Drugs online research references
Clin Sci Mol Med Suppl. 1976 Dec;3:481S-483S.
Haemodynamic long-term effects of beta-receptor-blocking agents in hypertension: a comparison between alprenolol, atenolol, metoprolol and timolol.
Lund-Johansen P, Ohm OJ.
1. Oxygen consumption and central haemodynamics were recorded at rest and during exercise in fifty-one men with essential hypertension (W.H.O. stage I) and repeated after 1 year on a single drug: alprenolol (n equals 10), atenolol (13) metoprolol (12) and timolol (16). 2. Mean arterial pressure was significantly reduced in all groups at rest (11-18%) and during exercise (5-11%). Heart rate was significantly reduced in all groups (20-28%) at rest and (17-26%) during exercise. Owing to increase in supine resting and exercise stroke volume in the alprenolol and atenolol group, cardiac index decreased less than heart rate---in contrast to the timolol group where cardiac index was decreased 26-32%. The calculated post-treatment total peripheral resistance was significantly increased at rest and during exercise in the timolol group. In the other groups the total peripheral resistance was significantly increased at rest when sitting, but not at rest when supine and during exercise. 3. It is concluded that the major haemodynamic changes induced in subjects with moderate and mild essential hypertension by these different beta-receptor blockers are the same, but that minor differences exist with respect to effect upon stroke volume and total peripheral resistance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15759&dopt=Abstract
Arch Int Pharmacodyn Ther. 1981 Sep;253(1):22-39.
Central cardiovascular effects of physostigmine in the cat; possible cholinergic aspects of blood pressure regulation.
de Wildt DJ, Porsius AJ.
The cental actions of the lipophilic cholinesterase inhibitor physostigmine were investigated by infusing very low doses (0.8 micrograms up to 18 micrograms per kg) into the left vertebral artery of the anaesthetized cat. A dose as low as 2.7 micrograms per kg reduced blood pressure by about 35%. High doses caused bradycardia. Occlusion of the right vertebral artery shifted the dose-response curve to the left. It seems likely that the hypotension was due to stimulation of muscarinic receptors in the pontomedullary region, since pretreatment with dexetimide administered via the vertebral artery strongly reduced the effect. Mecamylamine and the adrenergic blocking agents metoprolol and piperoxan, infused into the vertebral artery, could not reduce the depressor response and the bradycardic action. Both bilateral cervical vagatomy and peripherally applied N-methylatropine did not change the hypotensive action of physostigmine. This observation points towards a reduction of sympathetic outflow as the possible cause of the depressor effect. Atenolol, given intravenously, diminished the bradycardia to a great extent, whereas N-methylatropine did not significantly alter the negative chronotropic action of physostigmine. These results suggest a dominant role for the sympathetic system in reducing cardiac frequency. After intravenous administration, only doses higher than 28 micrograms per kg evoked hypotension, which could not be blocked by intravenously administered N-methylatropine. However, centrally infused dexetimide considerably antagonized this effect, indicating that the hypotension was brought about by a central action and not evoked peripherally. Application of the drug via the external carotid arteries resulted in hypotension after considerably higher doses than those following administration via the vertebral artery, indicating the pontomedullary region as the main site of action. It is concluded that the present experimental data obtained with physostigmine support the hypothesis that ACh might have a transmitter role in the central haemodynamic control.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6119963&dopt=Abstract
J Appl Physiol. 1988 Jun;64(6):2647-52.
Effects of beta-adrenergic agents in lungs of normal and air-embolized awake sheep.
Bonsignore MR, Jerome EH, Culver PL, Dodek PM, Staub NC.
Cardiovascular Research Institute, University of California, San Francisco 94143-0130.
It is unclear whether beta-adrenergic agonists or antagonists affect lung liquid and protein exchange by changing pulmonary hemodynamics or microvascular leakiness. In 23 unanesthetized, instrumented sheep with long-term lung lymph fistulas, we assessed the effect of the beta-agonist terbutaline or the beta-antagonists propranolol, nadolol, and atenolol, all infused intravenously, on lung lymph flow under base-line conditions and during the acute lung injury caused by 4 h of venous air embolism. Under base-line conditions, neither beta-stimulation nor blockade had any effect. During air embolism, terbutaline decreased pulmonary vascular resistance and lymph flow by 25%. Propranolol and nadolol (non-selective beta 1,beta 2-antagonists) but not atenolol (selective beta 1-antagonist) also decreased lymph flow by 22% on average. We favor the more conservative (hemodynamic) over the more liberal (altered permeability) explanation for our results. First, beta-stimulation clearly caused vasodilation, which lowered the pulmonary microvascular pressure at the site of injury. beta-blockade caused changes similar to alpha-stimulation (J. Appl. Physiol. 62: 2147-2153, 1987). We therefore interpret the beta-blockade as unmasking pulmonary arterial alpha-receptors stimulated by the air-embolism injury, thus allowing vasoconstriction upstream to the site of injury. We do not believe the explanation of the beta-agent effects requires any modulation of lung microvascular leakiness by beta-adrenergic agents.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2900234&dopt=Abstract
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