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PubMedDate not supplied

Cardiac phosphocreatine deficiency induced by GPA during postnatal development in rat.

The effect of chronic administration of beta-guanidinopropionic acid (GPA) on the protein profiling, energy metabolism and right ventricular (RV) function was studied in the rat heart during the weaning and adolescence period. GPA was given in tap water (1-1.5%) using pair drink controls. The feeding of animals with GPA solution for a six week period resulted in elevation of heart to body weight ratio due to body growth retardation. GPA accumulated in the myocardium up to 67.37 +/- 5.3 mumoles.g dry weight and the tissue content of total creatine, phosphocreatine and ATP was significantly decreased to 15%, 9% and 65% of control values respectively. Total activity of creatine kinase (CK) was not changed, but the proportion of mitochondrial (Mi) CK isoenzyme was decreased; the percentage of MB isoenzyme of CK was significantly higher. GPA treatment resulted in an elevation of the content of cardiac collagenous proteins and decrease of non-collagenous proteins in the heart; in parallel, a decrease of the collagen I to collagen III ratio was detected. The function of the RV was assessed using an isolated perfused heart with RV performing pressure-volume work. As compared to pair-drink controls, RV function was significantly impaired the GPA group: at any given right atrial filling pressure, the RV systolic pressure and the rate of pressure development were decreased by almost a factor of two. Elevation of the RV diastolic pressure with increasing pulmonary artery diastolic pressure was also significantly steeper in the GPA group which also showed decrease of cardiac output, especially at high outflow resistance. It may be assumed that chronic administration of GPA deeply influenced metabolic parameters, protein profiles and contractile function of the developing heart. On the other hand, concentrations of glucose, total lipids and triglycerides in blood plasma were not affected. All these data confirm the concept that the CK system is of central importance both for heart function and for the regulation of normal growth of cardiac myocytes.

Animals↗
PubMed1994

Distribution of angiotensinogen in diseased human hearts.

Extrahepatic synthesis and localization of angiotensinogen (ATN) have been described in animals, thus establishing the tissue renin-angiotensin (RA) system. However, there had been no reports of tissue RA systems in human organs, including the heart. In earlier, we have reported the possibility of ATN synthesis in the human heart using ribonuclease protection assay system. ATN mRNA was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that ATN is synthesized in the human heart. In this report, we looked for the distribution of ATN in diseased human heart. Northern blot hybridization of cDNA with total RNA extracted from human liver, brain, kidney, atrial and ventricular tissues revealed that ATN mRNA exists in cardiac ventricule. Immunohistochemical studies using a specific antibody to ATN revealed a stronger reaction in the endocardial layer of the human left ventricle, than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. This distribution pattern was similar to that of human atrial natriuretic peptide (hANP), which functions a smooth muscle relaxant. Double immunostaining of ATN and hANP demonstrated that all myocytes in the right atrium had immunopositive reactions to ATN, hANP or both of ATN and hANP. Double immunoelectron staining enabled us to show more detailed localization of ATN and hANP; hANP only existed in the specific granules and ATN existed in the myofibril, but not in the granule. Furthermore, our experiments provide evidence of ATN in healthy human hearts and also reveal a widespread immunopositive reaction for ATN in the left ventricle of diseased hearts.

Angiotensinogen↗
PubMed1975

Intraventricular conduction in man studied with an endocardial electrode catheter mapping technique. Patients with normal QRS and right bundle branch block.

The sequence of intraventricular conduction has been studied in a total of 60 patients, 38 of whom had normal QRS morphology and 37 of whom had right bundle branch block (RBBB) either present continuously or produced as functional aberrant RBBB by the introduction of atrial premature depolarizations or by rapid atrial pacing. Activation times were measured by intracardiac electrode catheters positioned at the right ventricular inflow tract (RVIT), right ventricular apex (RVA), right ventricular outflow tract (RVOT), left ventricular apex (LVA) and left ventricular outflow tract (LVOT). The activation after beginning of QRS in milliseconds plus or minus 1 SD and the number of patients studied at each location were: RVIT--normal 23 plus or minus 13 (15 patients); RVIT-RBBB 49 plus or minus 16 (15 patients); RVA--normal 18 plus or minus 9 (28 patients); RVA-RBBB 54 plus or minus 16 (30 patients); RVOT--normal 40 plus or minus 10 (28 patients); RVOT-RBBB 78 plus or minus 21 (30 patients);LVA--normal 9 plus or minus 9 (18 patients); LVA-RBBB 6 plus or minus 10 (10 patients); LVOT--normal 45 plus or minus 13 (10 patients); LVOT-RBBB 32 plus or minus 9 (7 patients). Significant differences observed were: RVA-normal versus RVA-RBBB P smaller than 0.001; RVOT-RBBB P smaller than 0.001; RVA-normal versus LVA-normal P smaller than 0.005; LVA-normal versus LVA-RBBB NS, LVOT-normal versus LVOT-RBBB P smaller than 0.05. The LVOT change was unexpected and suggests changes in left ventricular depolarization may occur when right bundle branch block develops. In patients with RBBB the activation of the RVA (r equals 0.82) and of the RVOT (r equals 0.68) was directly related to the duration of QRS. Changes in activation time when RBBB was induced by rapid atrial pacing or by introduction of atrial premature depolarizations were: RVA (7 patients) 19 plus or minus 11 to 56 plus or minus 16 (P smaller than 0.001); RVOT (9 patients) 41 plus or minus 10 to 77 plus or minus 22 (P SMALLER THAN 0.001); LVA (5 patients) and LVOT (2 patients), small insignigicant changes. These data indicate that endocardial activation changes can be evaluated in the catheterization laboratory, that right ventricular conduction becomes slower in RBBB as a direct function of total QRS and that left ventricular conduction may be affected when RBBB develops.

Action Potentials↗
PubMed1975

Sinus nodal function in the intact dog heart evaluated by premature atrial stimulation and atrial pacing.

Sinus nodal function was analyzed in 25 dogs by premature stimulation of the right atrium. The return (AT-AR) and post-return (AR-A) cycles were plotted as a function of the premature cycle, and four zones were identified. Zone I (compensatory zone) was observed during the last 4.8 percent (mean value) of the sinus cycle (A-A). Zone II was observed during 43.6 to 95.2 percent (mean value) of the sinus cycle. During the latter part of zone II, AT-AR was nearly constant and AR-A remained nearly equal to A-A during the last 29 percent (mean value) of the cycle. Earlier in zone II three distinct patterns of return cycle responses were observed whereas post-return cycles either remained nearly equal to A-A or showed progressive lengthening. Zone III (interpolation) was observed in 10 animals during 39.5 to 46.2 percent (mean value) of the sinus cycle. AR-A was nearly equal to A-A in zone III. Interpolation was incomplete late and complete early in the zone. Zone IV (echo zone) was seen in another 10 animals during 40.9 to 45.3 percent (mean value) of the sinus cycle and in this zone AR-A was greater than A-A. No significant difference in these zones was seen among the animals anesthetized with pentobarbital or alpha-chloralose, or given 6-OH-dopamine. The AR-A was important in the analysis of these zones and appears to be essential to the interpretation of data derived from premature atrial stimulation. Responses to premature atrial stimulation through a catheter electrode positioned against the sinus nodal region compared favorably with responses to direct epicardial stimulation. After periods of continuous right atrial pacing a vairety of patterns of sinus nodal depression were observed at different rates and durations of stimulation. The frequent occurrence of a short sinus escape cycle followed by the maximal pause observed during rapid pacing rates suggests sinus nodal entrance block. This may be an important factor to consider in determining an optimal pacing rate for assessing sinus nodal function.

Anesthesia, Intravenous↗
PubMed2000

Patients with pulmonary fibrosis: cardiac function assessed with MR imaging.

PURPOSE: To detect abnormalities in cardiac function by using magnetic resonance (MR) imaging in patients with mild to moderate pulmonary fibrosis and to evaluate the relationship between pulmonary function and cardiac function. MATERIALS AND METHODS: Sixteen patients were compared with 16 sex- and age-matched healthy control subjects. Systolic function was assessed by using multisection multiphase cine MR imaging. Diastolic function was assessed with flow-sensitive MR imaging across the mitral and tricuspid valves. MR imaging results were compared with the severity of impairment in pulmonary function. RESULTS: Biventricular systolic function and left ventricular diastolic function were normal in patients, but right ventricular diastolic function was significantly impaired versus that of control subjects, with a ratio of peak flow during early diastolic (E) filling to peak flow during atrial contraction (A) of 0.85 +/- 0.40 versus 1.28 +/- 0.50 (P =.035). Biventricular E/A ratios were strongly correlated to age in patients and control subjects. The right ventricular E/A ratio in patients corresponded with values that are normally expected in people 20 years older. Diastolic left and right ventricular functions were significantly correlated with each other. There was no relationship between pulmonary function and cardiac function. CONCLUSION: Impairment of right ventricular diastolic function was found by using MR imaging in patients with mild to moderate pulmonary fibrosis, whereas left ventricular diastolic function and biventricular systolic function were preserved.

Adult↗
PubMed1990

Effects of increasing heart rate induced by efferent sympathetic neuronal stimulation, isoproterenol or cardiac pacing on myocardial function and oxygen utilization.

The effects of increasing heart rate by six different methods on cardiac function were investigated in 17 open-chest anesthetized dogs. Heart rate was increased approximately 30% by (1) right interganglionic nerve stimulation, (2) atrial pacing, (3) ventricular pacing, (4) atrioventricular sequential pacing, (5) right stellate ganglion stimulation, and (6) isoproterenol administration. During heart rate increases induced by atrial pacing left ventricular intramyocardial pressure, coronary blood flow, oxygen delivery per unit of myocardial oxygen consumption, and myocardial efficiency were unchanged. Ventricular pacing reduced left ventricular cavity and septal intramyocardial pressure, while circumflex coronary flow increased, resulting in reduced oxygen delivery relative to myocardial oxygen consumption. Similarly, atrioventricular sequential pacing increased circumflex coronary artery flow and myocardial oxygen consumption, and decreased septal intramyocardial pressure and oxygen delivery per unit of myocardial oxygen consumption. Right stellate ganglion stimulation and isoproterenol increased left anterior descending and circumflex coronary artery blood flow, intramyocardial pressure, and myocardial oxygen consumption. Estimated myocardial efficiency (left ventricle) was decreased by ventricular pacing and isoproterenol, and was unchanged by atrial pacing and right interganglionic nerve stimulation. Increases in heart rate induced by right interganglionic nerve stimulation did not alter myocardial oxygen consumption, or the index of cardiac efficiency. It is concluded that augmentation of heart rate by either ventricular or atrioventricular pacing impairs myocardial function so that there is a decrease of left ventricular efficiency and isoproterenol augments chronotropism and myocardial force relative to cardiac external work so there is a reduction in cardiac efficiency. In contrast, atrial pacing or right interganglionic nerve stimulation augments chronotropism such that myocardial oxygen consumption and efficiency are unchanged.

Animals↗
PubMed2000

Beneficial effects of MET-88, a gamma-butyrobetaine hydroxylase inhibitor in rats with heart failure following myocardial infarction.

Myocardial ischemia can cause myocardial infarction and as a consequence, heart failure. 3-(2,2,2-trimethylhydrazinium) propionate (MET-88) inhibits gamma-butyrobetaine hydroxylase and has cardioprotective effects on the ischemic heart. We now examined the effects of MET-88 in rats with congestive heart failure following myocardial infarction. Congestive heart failure was produced by left coronary artery ligation in rats. MET-88 at 100 mg/kg/day was orally administered from the 2nd day after surgery. We performed a survival study for 181 days, and measured ventricular remodeling, cardiac function, and myocardial high-energy phosphate levels after treatment for 20 days. MET-88 prolonged survival with a median 50% survival of 103 days compared to 79 days for the heart-failure control rats. The expansion of the left ventricular cavity (ventricular remodeling) in heart-failure rats was prevented by treatment with MET-88, and the effect of MET-88 was similar to that of captopril at 20 mg/kg. MET-88 attenuated the rise in right atrial pressure in heart-failure rats and augmented cardiac functional adaptability against an increased load. Also, MET-88 improved the myocardial energy state in heart-failure rats. The present results indicate that MET-88 improves the pathosis in rats with heart failure induced by myocardial infarction.

Adenosine Diphosphate↗
PubMed1979

Cardiovascular effects of positive-pressure ventilation in normal subjects.

In normal subjects during 15-min positive-pressure ventilation with 10 cmH2O end-expiratory pressure (PEEP), cardiac output fell 19% due to a fall in stroke volume. Transmural mean right atrial pressure rose 3.1 cmH2O and right ventricular end-diastolic diameter increased 15%. Simultaneously, left ventricular end-diastolic diameter decreased 21%, ejection time increased 11%, and velocity of circumferential fiber shortening fell 30%. Thus, right ventricular filling increased and left ventricular filling decreased. The function of the right ventricle was impaired and the function of the left ventricle may have been impaired. Cardiac output gradually increased due to a 7% increase in heart rate as PEEP was continued for 1 h and transmural mean right atrial pressure also increased further by 2.4 cmH2O. Compensation for the reduced stroke volume occurred as filling pressures and heart rate rose, but ventricular function remained impaired for the entire duration of PEEP. On resuming spontaneous breathing, cardiac output and ventricular function returned to base-line levels. We conclude that the reduced cardiac output during PEEP is not due to a direct mechanical reduction in right ventricular filling.

Adult↗
PubMed2001

Conversion of extracorporeal membrane oxygenation to non-pulsatile left ventricular assist device. Is it out-of-date for non-pulsatile LVAD?

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) provides an immediate support for acute deterioration of hemodynamic and pulmonary status, but what is the best decision for these critical patients? Biventricular assist device (BVAD) or left ventricular assist device (LVAD)? We proposed a protocol of step-by-step conversion from ECMO to LVAD after assurance of the reversibility of right ventricle and pulmonary function. METHODS: After femoral venoarterial ECMO was inserted for the critical patients, the left atrial drainage was added to the ECMO firstly and the femoral arterial inflow was shifted to the ascending aorta for preventing possible peripheral vascular complications. Temporary clamp of right heart drainage was tried to test right heart function 24 to 48 hours later. The sweep gas flow of oxygenator could be reduced gradually to test the pulmonary function. Therefore, the right heart drain and the oxygenator could be withdrawn to become a non-pulsatile LVAD or shift to pneumatic LVAD directly. There were four clinical experiences with successful conversion without temporary right ventricular assist device. RESULTS: All of them were able to convert their ECMO to LVAD smoothly in 8.0+/-2.5 days. Three of them were shifted to non-pulsatile LVAD, and one was converted to HeartMate. All but one could be weaned from the ventilator. No BVAD was needed in these patients. Due to the shortage of donor hearts, only one had the chance to undergo heart transplantation. CONCLUSIONS: The protocol did provide a good guideline for decision-making for those under ECMO support necessitating bridge to transplantation.

Cardiotonic Agents↗
PubMed1994

A logical state model of circus movement atrial flutter role of anatomic obstacles, anisotropic conduction and slow conduction zones on induction, sustenance, and overdrive paced modulation of reentrant circuits.

Mapping studies of atrial flutter in both the canine sterile pericarditis model and the right atrial enlargement model commonly reveal single loop reentrant circuits in the lower posterior part of the right atrium. Functional bidirectional conduction block and natural anatomical obstacles comprise the central obstacle for reentrant impulse during circus movement atrial flutter. Because the relative roles of anatomical obstacles, in combination with functional barriers, anisotropic conduction, and slow conduction can not be readily assessed with current electrophysiological techniques, an atrial activation model was developed to study the mechanisms of circus movement atrial flutter. A discrete state model consisting of 4096 logically connected cardiac elements was used to simulate atrial activation; an inexcitable region simulating the inferior vena cava (IVC) was also incorporated in the model. Atrial flutter was induced by programmed premature stimulation. Anisotropic conduction velocity properties, regional variations in slow conduction, regional refractory gradients and stimulation parameters were specified for each simulation. The reentrant circuit generally consisted of a single reentrant impulse which circulated around a continuous line of functional bidirectional conduction block joined to the IVC. Rapid pacing, 5-30 ms shorter than the spontaneous reentrant cycle length, was applied to entrain and/or terminate the rhythm. The results of this study demonstrate that patterns of initiation, entrainment, termination and reinitiation of circus movement atrial flutter mimic results from in vivo activation mapping studies. We find that sustained circus movement atrial flutter circuits depend on: 1) natural anatomical obstacles to stabilize reentrant circuits, and 2) anisotropic conduction properties to reduce the degree of functional conduction block needed to maintain circus movement. Rapid pacing of simulated circus movement atrial flutter demonstrated that the entrainment criteria can be satisfied in a two-dimensional syncytium.

Animals↗
PubMed2006

Ventricular pacing lead location alters systemic hemodynamics and left ventricular function in patients with and without reduced ejection fraction.

OBJECTIVES: We compared left ventricular (LV) systolic and diastolic function during right ventricular (RV), LV, and biventricular (BiV) pacing in patients with narrow QRS duration with and without LV dysfunction. BACKGROUND: The optimal RV pacing lead location for patients with a standard indication for ventricular pacing remains controversial. METHODS: Left ventricular pressure and volume data were determined via conductance catheter during electrophysiology study in 31 patients divided into groups with ejection fraction (EF) > or =40% (n = 17) or EF <40% (n = 14). QRS duration was 91 +/- 18 versus 106 +/- 25 ms, respectively (p = NS). Hemodynamic data were recorded during atrial and dual chamber pacing from the RV apex, RV free wall, RV septum, LV free wall, and BiV. RESULTS: In patients with EF > or =40%, RV pacing at 1 or more sites, but not LV free wall or BiV pacing, significantly (p < 0.05) impaired cardiac output (CO), stroke work (SW), EF, and LV relaxation compared with atrial overdrive pacing. Right ventricular pacing also impaired hemodynamics and LV function in patients with EF <40%. However, LV and BiV pacing increased CO, SW, EF, and LV +dP/dt(MAX) in patients with LV dysfunction. Left ventricular and BiV pacing enhanced an index of global LV cycle efficiency in patients with depressed EF. The detrimental hemodynamic effects of RV pacing were attenuated by selecting the optimal RV pacing site. CONCLUSIONS: Right ventricular pacing worsens LV function in patients with and without LV dysfunction unless the RV pacing site is optimized. Left ventricular and BiV pacing preserve LV function in patients with EF >40% and improve function in patients with EF <40% despite no clinical indication for BiV pacing.

Arrhythmias, Cardiac↗
PubMedDate not supplied

[Exercise test in coronary insufficiency diagnosis].

If the anamnesis is not conclusive for a definite diagnosis of angina pectoris or if a complementary test is adviseable the ECG, which is hardly ever significant at rest, can become very significant under the influence of physical activity. The easiest methodology is a bicycle ergometer or a treadmill performance test which can be performed under ideal safety conditions and which gives the best possible information. Compared to the coronarography results in 319 patients, the performance test at either maximum heart rate or up to the appearance of the typical electrocardiographic alterations was positive in 75.5% of the cases. It is less instructive if the test is not systematically exhaustive. Its validity also varies depending on the number of coronary arteries affected by stenosis, on the type of the angina pectoris, and the aspect of the ECG at rest. If the test is performed up to the maximum heart rate, its sensitivity is superior to the ones using lsoprenaline or right atrial pacing as a means for influencing the ventricular function.

Coronary Disease↗
PubMed1996

Heart-lung transplantation in situs inversus.

Reconstruction was accomplished in a 2 heart-lung recipients with situs inversus resulting in a left-sided systemic venous atrium. We created a large common atrium that was closed on the left side, leaving an atrial cuff on the inferior right quadrant. To this we anastomosed the donor right atrium, which had been opened laterally between the cavae. This resulted in some clockwise rotation of the ventricles and anterior positioning of the apex. The right pulmonary veins passed superior to the atrial anastomosis and posterior to the donor right atrium. Cardiopulmonary function was excellent in both cases.

Adolescent↗
PubMed2005

Echocardiographic findings in patients meeting task force criteria for arrhythmogenic right ventricular dysplasia: new insights from the multidisciplinary study of right ventricular dysplasia.

OBJECTIVES: The purpose of this study was to quantify the echocardiographic abnormalities in probands who were newly diagnosed with arrhythmogenic right ventricular dysplasia (ARVD). BACKGROUND: The diagnosis of ARVD remains challenging. The Multidisciplinary Study of Right Ventricular Dysplasia was initiated to characterize the cardiac structural, clinical, and genetic aspects of ARVD. METHODS: Detailed echocardiograms were performed in 29 probands and compared with echoes from 29 normal control patients matched for age, gender, body size, and year of echo. Right atrial (RA) and right ventricular (RV) chamber dimensions, RV regional function, and the presence of morphologic abnormalities (hyper-reflective moderator band, trabecular derangement, and sacculations) were assessed. The RV systolic function was calculated as RV fractional area change (FAC). RESULTS: The RV dimensions were significantly increased, and RV FAC was significantly decreased in probands versus control patients (27.2 +/- 16 mm vs. 41.0 +/- 7.1 mm, p = 0.0003). The right ventricular outflow tract (RVOT) was the most commonly enlarged dimension in ARVD probands (37.9 +/- 6.6 mm) versus control patients (26.2 +/- 4.9 mm, p < 0.00001). A RVOT long-axis diastolic dimension >30 mm occurred in 89% of probands and 14% of controls. The RV morphologic abnormalities were present in many probands (trabecular derangement in 54%, hyper-reflective moderator band in 34% and sacculations in 17%) but not in controls. CONCLUSIONS: Probands with ARVD have significant RA and RV enlargement and decreased RV function, which can be easily assessed on standard echocardiographic imaging. These parameters should be measured when ARVD is suspected and compared with normal values.

Adolescent↗
PubMed1999

Radiology of the right ventricle.

RV changes may be generalized into dilatation and hypertrophy. Increased preload results in ventricular dilatation. Increased afterload causes hypertrophy. Change in the shape of the RV resulting from increased afterload and myocardial hypertrophy induces tricuspid regurgitation, which superimposes changes of chamber dilatation onto those of hypertrophy. Sustained ventricular dilatation and hypertrophy frequently progresses to RV failure. In these cases, RV systolic function decreases in association with elevation of RV and right atrial diastolic pressure. Changes in the wall thickness and shape of the RV are variable, and depend upon the severity of the volume or pressure load presented, as well as its duration and rate of progression. Because the RV is an anterior cardiac structure, it occupies little of any heart border. Therefore, the sensitivity of plain film examination to RV disease is limited. Inferential diagnosis of RV disease can often be made based upon identification of other radiographic changes, notably the state of the pulmonary circulation, and the position of the heart in the chest. Conventional contrast right ventriculography may be used to assess the size and position of the RV, as well as associated acquired and congenital lesions that result in RV dysfunction. Due to the unusual shape of the RV cavity, however, and the unpredictable manner in which it dilates, accurate quantitative analysis by this technique is limited. Furthermore, the common association between RV disease and pulmonary hypertension limits the applicability of this imaging technique for evaluating patients with RV disease. Multiplanar MR imaging allows direct demonstration of changes in RV size and wall morphology. Furthermore, application of Simpson's rule to tomographic slices acquired at ventricular diastole and systole allows direct, accurate, and reproducible quantitative analysis of ventricular volume and myocardial mass, allowing radiographic assessment in patients for diagnosis, as well as longitudinally during medical management or after surgical treatment for congenital and acquired diseases that result in RV dysfunction.

Cardiac Output, Low↗
PubMed1988

Anesthetic and hemodynamic effects of the alpha 2-adrenergic agonist, azepexole, in isoflurane-anesthetized dogs.

The authors studied the reduction in anesthetic requirement (MAC) and the hemodynamic effects of the highly selective alpha 2-adrenergic agonist azepexole in isoflurane-anesthetized dogs. Eleven male beagles were anesthetized with isoflurane in oxygen. After a 2-h equilibration period, they determined isoflurane MAC and baseline hemodynamic function. Azepexole (at 0.1, 0.3, and 1.0 mg/kg) was administered via a right atrial port over 15 min, while each dog was given isoflurane at the MAC dose for that animal. Twenty minutes after the end of infusion, at a time when hemodynamic variables were stable, they reassessed hemodynamic function. They then determined isoflurane MAC again. In other experiments, dogs were pretreated with either idazoxan (the alpha 2-adrenergic antagonist; n = 5) or naloxone (the opiate antagonist; n = 7) prior to the administration of azepexole. Isoflurane MAC was determined before and after each dose of azepexole. Isoflurane MAC decreased as the dose of azepexole increased, to the extent that at the highest dose (1 mg/kg) the decrement in MAC was more than 85%. This reduction of MAC caused by azepexole could be completely prevented by pretreatment with idazoxan, while naloxone was without effect. Azepexole did not change mean arterial blood pressure, but caused heart rate and cardiac output to progressively decrease. The MAC-reducing effect of azepexole appears to be mediated by alpha 2 adrenoreceptors. Given the extent of the reduction of MAC, it is unlikely that inhibition of central noradrenergic neurotransmission through agonism of presynaptic alpha 2 adrenoreceptors is the sole explanation, since complete disruption of central noradrenergic tracts decreases MAC by only 40%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗