SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Surgical repair of atrial septal defect in adults reduces right ventricular and right atrial diameters and volumes, and improves left ventricular filling.
Adenosine depresses atrioventricular (AV) nodal function by binding to specific A1 receptors which activate the acetylcholine, adenosine-regulated potassium current. In addition, adenosine can act to antagonize the effects of beta-adrenergic stimulation on AV nodal function. To assess the negative dromotropic effects of adenosine under beta-adrenergic stimulation, 15 patients were studied during clinical electrophysiologic study. During high right atrial pacing at a cycle length of 400 to 600 ms, adenosine was injected intravenously at an initial dose of 0.5 mg followed by a stepwise increment of 0.5 or 1.0 mg given at 5-minute intervals until a maximal dose of 12 mg was achieved or AV block developed. Intravenous isoproterenol (1 to 3 micrograms/min) was then infused to accelerate sinus rate by 20 to 30% during which intravenous injection of incremental doses of adenosine as described was repeated. The AV nodal conduction time (AH interval) was measured at each dose of adenosine. Dose-response curves of AV nodal conduction time (expressed as percent increase in AH interval) were studied during the control state and during isoproterenol infusion. The dose of adenosine required to produce AV nodal Wenckebach block, the increase in the AH interval by 50% (ED50) and the maximal response (Emax) were 3.4 +/- 0.9 mg, 1.8 +/- 0.9 mg and 60 +/- 4%, respectively, in the control state, and 3.7 +/- 0.8 mg, 2.0 +/- 0.7 mg and 56 +/- 4%, respectively, during isoproterenol infusion. No significant changes in ED50, Emax and the dose of adenosine yielding AV nodal Wenckebach block could be demonstrated between the control state and during isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
The kidney is a complex endocrine organ, and many of the renal hormones have actions that help regulate renal function. Although we have much more to learn about the role of most of these hormones in the regulation of renal function in both the newborn and adult kidney, there are some important aspects to keep in mind as we approach therapeutic interventions in sick newborn and premature infants. Because of the many interactions between hormonal systems, drugs that we may use for specific actions on one system may have effects on others as well (ACE inhibitors, cyclooxygenase inhibitors, dopamine antagonists). In addition, it is clear that the state of the organism may play a role in which of the renal hormones is active. Finally, the nonrenal hormonal systems that affect renal function (aldosterone, atrial natriuretic peptide, vasopressin, etc) may interact to change further expected results of any therapeutic intervention. Therefore, it behooves the clinician to monitor carefully renal function whenever modifications in therapy are made, whether it is a change in mechanical or pharmacologic intervention.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Left atrial appendage (LAA) function and flow patterns in 29 patients with chronic nonrheumatic atrial fibrillation were studied by transesophageal echocardiography. These 29 patients (16 men and 13 women; mean age, 63.8 years; range, 38 to 77 years) were classified into two groups according to different LAA flow patterns. Seventeen patients (group 1) had well-defined LAA emptying and filling Doppler flow signals, and the other 12 patients (group 2) had very low LAA flow signals. No significant differences were found in age, sex, mean duration of atrial fibrillation, left ventricular end diastolic dimension, and left ventricular ejection fraction between the two groups. However, group 2 patients had larger left atrial diameter (42.8 +/- 4.2 mm vs 36.6 +/- 8.8 mm; p < 0.05), lower LAA ejection fraction (26.4 +/- 15.2 percent vs 42.6 +/- 14.1 percent; p < 0.05), and lower LAA peak emptying velocity (0.13 +/- 0.03 m/s vs 0.36 +/- 0.16 m/s; p < 0.001). Higher incidence of LAA spontaneous echocardiographic contrast formation in group 2 patients (8/12 vs 1/17; p < 0.001) was noted. In conclusion, a subset of patients with nonrheumatic atrial fibrillation were found to have lower LAA blood flow and poorer LAA function. These patients had higher incidence of left atrial or LAA spontaneous echo contrast formation which had been proved previously to be a marker for future systemic thromboembolism.
Ischemic preconditioning (IPrec) improves post-ischemic dysfunctions of the myocardium along with activation of protein kinase C isozymes including PKCdelta. Moreover, expression of cardio-protective determinants can reduce ischemic damages. Because IPrec is limited in aged hearts, we assessed in an experimental model the impact of aging on PKCdelta and selected protective proteins in the preconditioned myocardium from adult (< or =55) and older (> or =70 years) humans. Adult myocardium showed PKCdelta up-regulation after IPrec along with improved post-ischemic contractility. Although there was no functional benefit, PKCdelta increased in older myocardium as well. Subsequent mRNA analyses demonstrated that IPrec stabilizes the mRNA expression of protective proteins (Hsp70, Bcl-2/-xL, IAPs) in both aging groups. Moreover, older hearts revealed increase in post-ischemic Hsp90beta. Our study indicates, that IPrec conserves the expression of cardio-protective determinants in aged hearts despite limited functional recovery.
This article examines the factors that affect the transmission of airway pressures to intrathoracic structures. The effects of positive end-expiratory pressure on central venous pressures, cardiac filling pressures, and right and left ventricular function are discussed. Various techniques for estimating intrathoracic pressures and their limitations are reviewed.
OBJECTIVE: The aim was to clarify the mechanism of the following observations: (1) left ventricular pressure recordings during diastole have shown that the minimum pressure at the base is greater than that at the apex; (2) echocardiographic measurements of the short axis dimension of the left ventricle during early filling have shown that the maximum rate of increase at the base occurs before that at mid-cavity. These observations cannot be explained on the basis of simple pressure-volume relationships and suggest that diastolic haemodynamics are more complex. METHODS: A numerical (computer) model of early diastolic filling was developed. The model represents the atrium and ventricle as distensible cylinders connected by a valve. Parameters in the model such as ventricular stiffness and rate and duration of relaxation can be varied and the resulting haemodynamic changes observed. RESULTS: Despite the simplicity of the model and the omission of several physiological variables, intracavity pressure gradients and the phase relation of radial wall movements are generated that appear to be similar to those found in the human heart. CONCLUSIONS: The results suggest that these observations can be explained by inflow causing a pressure disturbance at the base which propagates to the apex, and which is reflected back to the base. The time between peak rate of change of short axis dimension at the base and mid-cavity may thus be a practical way of assessing diastolic function independently of loading conditions. These values can easily be measured by M mode echocardiography.
Previous studies on allosteric interactions at muscarinic receptors have often focused on ligand-receptor binding interactions, because ligand binding seemed to reflect functional consequences. The prototypal allosteric agent alcuronium is known to bind with similar affinity to the M(2) subtype of muscarinic acetylcholine receptors whether or not the receptors are occupied by the agonist pilocarpine. To determine allosteric modulation of receptor signaling by alcuronium, the effects of pilocarpine were measured in contracting guinea pig left atria and on G-protein coupling in M(2)-transfected Chinese hamster ovary (CHO) cell membranes. Alcuronium dose-dependently suppressed pilocarpine-induced reduction of isometric contraction force in atria (pIC(50, Alc) = 5.63) without any effect on the EC(50) of pilocarpine, consistent with an allosteric mechanism. In contrast, alcuronium shifted the concentration-effect curve of the agonist oxotremorine M to the right without affecting the maximal effect, in a formally competitive manner (pK(A, Alc) = 5.54). If pilocarpine remained receptor bound in the presence of alcuronium, this indicates that pilocarpine can no longer act as an agonist. In support of this hypothesis, pilocarpine acted as a competitive antagonist against oxotremorine M in the presence of 10 microM alcuronium. Measuring guanosine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding in CHO-M(2) membranes yielded similar results. Alcuronium suppressed pilocarpine-induced stimulation of [(35)S]GTPgammaS binding (pIC(50, Alc) = 5.47) without shift in EC(50), whereas it competitively shifted the response to oxotremorine M (pK(A, Alc) = 5.97). [(3)H]Oxotremorine M binding data corresponded with the functional findings. In conclusion, alcuronium converted the agonist pilocarpine into an antagonist-a novel type of functional allosteric interaction.
Aldosterone antagonism has emerged as an important strategy for end-stage congestive heart failure. To evaluate the potential contribution of aldosterone towards the cardiac complications of diabetes, this study examined the effects of chronic aldosterone receptor blockade (with spironolactone) on isolated working heart function in streptozotocin (STZ) - induced diabetic rats. Wistar rats were divided into four groups: control, control spironolactone-treated, diabetic, and diabetic spironolactone-treated. Following chronic spironolactone treatment (8 weeks), cardiac function was assessed in terms of the rate of contraction (+dP/dT), rate of relaxation (-dP/dT), and left ventricular developed pressure (LVDP). Untreated diabetic rats exhibited marked cardiac dysfunction when compared with age matched controls (p < 0.001). Long-term spironolactone treatment did not improve these parameters. These data demonstrate the lack of beneficial effects of aldosterone receptor blockade on isolated working heart function in diabetes.
Vascular reserve, which defines the capacity for further vasodilation in a given physiological or pathological condition, has not been measured in the canine atria. This study defines, in normal dogs, the regional vascular reserve simultaneously measured in the atria (appendage, nonappendage regions) and in the ventricles during rest and two levels of exercise. Blood flow was determined using 11.4 +/- 0.1 microns radiolabeled microspheres. Vascular reserve (percent for each region) is the ratio of vascular conductance during each condition to maximum vascular conductance. Maximum vascular conductance was estimated by infusing adenosine intravenously. For a given physiological condition regional vascular conductance varied two- to threefold. The vascular reserve of each of the regions decreased progressively from rest to mild exercise to moderate exercise. Regional vascular reserve for both atria, the right ventricle, and the epicardial layer of the left ventricle was essentially uniform for a given condition: rest 93 +/- 0.4%, mild exercise 81 +/- 1.2%, and moderate exercise 69 +/- 1.5%. This similarity in vascular reserve implies that for a given physiological condition a common mechanism precisely regulates myocardial perfusion in these cardiac regions as a function of the total vasodilator capacity.
Adenosine, an endogenously produced nucleoside, has direct negative chronotropic and inotropic effects on right and left atrial tissues, respectively. Age-related differences in the effects of A1 adenosine receptor activation on atrial rhythmic and contractile function were investigated in adult (6-8 months) and senescent (23-24 months) Fischer 344 (F344) rats. Senescent right atria (RA) were more sensitive to the negative chronotropic effects of R-phenylisopropyladenosine (R-PIA), a selective A1 receptor agonist, than adult RA (EC50: 4.8 +/- 0.7 vs 10.8 +/- 1.5 nM). However, senescent left atria (LA) were 15.4% less responsive to the maximal negative inotropic effects of R-PIA than adult LA. R-PIA did not significantly change resting force from basal values in either age group, but 90% relaxation time was prolonged threefold in senescent LA compared with adults. Radioligand binding experiments with 1,3-[3H]dipropyl-8-cyclopentylxanthine, a selective adenosine A1 receptor antagonist, showed a 56% greater density (Bmax) of adenosine A1 receptor in senescent than adult without differences in affinities (Kd). The increased sensitivity of senescent RA to the negative chronotropic effects of adenosine A1 receptor stimulation suggests a role for adenosine in abnormal sinus node function that occurs more frequently with age. Adenosine A1 receptor stimulation has more effect on relaxation than contraction in senescent LA compared with LA from adult F344 rats. However, the increase in density of adenosine A1 receptors suggests a functional dissociation between the availability of binding sites and receptor activation.
STUDY OBJECTIVE: Acute renal failure, which is a serious complication following open heart surgery, has a high mortality rate. Previous reports have shown that the calcium antagonist diltiazem is beneficial either as an adjunct to cardioplegic solution or perioperative treatment for preservation of postoperative cardiovascular function. We studied the effects of diltiazem on renal function, plasma atrial natriuretic peptide levels, and the renin-angiotensin-aldosterone system in patients who had undergone coronary artery bypass grafting. PATIENTS AND MEASUREMENTS: Diltiazem was administered, 0.1 mg/kg, in a bolus injection followed by continuous infusion at a rate of 2 micrograms/kg/min during surgery, and 30 mg through a nasogastric tube at every 8 h. Hemodynamics, renal function, and plasma hormone levels were measured in the diltiazem-treated group (n = 13) and the nontreated group (n = 10). RESULTS: Heart rate, mean arterial pressure, and systemic vascular resistance index in the diltiazem-treated group were significantly lower than those in the nontreated group following cardiopulmonary bypass. Urine volume, creatinine clearance, and free water clearance were well preserved in the diltiazem-treated group. However, plasma renin activity and aldosterone levels were significantly higher in the diltiazem-treated group with the same changes in plasma atrial natriuretic peptide levels. CONCLUSION: Perioperative treatment with diltiazem has a beneficial effect on postoperative renal function, and reflex sympathetic activation induced by peripheral vasodilation activated the renin-angiotensin-aldosterone system.
We compared several electrophysiological variables before and after Mustard and Senning procedures in 14 mongrel dogs and made the following three observations. First, after the Senning operation, the atrial activation in the areas of the anterior and middle internodal tracts is undamaged. After the Mustard procedure, however, conduction through the interatrial septum is practically abolished. Both techniques damage the area of the posterior internodal tract. On the whole, there is greater dispersion of atrial epicardial mapping with the Senning operation. Second, several degrees of depression in the sinus node automatism and intraatrial conduction were observed with both techniques. Third, atrioventricular block in various degrees was observed only after the Mustard procedure. The atrioventricular dissociation observed after the Senning operation was dependent on sinus pacemaker dysfunction only. We think that from the electrophysiological point of view, the Senning procedure is a valid alternative for repair of transposition of the great arteries.
Explore the source record for details and available documents.
Single-fiber atrial type B receptor activity was recorded from the cervical vagus nerves in 8 dogs during head-out water immersion (HOWI) to simulate weightlessness. The receptor activity was not affected by the water immersion, changing insignificantly from 4.4 +/- 0.9 (SEM) impulses per cardiac cycle (imp/cycle) before HOWI to 4.3 +/- 0.5 imp/cycle immediately on HOWI. At the end of 30 min of HOWI, the receptor activity was 3.9 +/- 1.2 imp/cycle (p > 0.05) while immediately after the immersion it was 4.1 +/- imp/cycle again statistically insignificant (p > 0.05). When expressed as imp/min, the activity before HOWI (803 +/- 142) rose marginally to 826 +/- 116 at the beginning of immersion (p > 0.05), but this trend was not maintained. The urine flow which was measured in 4 female dogs in a different set of experiments, did, however, increase significantly immediately on immersion from 0.89 +/- 0.21 (SEM) to 1.9 +/- 0.35 ml/min (p < 0.02). Therefore, in the dog model developed for single-fiber study during HOWI, atrial type B receptor activity is not affected, and the diuresis which was observed during HOWI could be attributed to other mechanisms.
From May 1995 to October 1996, 20 patients with mitral valve disease underwent the maze procedure for chronic atrial fibrillation and mitral valve replacement or mitral valvuloplasty. Epicardial mapping data demonstrated that the large macrorecurre flutter circuit was located in left atrium (14/20) and complex fibrillation in right atrium (18/20) of the majority of patients. No early death occurred. 20 patients were followed up for at least 3 months (range 3-20 months) and 14 patients for at least 1 year after operation, sinus rhythm and atrioventricular synchrony were restored (100%), atrial fibrillation was not induced by electrophysiologic study. The right and left atrial transport function was preserved (100%) by Doppler echocardiogram tracings. One patient died from acute necrotic hepatitis, 4 and half months after operation. Cox maze procedure was modified, atrial flutter and atrial fibrillation never occurred. In this study, the electrophysiologic mechanism of chronic atrial fibrillation associated with mitral valve disease, indications of operation and clinical results are discussed.