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A technique developed for isolated canine papillary muscle function in various plasmas; and utility ascertained with plasma containing myocardial depressant factors.

Isolated papillary muscles from young dogs were studied to determine the feasibility of utilizing plasma, without added foam depressants, as a test solution to support muscle function. Diluted canine plasma, undiluted canine plasma, plasma with adjusted protein content, monkey plasma, and plasma containing myocardial depressant factors (MDF) were evaluated. For each test, each papillary muscle served as its own control, with either Krebs-Henseleit solution or a control plasma to establish a basis for evaluation of the test plasma. A technique was implemented to oxygenate the muscle, in plasma, without foam production and to monitor pH continuously. These studies indicated that plasma (diluted, undiluted, or with protein adjustments to accommodate experimental procedural requirements) was a satisfactory test solution. Furthermore, plasma from species unrelated to the dog could be utilized. In utilizing plasma, it was essential to establish or adjust the pH and osmolarity for normal muscle function. These studies with plasma containing MDF indicated that MDF depressed canine papillary muscle function. The Vmax values and Po values were decreased and latency was increased. The effects of MDF in canine papillary muscle preparations were completely reversible in short-term studies (up 10 10 hours' duration).

Animals↗

Papillary muscle repair surgery in ischemic mitral valve patients.

BACKGROUND: Ischemic mitral regurgitation (MR), when ischemia/infarction has resulted in fibrotic degeneration and elongation of papillary muscles, carries a high risk for the patient and a technical challenge for the surgeon. We have developed a papillary-shortening plasty for this specific pathology. METHODS: Papillary muscle repair was performed in 88 patients (7.2%) where degenerated and fibrotic elongated papillary muscles were found, which resulted in a prolapse of one or more parts of the mitral valve leaflets (MR III-IV). All patients had a papillary muscle-shortening plasty using a pericardium pledged-reinforced polytetrafluoroethylene suture and a ring annuloplasty. Because the cause of regurgitation in this specific group of patients was ischemic, concomitant coronary bypass grafting was required in all patients, with 2.2 grafts/patient. RESULTS: There were five hospital deaths (5.7%). Postoperative mitral valve function was satisfactory in all patients: no residual mitral regurgitation (MR 0) was found in 80 patients (90.9%), mild regurgitation (MR I) in 5 patients (5.7%), and moderate regurgitation (MR I-II) was observed in 3 patients (3.4%). Within a short mean follow-up period of 18.6 months (3 to 40 months), there was one late death (1.2%). The actuarial freedom from reoperation and thromboembolic complications was 100%, but there were two anticoagulation-induced gastric bleeding complications (2.3%). All patients were in New York Heart Association functional class I or II at the time of follow-up. CONCLUSIONS: Our data show that careful assessment of papillary muscle pathology is mandatory, and that a papillary muscle-shortening plasty is a simple but valuable surgical tool to repair the mitral valve in this specific group of high-risk patients with ischemic mitral regurgitation.

Adult↗

Papillary muscle misalignment causes multiple mitral regurgitant jets: an ambiguous mechanism for functional mitral regurgitation.

BACKGROUND AND AIMS OF THE STUDY: The study aim was to test the hypothesis that asymmetric alignment (misalignment) of the papillary muscles is sufficient to cause incomplete mitral leaflet coaptation and functional mitral regurgitation (MR). METHODS: Different spatial relationships between the papillary muscles and the mitral annulus were investigated in isolated porcine mitral valves in vitro to assess the impact on mitral valve competence. The systolic occlusional leaflet area (OLA) needed to cover the mitral orifice and the anterolateral (ACOM) and posteromedial (PCOM) commissural portion (OLA(ACOM), OLA(PCOM)) were assessed by 2D echocardiography to quantitate incomplete mitral leaflet coaptation. The regurgitant fraction (RF) and MR jet location were assessed by a flow meter and color Doppler ultrasound. RESULTS: Posterolateral dislocation of the posteromedial papillary muscle impaired mitral leaflet coaptation at the corresponding half-portion of the mitral orifice (OLA(PCOM): 351-397 mm2 versus 296 mm2 (normal); p < 0.001) and modified the contralateral part (OLA(ACOM): 354-387 mm2 versus 304 mm2 (normal); p <0.001). The mitral leaflet coaptation line moved in apical and posterior directions, creating a commissural MR orifice at the PCOM side. At the ACOM side, anterior leaflet prolapse and restricted posterior leaflet mobility created an additional commissural regurgitant jet (RF = 0.11-0.13). Symmetrical papillary muscle misalignment restricted mitral leaflet mobility on both sides of the orifice in a synergistic manner (OLA(PCOM): 416-459 mm2 and OLA(ACOM): 427-489 mm2; both p <0.001 versus normal). The central MR jet orifice, which extended towards both commissures, caused more significant MR (RF = 0.15-0.26). CONCLUSIONS: Papillary muscle misalignment caused mitral regurgitant jet ambiguity with an anterior MR jet location following posteromedial papillary muscle displacement. These findings may improve understanding of the relation between myocardial lesion and mitral regurgitant jet location and thereby facilitate rational strategies for valvular interventions.

Animals↗

Mechanical properties of papillary muscle in cardiac failure: importance of pathogenesis and of ventricle of origin.

In an attempt to better understand what causes impairment of failing myocardium, the mechanical characteristics of papillary muscles from three different models of congestive heart failure were compared at varying stages of hypertrophy and failure: adriamycin cardiotoxic rabbit, cardiomyopathic hamster and infra-renal aorto-caval shunted dog. Except for right ventricular muscles from the shunted dogs, in all groups there was a significant decrease in total twitch tension, +dT/dt, -dT/dt, Vmax, +dL/dt, and -dL/dt. However, there were major differences in twitch duration between the three models with time to attain peak tension and peak shortening and time to attain half tension decline decreasing in right ventricular papillary muscles from adriamycin rabbits but increasing in right ventricular papillary muscles from shunted dogs and no change occurring in left ventricular papillary muscles from cardiomyopathic hamsters or shunted dogs. Load dependence as assessed by time to relaxation index for 30% afterload contractions was decreased in all but right ventricular muscles from shunted dogs. These results indicate that despite some common characteristics, major differences exist between papillary muscles from different models of congestive heart failure depending on the pathophysiological process involved and the ventricle of origin.

Animals↗

[A case of acute postinfarction mitral regurgitation and cardiogenic shock caused by a total rupture of the papillary muscle].

We report a case of mitral regurgitation caused by a total rupture of the posterior papillary muscle that had occurred after acute myocardial infarction. A 72-year-old woman was transferred to our hospital for cardiogenic shock. Echocardiogram revealed massive mitral regurgitation and prolapse of posterior mitral leaflet presumably due to a rupture of a papillary muscle. Cardiac catheterization demonstrated a total occlusion in the segment 2 of the right coronary artery. She had developed progressively increasing heart failure even though the patient had received a successful PTCA for a total occlusion of the right coronary artery. She underwent an emergency mitral valve replacement with preservation of the posterior leaflet using a SJM prosthetic valve. Intraoperative findings were confirmative of total rupture of the posterior papillary muscle. A postoperative course was uneventful. This case is the seventh case which has been reported as the successful operation of a total rupture of the papillary muscle in Japan.

Aged↗

Papillary muscle traction in mitral valve prolapse: quantitation by two-dimensional echocardiography.

Previous angiographic observations in patients with mitral valve prolapse have suggested that superior leaflet displacement results in abnormal superior tension on the papillary muscle tips that causes their superior traction or displacement. It has further been postulated that such tension can potentially affect the mechanical and electrophysiologic function of the left ventricle. The purpose of this study was to confirm and quantitate this phenomenon noninvasively by using two-dimensional echocardiography to determine whether superior displacement of the papillary muscle tips occurs and its relation to the degree of mitral leaflet displacement. Directed echocardiographic examination of the papillary muscles and mitral anulus was carried out in a series of patients with classic mitral valve prolapse and results were compared with those in a group of normal control subjects. Distance from the anulus to the papillary muscle tip was measured both in early and at peak ventricular systole. In normal subjects, this distance did not change significantly through systole, whereas in the patient group it decreased, corresponding to a superior displacement of the papillary muscle tips toward the anulus in systole (8.5 +/- 2.6 vs. 0.8 +/- 0.7 mm; p less than 0.0001). This superior papillary muscle motion paralleled the superior displacement of the leaflets in individual patients (y = 1.0x + 0.8; r = 0.93) and followed a similar time course.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Papillary muscle repositioning for repair of anterior leaflet prolapse caused by chordal elongation.

OBJECTIVE: Anterior leaflet prolapse is still a challenge. Various techniques have been described, but very little is known of the long-term outcome. We describe the long-term results of papillary muscle repositioning, with up to 15 years' follow-up. METHODS: From 1989 through 2005, 120 patients with anterior leaflet prolapse (97 bileaflet and 23 isolated anterior leaflet) were treated with papillary muscle repositioning when chordae were elongated. All patients had severe mitral regurgitation. The mean left ventricular end-systolic diameter on echocardiography was 39.4 +/- 5.2 mm. The predominant cause was degenerative: dystrophic disease in 62 and Barlow's disease in 43. Papillary muscle repositioning was carried out on the posterior papillary muscle in 92.5% and on the anterior papillary muscle in 31.7%. A ring annuloplasty was performed in 117 cases. Fifty-seven (47.5%) patients had a tricuspid annuloplasty. RESULTS: There were no in-hospital deaths or patients lost to follow-up. Mean follow-up was 6.3 +/- 0.4 years (maximum, 15.6 years). Cumulative actuarial survival at 5, 10, and 15 years was 97.2%, 94.1%, and 81.4%, respectively. Two (1.7%) patients required reoperation at 1 and 5 years after repair. No significant risk factor was identified for late mortality or reoperation. At the latest assessment, 88 (73.3%) patients were asymptomatic. Echocardiography showed no or trivial mitral regurgitation in 89 (74.2%) patients, mild mitral regurgitation in 8 patients, and moderate mitral regurgitation in 9 patients. CONCLUSIONS: Anterior leaflet prolapse caused by elongated chordae can always be addressed with papillary muscle repositioning. Results indicate that it is a safe and durable technique, providing good long-term results in the management of degenerative pathology of the anterior leaflet.

Cardiac Surgical Procedures↗

Pitfalls in clinical recognition and a novel operative approach for hypertrophic cardiomyopathy with severe outflow obstruction due to anomalous papillary muscle.

BACKGROUND: Ventricular septal myotomy/myectomy (Morrow procedure) is the standard surgical option for severely symptomatic patients with hypertrophic cardiomyopathy (HCM) and marked basal obstruction to left ventricular outflow due to mitral valve systolic anterior motion. In some patients, however, congenital malformations of the mitral apparatus may be responsible for outflow obstruction; the failure to recognize this morphology before operation could have adverse consequences. METHODS AND RESULTS: We recently evaluated 2 patients with obstructive HCM operated on at Mayo Medical Center in 1997 who demonstrated direct anomalous papillary muscle insertion into the anterior mitral leaflet, producing muscular midcavity obstruction. This anomaly is potentially identifiable with echocardiography by exaggerated anterior displacement of hypertrophied papillary muscles within the left ventricular cavity and the direct continuity between papillary muscle and anterior leaflet associated with a rigid motion pattern of the mitral apparatus. Echocardiographic diagnosis, however, was confused in both patients by the association of systolic anterior motion of the mitral valve, probably produced by freely mobile margins of the mitral leaflet unencumbered by papillary muscle insertion, and in 1 patient probably representing a second and more basal level of obstruction. Because outflow tract morphology was judged unsuitable for conventional myotomy/myectomy, a novel surgical strategy was designed to remove the outflow gradient in which an extensive myectomy trough (wider at its apical than basal extent) was created within the ventricular septum to papillary muscle level; also, in 1 patient, attachment of anterolateral papillary muscle with the lateral free wall was partially severed to increase mobility of the mitral apparatus. After surgery, both patients reported substantial relief of symptoms and improved exercise tolerance and also showed reduced or abolished basal outflow obstruction. CONCLUSIONS: In HCM, outflow obstruction due to anomalous papillary muscle insertion directly into anterior mitral leaflet is challenging to identify but should always be contemplated before operative intervention. This important (but often unsuspected) congenital malformation may require alternative surgical strategies to standard myotomy/myectomy, similar to those described here.

Adolescent↗

Histologic findings in left ventricle papillary muscle arteries from human hearts.

We describe original histologic findings of left ventricle papillary muscle (LVPM) arteries in people under 30 years of age. We examined 666 samples taken from the tip, mid-portion and base of papillary muscles in 56 males and 55 females, as well as several samples from the rest of the left ventricle. The number of smooth muscle cells (SMC) in the tunica media of the LVPM arteries led us to divide the samples examined into three groups: (i) group 1, 355 samples (53%) with a normal number of SMC and a normal lumen (the number of group 1 samples increased from the tip (21%) to the base (47%)); (ii) group 2, 252 samples (38%) with a mild to moderately increased number of SMC (the number of these samples decreased from the tip (44%) to the base (22%)); and (iii) group 3, 59 samples (9%) with abundant SMC that were more than twofold greater in size and number of normal arteries, in contrast with the other two groups. The shape of the SMC in group 3 samples was round and the extremely narrow, centrally located lumen of these SMCE had a round or oval shape. These changes were restricted only to papillary muscle arteries and the number of group 3 samples decreased from the tip (63%) to the mid-portion (37%). No inflammatory reaction or chronic ischemic changes were found in the LVPM arteries and surrounding area. The SMC changes in groups 2 and 3 were found in subjects aged more than 2 months. These findings will provide anatomists, cardiologists, pathologists and physiologists with valuable knowledge and will trigger further investigation into the etiology of the structural changes observed and their evolution with age.

Adolescent↗

Histopathological study of the papillary muscles and apex cordis of the hypertrophied left ventricle.

Hypertrophy of the papillary muscle and apex cordis of the left ventricle was studied histopathologically using 84 hearts obtained at autopsy. The hearts were divided into three groups: a hypertrophy group (heart weight more than 350 g); a borderline group (heart weight between 350 and 300 g) and a control group (heart weight less than 300 g). The size of the papillary muscle increased with increase in heart weight. Derangement of myocyte linings and fibrosis at the papillary muscle base became apparent with hypertrophy. In addition derangement and fibrosis extented from the internal to middle layers of the free wall with progressing hypertrophy. Derangement seemed to precede hypertrophy and fibrosis. A cluster of huge myocyte-like Purkinje's cells were associated with the center of the derangement. At the apex, criss-cross derangement developed from right and left side derangement with increasing hypertrophy. It is speculated that the focal derangement plays an important role in producing hypertrophy in response to mechanical stress with subsequent development of hypertrophy and fibrosis with some asymmetry.

Cardiomegaly↗

Uridine triphosphate prolongs action potential duration of guinea pig papillary muscles via P2Y2 purinoceptors.

AIM: To study the electrophysiologic effects of uridine triphosphate (UTP) on the guinea pig papillary muscles in vitro and purinoceptors related with the action of UTP. METHODS: Intracellular microelectrode method was used to record action potentials (AP) in guinea pig papillary muscles. RESULTS: UTP, adenosine triphosphate (ATP), and adenosine diphosphate (ADP) prolonged the action potential duration (APD) concentration dependently in guinea pig papillary muscles. The potency order was UTP=ATP > ADP. There was cross desensitization between the response to ATP and that to UTP, and neither Ado nor alpha, beta-MeATP caused great change in AP of the papillary muscles. The prolongation of APD by UTP was not affected by sustained perfusion with aminophylline. As an osmotic pressure control equivalent to UTP 3 mmol/L, ceftriaxonum 3 mmol/L or NaCl 9 mmol/L induced a marked but slight prolongation of APD. CONCLUSION: UTP produced APD prolongation through specific and nonspecific actions, and the specific response to UTP was mediated by P2Y2 purinoceptors.

Action Potentials↗

Myocardial contractile actions of endothelin-1 in rat and rabbit papillary muscles. Role of endocardial endothelium.

The actions of endothelin on the contractile and twitch configuration characteristics of rat and rabbit papillary muscles were evaluated before and after endocardial endothelium removal. In rabbit papillary muscles, endothelin produced a dose-dependent (10(-11) to 10(-7) M) increase in tension (T) (from 2.7 +/- 0.2 to 8.9 +/- 0.7 g/mm2, p less than 0.01), dT/dt, and Vmax (from 1.14 +/- 0.03 to 3.0 +/- 0.13 Lmax/sec, p less than 0.01), a decrease in time to peak tension (from 251 +/- 9 to 216 +/- 7 msec, p less than 0.05), and an increase in time to half relaxation (from 168 +/- 9 to 293 +/- 14 msec, p less than 0.01). Increasing calcium concentration in the bath from 1.25 to 15 mM greatly attenuated these changes. In the presence of propranolol (10(-5) M), endothelin increased all indexes of contractility but to a lesser extent (T = 2.6 +/- 0.3 to 6.5 +/- 0.2 g/mm2, p less than 0.01; Vmax = 1.16 +/- 0.10 to 2.06 +/- 0.10 Lmax/sec, p less than 0.01). Myocardial catecholamine depletion with reserpine had effects similar to those of propranolol. The myocardial contractile and twitch configuration characteristics of endothelin were similar to those of phenylephrine (10(-4) M), a strong stimulator of the phosphatidylinositol pathway and a moderate beta-adrenergic stimulator. The effects of phenylephrine and endothelin were modified in a similar manner by propranolol (10(-5) M). The presence of nicardipine (3 X 10(-7) M) decreased the absolute increase in contractility caused by endothelin but did not alter the percent change or shift the dose-response curve of endothelin. The actions of endothelin in rat papillary muscles studied at physiological calcium concentrations (Ca2+ = 1.25 mM) were less marked than those of rabbit studied at physiological calcium (Ca2+ = 1.25 mM) but similar to those of rabbit studied at high calcium concentrations (Ca2+ = 15 mM). Removing the endocardial endothelial layer of rabbit papillary muscles did not alter the absolute changes in contractility caused by endothelin but shifted the dose-response curve to the left and markedly altered the effects of endothelin on twitch configuration characteristics. Thus, it would appear that endothelin increases contractility and modifies twitch configuration. It does so more at lower rather than higher extracellular calcium concentrations and in a species, such as rabbit, that responds more to interventions that increase intracellular calcium.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

A clinicopathological study on the papillary muscle dysfunction.

A total of 11 cases of papillary muscle dysfunction (PMD) was found among 600 consecutive autopsy (1.8%). There were 5 men and 6 women, with their ages ranging from 64 to 92 years. Auscultation and phonocardiograms revealed holosystolic murmurs in 9 cases and early systolic murmurs in 2. There were accentuated 1st sound in 8 cases, 3rd sound in 7, and 4th sound in 5. PMD was classified into 3 types according to the clinical course and pathologic examinations. In type A (6 cases), myocardial infarction (MI) preceded the occurence of mitral regurgitation (MR) by 3 or 4 years, with pathological verification of old MI. In type B (1 case), MR developed during acute MI. In type C (4 cases), pathological examinations disclosed various degrees of myocardial fibrosis, in which clinical diagnosis was MR of unknown etiology. In a total of 113 cases of MI, 36 cases (32%) showed papillary muscle infarction (PMI), which occurred with significantly high incidence in (1) male, (2) large MI, and (3) subendocardial or lateral MI. Among 36 cases of PMI, 9 cases developed PMD, which showed high incidence in inferior MI and in female. Various other factors concerning PMD and PMI were examined, and it was pointed out that not only PMI but also severe lesions in corresponding ventricular wall were necessary for the development of PMD.

Aged↗

Surgical treatment of papillary muscle rupture.

Between 1971 and 1979, 16 patients underwent mitral valve replacement for papillary muscle rupture after infarction. Nine of these patients were operated on within 3 days of papillary muscle rupture. Eight patients had low cardiac output syndrome prior to operation. Six patients had concomitant coronary artery bypass, and 1 patient had resection of an associated left ventricular aneurysm. There were 3 operative deaths (19% mortality). Surviving patients have been followed for a total of 49 patient-years. There have been 2 late deaths, each a result of coronary artery disease. Six of the 11 surviving patients are asymptomatic; the others are in New York Heart Association Functional Class II or III. The actuarial 5-year survival was 75%. These data support the concept that an aggressive attitude should be taken toward early diagnosis and surgical treatment of postinfarction papillary muscle rupture.

Aged↗

Postinfarct cardiac free wall rupture: the relationship of rupture site to papillary muscle insertion.

The objective of this study was to examine for any relationship between the sites of papillary muscle insertion in left ventricular free wall (LVFW) and the site of LVFW rupture postinfarct. Twenty-five consecutive patients with LVFW rupture (12 men and 13 women, mean age 72.3 yr, range = 48 to 93) at the University of Ottawa Heart Institute during the period of July 1, 1988 to 1992 were studied. Clinical charts were reviewed, and the Formalin-fixed hearts were re-examined grossly and microscopically. Each patient died of tamponade or after surgery for tamponade. Eight (32%) of the 25 infarcts were anteroseptal or anterior, 11 of 25 (44%) were lateral, and 6 of 25 (24%) were inferior or inferoseptal. Four (16%) of the 25 infarcts were less than 2 days old, 9 of 25 (36%) were 2 to 5 days old, and 12 of 25 (48%) were 5 to 10 days old. A separate pre-existent and healed infarct was noted in 36% of patients; however, rupture adjacent to these areas of old infarct occurred in only 8% of cases. In 15 of 25 (60%) cases, free wall rupture occurred in the lateral wall between and at the level of the two papillary muscles. In a further 5 of 25 (20%) cases, the rupture was beside one of the papillary muscles but in anterior or posterior walls. In 20 of 25 (80%) cases, the endocardial tear associated with the LVFW rupture was within 1 cm of the base of one of the papillary muscles as they inserted in LVFW.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Postinfarction double papillary muscle rupture in three surgically excised mitral valves.

Three patients ranging in age from 58 to 72 years underwent mitral valve replacement for cardiogenic shock and severe mitral insufficiency associated with acute myocardial infarction. Correlation of the gross and microscopic findings confirmed the presence of partial rupture of both papillary muscles in all three cases. Papillary muscle rupture is an infrequent complication of acute myocardial infarction; double papillary muscle rupture an extreme rarity, previously only reported at autopsy. To our knowledge, the occurrence of postinfarction dual papillary muscle rupture in surgically excised valves has not been previously reported in the literature.

Aged↗

[Usefulness of helical scanning CT in assessment of left ventricular papillary muscle contractility].

Three-dimensional data on the left ventricle at quasi-end-diastole and quasi-end-systole were acquired by helical scanning CT in 12 patients. Short axial images of the left ventricle and long axial images of the papillary muscle were created using multiplanar reconstruction. Left ventricular dimensions and the length of the papillary muscle were measured, and fractional shortening of the papillary muscle was calculated. There was a good correlation between left ventricular dimensions measured by echocardiogram and helical scanning CT (end-diastole: r = 0.94: end-systole: r = 0.86; fractional shortening of left ventricular dimension: r = 0.84). Papillary muscle fractional shortening was 6.3% in the ischemic group and 21.5% in the non-ischemic group (p < 0.005). Helical scanning CT is clinically useful for the assessment of left ventricular papillary muscle function.

Adult↗

Contribution of endogenous opioids and nitric oxide to papillary muscle contractile impairment in cholestatic rats.

Attenuated responsiveness to adrenoceptor stimulation has been proposed as an important factor underlying cardiovascular complications of cholestasis. We examined isolated papillary muscle responsiveness to alpha (phenylephrine) and beta-adrenoceptor (isoproterenol) agonists in 7-day bile duct-ligated rats. We investigated the role of nitric oxide (NO) and endogenous opioids in papillary muscle hyporesponsiveness to isoproterenol stimulation. In order to evaluate the effect of NO and endogenous opioids, animals were treated with chronic subcutaneous injections of N(omega)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg/day) or naltrexone (20 mg/kg/day), or isolated papillary muscles were exposed acutely to the same drugs (10(-4) and 10(-6) M, respectively) in an organ bath. The basal contractile force of papillary muscle, +dT/dtmax and -dT/dtmax, was significantly decreased in bile duct-ligated rats compared to sham-operated ones (P<0.05, for each value). The concentration-response curve for phenylephrine and isoproterenol demonstrated a reduced maximum effect in bile duct-ligated rats compared to the sham-operated group (P<0.01 and 0.05, respectively). Basal contractile abnormalities of bile duct-ligated rats were corrected by L-NAME or naltrexone treatment, either acute or chronic. While chronic L-NAME treatment resulted in a left-ward shift (P<0.05), it had no effect on the maximum effect in bile duct-ligated rats. Acute L-NAME treatment did not influence isoproterenol responsiveness. Acute and chronic naltrexone treatment resulted in partial and complete correction of the hyporesponsiveness of bile duct-ligated rats, respectively (P<0.05). This investigation demonstrates that the papillary muscles of 7-day bile duct ligated-rats have an impaired basal contractility and hyporesponsiveness to both alpha and beta-adrenoceptor stimulation. It also provides evidence for the involvement of increased opioidergic tone and NO overproduction in cholestasis-induced cardiac impairment.

Adrenergic alpha-Agonists↗