Drugs online research references
Arq Bras Cardiol. 1989 Jan;52(1):19-22.
[Postoperative atrial fibrillation in myocardial revascularization]
[Article in Portuguese]
Sgarbieri RN, de Freitas JN, Evora PR, Brasil JC, Ribeiro PJ, Otaviano AG, Bongiovanni HL, Menardi AC, Ferez MA.
Many studies have demonstrated fairly high incidence of supraventricular arrhythmias after coronary artery bypass surgery, and have tried to identify preoperative, operative and postoperative factors related to their appearance. The present paper analysed 186 patients submitted to coronary artery bypass and reported a incidence of atrial fibrillation of 6.04% (11 cases). The male sex was dominant (81.2%) with ages varying from 49 to 73 (mean 54.58) years. The preoperative incidence of diabetes, smoking and systemic hypertension were, respectively, 18.2%, 54.51% and 36.4%. The mean number of vessels bypassed was 2.42 +/- 1.19 and the left circumflex artery was involved in 81.20% of these cases. Cardiopulmonary bypass time was 100 +/- 39.6 min and ischemic arrest time of 79.6 +/- 37.7 min. Single double stage cannulae for venous drainage were used in 45.5% of the patients and ventricular fibrillation and cardiac overdistention occurred in 63.60% immediately after CPB. Atrial fibrillation presented around 1.66 +/- 2.17 days in the postoperative period and 45.5% of the patients had more than one distinct episode of the arrhythmia. Treatment constituted of cardioversion in 25%, atenolol oral in 18.75% and digitalis associated to quinidine in 56.25%. These numbers permit us to suggest that some of the above factors may contribute to the genesis of arrhythmias, such as single double stage cannulation for venous drainage, inadequate myocardial protection, overdistention and cardiac fibrillation and, mainly, the presence of proximal circumflex artery obstructions responsible for atrial ischemia before and during surgery.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2818236&dopt=Abstract
Kardiologiia. 1991 Feb;31(2):34-6.
[Changes in diastolic filling of the heart during isometric exercise test in patients with ischemic heart disease treated with atenolol]
[Article in Russian]
Surovov IuA, Ul'ianova KN, Sedov VP, Sidorenko BA.
Changes in left diastolic filling which had been caused by treatment with the beta-adrenoblocker atenolol given in a dose of 50-100 mg/day were studied in 66 patients with Functional Class I-II exercise-induced angina pectoris. Echocardiography was performed during isometric exercise tests before and 7-9 days after drug administration. It was ascertained that not only ino- and chronotropic mechanisms, but redistribution in diastole patterns in the direction of increasing atrial systole were involved to adequately maintain cardiac output during exercise. Ejection fraction became higher in response to exercise with predominant myocardial mass, whereas atrial systolic fraction, with predominant dilatation. The drug produced its negative inotropic effect in the patients with predominant left ventricular dilation; a decrease in the rapid filling fraction was not followed by an increase in the atrial systolic fraction, which may be regarded as an early sign of myocardial failure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2041287&dopt=Abstract
Life Sci. 1983 Jul 25;33(4):371-6.
Presynaptic mediation by alpha 2-, beta 1- and beta 2-adrenoceptors of endogenous noradrenaline and dopamine release from slices of rat hypothalamus.
Ueda H, Goshima Y, Misu Y.
Using high performance liquid chromatography with an electro-chemical detector, we studied effects of different compounds on the impulse-evoked release of endogenous noradrenaline (NA) and dopamine (DA) release from slices of the rat hypothalamus. Adrenaline (10(-7) M), with a potent alpha-agonistic action decreased both NA and DA release, and these effects were blocked by pretreatment with yohimbine (10(-7 M). The alpha 2-antagonist, yohimbine alone (10(-8) - 10(-6) M) concentration-dependently increased these releases, while alpha 1-antagonist, prazosin showed weak increase on NA but not DA release at 10(-6) M. Isoproterenol (10(-10) - 10(-8) M) concentration-dependently increased these releases and the effects were antagonized by pretreatment with a non-selective beta-antagonist, 1-propranolol, a beta 1-antagonist, atenolol or a beta 2-antagonist, butoxamine. 1-Propranolol (3 X 10(-7) M) alone, but not the d-isomer inhibited the releases. Thus, in the rat hypothalamus, the release of NA and DA may be mediated via presynaptic alpha 2-, beta 1- and beta 2-adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6135966&dopt=Abstract
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