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1.
Cardiovasc Res ; 14(8): 490-4, 1980 Aug.
Article in English | MEDLINE | ID: mdl-7438151

ABSTRACT

The flip-flop producing a pulse proportional to the transit time of an ultrasonic burst between two piezoelectric crystals was often reset by transmission artefacts in sonomicrometers. A design improvement was made. The insertion of two monostable vibrators and one nand gate corrected the resetting caused by transmission artefacts. The new design produced a flip-flop pulse that was proportional to the transit time of the ultrasonic burst through the aorta. Ascending aortic diameter was monitored in unanaesthetised dogs for 6 to 8 weeks using the new design.


Subject(s)
Aorta/anatomy & histology , Ultrasonics/instrumentation , Ultrasonography , Animals , Biometry , Dogs , Electronics, Medical , Female , Male , Monitoring, Physiologic/instrumentation
2.
J Pharmacol Exp Ther ; 200(1): 195-206, 1977 Jan.
Article in English | MEDLINE | ID: mdl-833757

ABSTRACT

Ro 2-2985 increased mean arterial blood pressure in both the venous bypass preparation and the intact animal; however, total peripheral resistance increased in the venous bypass preparation with a constant cardiac output but decreased in the intact animal with an increase in cardiac output. These observations indicate a drug-related increase in the distensibility of the aorta at the same arterial pressure. In vivo ventricular function curves were shifted to the left indicating enhanced myocardial performance with the translocation of large volumes of blood to the central circulation since total body venous compliance was significantly decreased. Beta adrenergic blocking doses of propranolol blocked the positive inotropic effect of Ro 2-2985 while myocardial depression produced by toxic doses of propranolol was reversed. This observation suggests several mechanisms for the Ro 2-2985 metabolic mediation of myocardial muscle contraction. The cardiovascular effects produced by Ro 2-2985 were accompanied by a marked polycythemia and a decrease in plasma volume without a change in total circulating blood volume, while blood glucose values showed a nonsignificant increase. Ro 2-2985 produced a marked increase in cardiac output. The increase in myocardial performance appears to be complex since myocardial force of contraction, dT/dt, dP/dt:P40 and Vmax were all increased. RO 2-2985 increased coronary flow without an increase in resistance. There were no significant increases in myocardial arteriovenous glucose, lactate, K+, Ca++, Na+ or Cl.


Subject(s)
Anti-Bacterial Agents/pharmacology , Hemodynamics/drug effects , Lasalocid/pharmacology , Animals , Blood Pressure/drug effects , Blood Volume/drug effects , Cardiac Output/drug effects , Coronary Vessels/physiology , Dogs , Drug Interactions , Electrocardiography , Energy Metabolism/drug effects , Female , Heart/drug effects , Heart Rate/drug effects , Male , Myocardial Contraction/drug effects , Myocardium/metabolism , Propranolol/pharmacology , Time Factors
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