients with dysfunctional labor augmented with oxytocin safely reduced the need for cesarean delivery, particularly among patients with inadequate uterine contractility.

Adrenergic beta-Antagonists↗
PubMed1995

The inhibitory effects of propranolol on genital reflexes in male rats.

We have previously reported that propranolol adversely affects sexual behavior in male rats. To elucidate whether the effects of propranolol might involve decrements in ability, we examined two components of sexual function ex copula--ejaculatory reflex capacity and erectile reflexes. In the first study, we examined the effects of various doses of (+/-)-propranolol (1.25-10 mg/kg) administered subcutaneously. Marked inhibition was observed, evidenced by increases in the latency to ex copula ejaculation and to initial erection and decrements in the number of seminal emissions and in the number of erectile reflexes. Analyses of dose-response relationships indicated that the degree of inhibition increased with increasing dose. In the second study, we evaluated the stereo-selectivity of the responses. Both (+)- and (-)-propranolol (1.25 mg/kg) significantly inhibited ejaculatory reflex potential, and although (+)- and (-)-propranolol significantly inhibited erectile reflexes, (-)-propranolol had a greater effect. The data are interpreted to indicate that a) propranolol-induced sexual dysfunction involves both motivational and ability aspects; and b) propranolol-induced inhibition of genital reflexes may be due, at least in part, to mechanisms other than beta-adrenoceptor blockade.

Adrenergic beta-Antagonists↗
PubMed1990

Propranolol inhibits cyclic AMP accumulation and amylase secretion in parotid acinar cells stimulated by isobutylmethylxanthine and forskolin.

Propranolol inhibited cyclic AMP (cAMP) accumulation stimulated by 3-isobutyl-1-methylxanthine (IBMX) or forskolin in rat parotid acinar cells. The inhibition by propranolol was highly potent; 10(-7) M propranolol was sufficient for the maximum inhibition (approx. 50% at 5 min). The inhibitory effect was observed in both intact and saponin-permeabilized parotid cells, but the effect was more prominent in permeabilized cells than in intact cells. Other beta-blockers, like alprenolol and atenolol, were as effective as propranolol, but butoxamine (beta 2-selective) was slightly less effective. The inhibition by propranolol was similarly detected in the cells prepared from pertussis-toxin-pretreated rats, suggesting that inhibitory guanine nucleotide regulatory protein (Gi) is not involved in the inhibitory mechanism. Propranolol also inhibited the exocytosis of amylase stimulated by IBMX or forskolin. In the presence of propranolol and IBMX, the responsiveness of saponin-permeabilized cells to exogenous cAMP was markedly increased, indicating that propranolol neither promotes the degradation of cAMP nor prevents the inhibitory effect of IBMX on cAMP phosphodiesterase.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Early chronic administration of propranolol reduces the severity of portal hypertension and portal-systemic shunts in conscious portal vein stenosed rats.

We investigated the effects of early chronic administration of propranolol on systemic and splanchnic hemodynamic changes, and the development of portal-systemic shunts in conscious, unrestrained, portal vein stenosed rats. Compared to rats receiving placebo, early chronic propranolol (75 mg kg-1 day-1) administration to rats begun 3 days before portal vein stenosis and then continued for 10 consecutive days, resulted in a significant decrease in both portal pressure (11.8 +/- 1.5 mmHg) and portal-systemic shunts (48 +/- 18%) which were measured 2 to 3 h after the final dose of propranolol (15.2 +/- 1.5 mmHg and 84 +/- 5%, respectively). These beneficial effects were also observed 18 to 24 h after the final dose of chronic propranolol. In rats given propranolol continuously for 5 days starting 5 days after portal vein stenosis, portal pressure (11.8 +/- 1.2 mmHg) was significantly lower than in the placebo group but portal-systemic shunts (76 +/- 14%) were not significantly different. In rats receiving a single dose of propranolol (75 mg/kg) 10 days after portal vein stenosis and measured 2 to 3 h after propranolol administration, portal pressure (12.8 +/- 1.0 mmHg) was significantly lower than in the placebo group. Portal-systemic shunts (72 +/- 17%), however, showed no significant difference from the placebo group. Similar values in portal pressure (13.3 +/- 1.2 mmHg) and portal-systemic shunts (83 +/- 21%) were also observed in rats 18 to 24 h after a single dose of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of propranolol on intestinal microcirculation of normal and portal hypertensive rats.

BACKGROUND/AIMS: The goal of the present study was to compare the efficacy of locally and systemically administered propranolol in normal and prehepatic portal hypertensive rats, and to test the hypothesis that beta-adrenoceptor blockade reduces intestinal arteriolar diameter by allowing unopposed alpha-adrenergic activity. METHODS: The small intestine was prepared for in vivo microcirculatory studies and transferred to an intravital microscope where arteriolar diameter and erythrocyte velocity were continuously monitored. First order arteriolar (1A) blood flow was calculated from the product of mean velocity and microvessel cross-sectional area. In separate experiments, diameter responses of 2A and 3A were monitored. Once steady-state conditions were achieved, the preparation was challenged by topically applied doses of propranolol (0.01-100.00 microM) in the presence and absence of the alpha-receptor antagonist, phentolamine. In a separate group of experiments, the effects of systemically administered propranolol (10 mg/kg body weight) were evaluated before and after local alpha-adrenoceptor blockade. RESULTS: Propranolol produced significant vasoconstriction and decreased blood flow in both normal and portal hypertensive rats. Portal hypertensive arterioles exhibited an attenuated response to propranolol. Local administration of phentolamine completely blocked the propranolol-induced diameter changes. Comparison of equivalent concentrations of local and systemic propranolol indicated that both routes of administration were equally effective. CONCLUSION: The results of the present study suggest that the cardiovascular actions of propranolol are predominantly mediated through blockade of peripheral beta 2-adrenoceptor.

Animals↗
PubMed1995

Effect of propranolol on portosystemic collateral circulation estimated by per-rectal portal scintigraphy with technetium-99m pertechnetate.

BACKGROUND/AIMS: Propranolol is widely used in the prevention of variceal bleeding. However, in certain patients with cirrhosis, the portal hypotensive effect of propranolol cannot be obtained. An explanation for portal unresponsiveness to propranolol could be an increase in portocollateral vascular resistance mediated by this drug. METHODS: In 33 patients with cirrhosis the effect of chronic administration of propranolol on portocollateral blood flow from the inferior mesenteric vein was examined by means of per-rectal portal Tc-99m pertechnetate scintigraphy. RESULTS: Propranolol significantly reduced the shunt index by 15.3 +/- 4.2%. This reduction was observed only in patients with cirrhosis classified as Child-Pugh A and B groups, but not group C. Differences between groups in portosystemic shunt index changes after propranolol were significant (F = 3.4, p < 0.05). CONCLUSIONS: The data presented suggest that propranolol changes the distribution of blood between the portal and systemic circulation, which is probably due to the increase in vascular resistance of portocollateral vessels. The magnitude of the vascular response to propranolol depends on the severity of liver disease.

Adolescent↗
PubMed1984

Evaluation of antidotes against the acute cardiovascular toxicity of propranolol.

Rats anesthetized with pentobarbital and ventilated artificially were intoxicated with 1 mg/kg X min propranolol i.v. After 30 min heart rate, mean arterial blood pressure and peripheral resistance had dropped by about 50% and cardiac output by about 25% and were stable for up to 120 min. Isoprenaline proved to be the best antidote for the treatment of propranolol intoxication antagonizing the bradycardia by 76% and the hypotension completely. The antagonistic activities of orciprenaline and prenalterol were lower than those of isoprenaline. Dopamine, adrenaline and noradrenaline antagonized propranolol-induced hypotension but did not considerably influence the bradycardia whereas dobutamine was nearly ineffective in both respects. Glucagon and aminophylline displayed some chronotropic activity without influencing propranolol-induced hypotension. Calcium chloride, on the other hand, produced a moderate elevation of blood pressure but only a small chronotropic activity, and atropine was inactive in both respects. Isoprenaline also restored the cardiac function of propranolol-poisoned rats if administered by infusion and, furthermore, increased the lethal dose of propranolol from 77 to 165 mg/kg. The strong antagonistic activity of isoprenaline against propranolol-induced cardiovascular depression was also confirmed by experiments in pigs. In conclusion, isoprenaline is the most active antidote for the treatment of propranolol intoxication in the rat though the administration of massive doses are required. The vasodilatory effect of isoprenaline can be overcome by the additional administration of a vasoconstricting agent like dopamine.

Animals↗
PubMed1991

Measurements by microdialysis of free tissue concentrations of propranolol.

To determine the free concentration of a drug (propranolol) in the interstitial space in humans in vivo, seven male students were investigated by microdialysis of the periumbilical subcutaneous tissue. The microdialysis catheters were calibrated in vivo and the propranolol concentration was determined by high-performance liquid chromatography. Ten hours after intake of 80 mg of propranolol, the total plasma and free interstitial propranolol concentrations were 80 +/- 43 and 7 +/- 2 nM, respectively. After a second dose, maximum concentration was reached after 80 +/- 10 min and 98 +/- 12 min, in plasma, and the concentrations in the interstitial water were 594 +/- 138 and 27 +/- 7 nM, respectively. In a second study, microdialysis was performed on the left ventricular wall in six pigs receiving an intravenous injection of 5 mg of propranolol followed by a constant propranolol infusion for 40 min (5 mg propranolol per h). The maximum concentrations of propranolol were 97 +/- 29 and 6 +/- 2 nM in plasma and in interstitial water, respectively. The data suggest that microdialysis is a useful tool for recording the free concentrations of a drug in the interstitial space.

Adult↗
PubMed2005

Biofeedback assisted diaphragmatic breathing and systematic relaxation versus propranolol in long term prophylaxis of migraine.

OBJECTIVES: To evaluate utility of biofeedback assisted diaphragmatic breathing and systematic relaxation in migraine and to compare their efficacy with propranolol in long term prophylaxis of migraine. METHODS: 192 migraine patients were randomly distributed into two groups. Propranolol group received propranolol 80 mg/day while biofeedback group received electromyogram (EMG) and temperature biofeedback assisted diaphragmatic breathing and systematic relaxation training accompanied by home practice for 6 months. RESULTS: Significant clinical response was seen with biofeedback in 66.66% and with propranolol in 64.58% of patients. Frequency, severity, duration of attacks and number of vomiting episodes were significantly reduced in both the groups at 6 months but inter-group differences were statistically insignificant. During 1 year post-treatment period, significantly lesser resurgence of migraine was seen in biofeedback group as whole (9.37%) and in biofeedback responders in biofeedback group (9.37%) in comparison to resurgence of migraine in propranolol group as whole (38.54%) and in propranolol responders in propranolol group (53.22%) respectively. CONCLUSIONS: Biofeedback assisted diaphragmatic breathing and systematic relaxation were very useful in migraine and had significantly better long-term prophylactic effect than propranolol in migraine.

Adolescent↗
PubMed2006

A double-blind, placebo-controlled trial of amantadine, propranolol, and their combination for the treatment of cocaine dependence in patients with severe cocaine withdrawal symptoms.

BACKGROUND: This trial evaluated the efficacy of amantadine, propranolol and their combination in cocaine dependent patients with severe cocaine withdrawal symptoms. METHODS: Cocaine withdrawal symptom severity was measured by the cocaine selective severity assessment (CSSA). One hundred and ninety-nine patients with high scores on the CSSA participated in a 10-week double-blind trial. Patients were randomly assigned to receive amantadine (300 mg/day), propranolol (100mg/day), a combination of amantadine (300 mg/day) and propranolol (100mg/day) or matching placebo capsules. The primary outcome measure was cocaine abstinence. RESULTS: In the intent-to-treat sample, there were no significant differences between the four medication groups in treatment retention. The odds of cocaine abstinence showed a marginally significant increase over time in the propranolol group (p=0.06) but not in the other three groups. In highly medication-adherent patients, treatment retention was significantly better in the propranolol group compared to the placebo group (p=0.01) and the odds of cocaine abstinence increased significantly over time in the propranolol group but not in the other three groups. CONCLUSION: In the intent-to-treat sample, none of the three active treatments (propranolol, amantadine or their combination) was significantly more effective than placebo in promoting abstinence from cocaine among patients who entered treatment with more severe cocaine withdrawal symptoms. Among patients highly adherent to study medication, propranolol treatment was associated with better treatment retention and higher rates of cocaine abstinence compared to placebo.

Adrenergic beta-Antagonists↗
PubMed2005

Propranolol inhibits the human ether-a-go-go-related gene potassium channels.

Propranolol is a noncardioselective beta-adrenergic antagonist that has been recently reported to prolong the QTc interval on the surface electrocardiogram in humans when overdosed [Farhangi, V., Sansone, R.A. (2003). QTc prolongation due to propranolol overdose. Int. J. Psychiatry Med. 33, 201-202.]. To examine the underlying mechanisms for these clinical findings, we studied the effects of propranolol on the human cardiac potassium channels encoded by the ether-a-go-go-related gene (ERG) using the whole cell voltage-clamp technique. We found that propranolol blocked hERG currents in a concentration-dependent manner with an IC50 of 9.9+/-1.3 microM which is relevant to the predicted plasma level of propranolol in this case report. The present study demonstrated that propranolol can inhibit hERG channels. The interaction between propranolol and hERG channels could lead to delayed cardiac repolarization and might be a molecular mechanism for the previously reported QTc prolongation when propranolol is overdosed.

Adrenergic beta-Antagonists↗
PubMed2004

The use of a dendrimer-propranolol prodrug to bypass efflux transporters and enhance oral bioavailability.

The aim of the study was to determine the effects on the transport of propranolol across monolayers of the human colon adenocarcinoma cell line, Caco-2, of forming a prodrug by conjugating to generation 3 (G3) and lauroyl-G3 PAMAM dendrimers. Propranolol is a poorly soluble drug and known substrate of the P-glycoprotein (P-gp) efflux transporter. Propranolol-G3 dendrimer conjugates were synthesised by surface attachment of two, four or six propranolol molecules. The apical (A) to basolateral (B) apparent permeability coefficient, P(app), of propranolol was increased and its B-->A P(app) decreased following conjugation to G3 dendrimers. Conjugation of propranolol to lauroyl-G3 dendrimers further increased its A-->B P(app). Our findings show that the A-->B P(app) of propranolol conjugates was reduced in the presence of the endocytosis inhibitor colchicine and was lower at 4 degrees C than at 37 degrees C, suggesting that the enhancement mechanism involves endocytosis-mediated transepithelial transport. The A-->B P(app) of conjugated propranolol was not altered in the presence of the P-gp inhibitor cyclosporin A suggesting that conjugation of drug to dendrimer allows the bypassing of the efflux transporter. The results suggest that dendrimer-drug prodrugs may be used to increase drug solubility and bypass drug efflux transporters, therefore increasing drug bioavailability.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Composite membrane of bacterially-derived cellulose and molecularly imprinted polymer for use as a transdermal enantioselective controlled-release system of racemic propranolol.

A composite membrane for transdermal delivery of S-propranolol enantiomer was developed based on the controlled pore functionalization of bacterial cellulose membranes using a molecularly imprinted polymer (MIP) layer synthesis. The reactive pore-filling of an asymmetric porous cellulose membrane with a MIP thin-layer was effected using a silanized coupler as an additional anchor for the MIP. MIP thin-layers with specific binding sites for S-propranolol were synthesized by copolymerization of methacrylic acid with a cross-linker, ethylene glycol dimethacrylate in the presence of S-propranolol as the template molecule and the latter was subsequently extracted. Selective transport of S-propranolol through the MIP composite membrane was obtained, although this was determined mostly by the parent cellulose membrane with some ancillary contributory effect from the MIP layer. In addition, an enantioselectivity in the transport of propranolol prodrug enantiomers was found, suggesting that the shape and functional groups orientation, which are similar to that of the print molecule were essential for enantiomeric recognition of the MIP composite membrane. The enantioselectivity of S-MIP membranes was also shown when the release of propranolol enantiomers was studied in vitro using rat skin, with racemic propranolol contained in the donor compartment. The composite membrane of bacterially-derived cellulose and molecularly imprinted polymer may have great potential for use as a transdermal enantioselective controlled-release system for racemic propranolol.

Administration, Cutaneous↗
PubMed2003

Effects of propranolol on recovery of heart rate variability following acute myocardial infarction and relation to outcome in the Beta-Blocker Heart Attack Trial.

This study evaluated the effects of propranolol on recovery of heart rate variability (HRV) after acute myocardial infarction and its relation to outcome in the Beta-blocker Heart Attack Trial (BHAT). Beta blockers improve mortality after acute myocardial infarction, but through an unknown mechanism. Depressed HRV, a measure of autonomic tone, predicts mortality after acute myocardial infarction. Whether beta blockers influence recovery of HRV after acute myocardial infarction, and thereby improve outcome, is unknown. We compared 24-hour HRV parameters at 1 week after acute myocardial infarction and after 6 weeks of treatment with propanolol (n = 88) or placebo (n = 96). The relation between 25-month outcome (death/acute myocardial infarction/congestive heart failure), propranolol treatment, and HRV was further analyzed. After 6 weeks, high-frequency (HF) power (log-normalized), an index of vagal tone, increased more in propranolol-treated patients (4.28 +/- 0.1 to 5.17 +/- 0.09 ms(2)) than in placebo-treated patients (4.26 +/- 0.09 to 4.77 +/- 0.1 ms(2), p <0.05). Sympathovagal balance measured by the low-frequency (LF) to HF ratio increased in placebo-treated patients (3.55 +/- 0.24 to 3.86 +/- 0.24) but decreased in those treated with propranolol (3.76 +/- 0.29 to 3.17 +/- 0.23, p <0.01). Other frequency-domain parameters increased over time but were not affected by propranolol. Propranolol blunted the morning increase in the LF/HF ratio. Recovery of HF, the strongest HRV predictor of outcome, and propranolol therapy independently predicted outcome. In summary, after acute myocardial infarction, propranolol therapy improves recovery of parasympathetic tone, which correlates with improved outcome, and decreases morning sympathetic predominance. These findings may elucidate the mechanisms by which beta blockers decrease mortality and reduce the early morning risk of sudden death after acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Dose-sensitive excitation and inhibition of spontaneous amygdala activity by propranolol.

The effect of systemically administered propranolol was determined on spontaneous activity of neurons in the central nucleus (CeA) of the amygdala, a brain site implicated in fear-related learning and memory. Extracellular recordings of single units in the CeA were obtained in vivo from rats administered saline or the centrally and peripherally acting beta-adrenergic receptor blocker propranolol (4, 7, 10 mg/kg i.p.). The high dose (10 mg/kg) of propranolol markedly increased spontaneous activity of CeA neurons. In contrast, the low (4 mg/kg) and intermediate (7 mg/kg) doses of propranolol significantly decreased spontaneous CeA activity, with the suppressant effect of propranolol on CeA firing rates weakening as the dosage increased from 4 to 7 mg/kg. These results suggest that (1) spontaneous activity of CeA neurons is tonically influenced by competing excitatory and inhibitory modulatory circuits, and (2) propranolol's effect on the two modulatory circuits is dose dependent: the high dose increasing spontaneous CeA activity by preferentially blocking an inhibitory circuit, the low dose decreasing spontaneous CeA activity by preferentially blocking an excitatory circuit, and the intermediate dose weakly suppressing CeA activity by blocking both the excitatory and inhibitory modulatory circuits. Disinhibition of CeA activity by the high dose of propranolol may explain the enhancement of retention observed in the passive-avoidance task when this dose of the drug is administered systemically, and may have implications for the use of propranolol clinically in treating aversive-memory-related anxiety disorders such as posttraumatic stress syndrome.

Adrenergic beta-Antagonists↗
PubMed1978

Beta-blockade and blood-levels after low-dose oral propranolol: The hepatic "first-pass" threshold revisited.

Heart-rate, arterial pressure, and plasmarenin activity were determined in six normal subjects at rest and after an injection of 8 microgram isoprenaline with and without prior propranolol administered orally in a dose of 5 mg 8-hourly for a total of five doses. After propranolol, resting heart-rate, systolic pressure, and plasma-renin activity all fell significantly (P less than 0.05 to less than 0.001). When the isoprenaline-induced changes of heart-rate, diastolic pressure, and plasma renin activity without propranolol were compared to those with propranolol, these responses were greatly diminished (P less than 0.01 to less than 0.001). The percent blockade by propranolol of the isoprenaline-induced changes ranged from 65% for diastolic pressure to 77% for heart rate and 78% for plasma-renin activity. Propranolol levels determined by conventional fluorometry were below accurate detection limits, whereas those determined by gas-liquid chromatography ranged from 2.3 to 8.5 ng/ml. These findings, which demonstrate beta-blockade with low-dose propranolol, are not consistent with the existence of a postulated threshold for the hepatic "first-pass effect" in man, which is said to require saturation by single doses of 30 mg or more before propranolol enters the systemic circulation.

Administration, Oral↗
PubMedDate not supplied

Effectiveness of low dose captopril versus propranolol therapy in infants with severe congestive failure due to left-to-right shunts.

UNLABELLED: To evaluate the therapeutical effects of the angiotensin converting enzyme inhibitor Captopril to the beta-blocker Propranolol in infants with congestive failure due to pulmonary overcirculation, we retrospectively analysed clinical, neurohormonal and hemodynamic data in 22 infants, 11 of whom were treated with Captopril (Group 1), 11 with Propranolol (Group 2). Age, weight, number of palliative operations, plasma renin activities and pulmonary to systemic flow ratios (3.5 vs. 3.5) were not significantly different prior to Captopril or Propranolol therapy. If treatment with digoxin and diuretics did not succeed, the infants were additionally treated with Captopril (1 mg/kg) for a mean of 7.4 months, or with 1.9 mg/kg Propranolol for 9.2 months. RESULTS: 1 mg/kg Captopril did not effectively suppress angiotensin converting enzyme in the steady state at trough level (92+/-52 vs. 87+/-50 nmol/min/ml). In the Propranolol group, the clinical heart failure score (2.6+/-1.5 vs. 7. 4+/-2.5) and plasma renin activities (14+/-10 vs. 101+/-70 ng/ml/h) were significantly lower, compared to the Captopril group. Length of hospital stay (23+/-9 vs. 52+/-24 days) was lower and weight gain (126+/-38 vs. 86+/-84 g/week) was higher within 3 months after starting Propranolol therapy. Significantly lower left atrial pressures (6.2+/-2.2 vs. 13.4+/-9.2 mmHg) and lower endiastolic ventricular pressures (7.6+/-2.5 vs. 12.6+/-4.0 mmHg) during pre-operative cardiac catheterization indicated a better diastolic ventricular function under chronic Propranolol treatment. CONCLUSION: Although high dose Captopril was not evaluated in this study, when compared to patients on low Captopril dosages, infants who received Propranolol treatment showed improvement in heart failure scores, shorter lengths of hospital stay, lower plasma renin activities and better diastolic ventricular functions.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Accuracy of portal and forearm blood flow measurements in the assessment of the portal pressure response to propranolol.

BACKGROUND/AIMS: The portal pressure response to propranolol varies significantly in individual patients with cirrhosis. At present, propranolol responders can be identified only by measuring the hepatic venous pressure gradient. The aims of this study were: 1) to investigate whether the noninvasive monitoring of portal blood flow by pulsed Doppler ultrasound and forearm blood flow by strain-gauge plethysmography can predict the hepatic venous pressure gradient response to propranolol in patients with cirrhosis, and 2) to analyze the factors that may influence this response. METHODS: Hemodynamic measurements were undertaken in 80 patients with cirrhosis before and after receiving propranolol (0.15 mg/kg i.v., n = 60) or placebo (n = 20). RESULTS: No changes were observed in the placebo group. Propranolol lowered (p < 0.01) hepatic venous pressure gradient from 17.6 +/- 3.8 to 14.7 +/- 3.8 mmHg, portal blood flow from 1122 +/- 363 to 897 +/- 332 ml/min and forearm blood flow from 7.52 +/- 3.1 to 6.12 +/- 2.3 ml/min%. Changes in hepatic venous pressure gradient were correlated (p < 0.01) with those of portal blood flow (r = 0.82) and forearm blood flow (r = 0.54). The reduction in hepatic venous pressure gradient was > 20% in 23 patients ("responders"). The accuracy of portal Doppler flowmetry in identifying responders was higher than that of forearm plethysmography (88.3 vs. 68.3%, p < 0.05). Multivariate analysis proved that previous variceal bleeding was the only factor independently associated with a lack of response to propranolol (relative risk 3.42, 95% CI 1.5-7.4, p < 0.01). Hepatic venous pressure gradient reduction by propranolol was higher in non-bleeders than in bleeders (-19.9 +/- 9.4 vs. -11.3 +/- 8.6%, p < 0.01). CONCLUSIONS: Portal Doppler ultrasound can be used as a reliable surrogate indicator of the hepatic venous pressure gradient response to acute propranolol administration. In addition, our study indicates that this response is mainly influenced by previous variceal hemorrhage.

Adrenergic beta-Antagonists↗