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Hypertension. 1981 Mar-Apr;3(2):262-8.
Short-term systemic hemodynamic adaptation to beta-adrenergic inhibition with atenolol in hypertensive patients.

Simon G, Franciosa JA, Gimenez HJ, Cohn JN.

Early systemic hemodynamic adjustments to antihypertensive therapy with the cardioselective beta inhibitor, atenolol, were investigated in 12 hospitalized men, mean age 52 years, with uncomplicated mild-to-moderate essential hypertension. Twice daily measurements of cardiac output (CO) by CO2 rebreathing, blood pressure by cuff, and heart rate were performed in all subjects for 3 days before and 5 days after initiation of oral atenolol therapy (50 or 100 mg daily). Cardiac output by CO2 rebreathing was checked with dye dilution just before, and 4 hours and 4 days after the start of therapy. Plasma volume (radioiodinated albumin) was measured before therapy and on Day 5 of therapy. The CO results obtained with the two methods were not significantly different (r = 0.88, p less than 0.01, n = 12). A reduction in heart rate, 18 +/- 2 beats/min (mean +/- SE), occurred in all patients while taking atenolol. By 4 hours after the first dose of atenolol, CO fell from 5.49 +/- 0./30 to 4.24 +/- 0.21 liters/min (p less than 0.01), while the control mean arterial pressure (MAP) of 108 +/- 4 mm Hg was not significantly changed, 110 +/- 4 mm Hg. At 24 hours, CO returned near baseline (5.10 +/- 0.21 liters/min) but MAP was reduced (95 +/- 3 mm Hg, p less than 0.001) and remained so thereafter. CO remained at baseline at 48 hours (5.50 +/- 0.29 liters/min) but fell again (p less than 0.01) to 4.81 +/- 0.11 on Day 4 and to 4.68 +/- 0.25 liters/min on Day 5 of atenolol therapy. Plasma volume, 3110 +/- 100 ml before therapy, was reduced to 2850 +/- 100 by Day 5 of atenolol therapy (p less than 0.01). The findings indicate a delayed onset of the antihypertensive action of atenolol. The transient return to baseline of CO on Day 2 and 3 of atenolol therapy suggests a reverse autoregulatory adjustment to the initial fall in CO.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6111532&dopt=Abstract




J Cardiovasc Pharmacol. 1989 Sep;14(3):412-8.
Positive inotropic and hemodynamic properties of flosequinan, a new vasodilator, and a sulfone metabolite.

Falotico R, Haertlein BJ, Lakas-Weiss CS, Salata JJ, Tobia AJ.

Research Laboratories, Ortho Pharmaceutical Corporation, Raritan, New Jersey 08869.

Flosequinan, a new orally active vasodilator, and its sulfone metabolite were evaluated for inotropic activity in isolated ferret papillary muscles and pentobarbital anesthetized open-chest dogs. In vitro, flosequinan and its sulfone derivative increased tension development in a concentration-dependent manner (1-50 microM) in electrically stimulated papillary muscles pretreated with the beta-adrenergic blocking agent atenolol (2 microM). Peak increases in tension of 75 +/- 17%, and 111 +/- 46% with potencies (EC50) of 15 and 10 microM were observed for flosequinan and its metabolite, respectively. In vivo, flosequinan increased left ventricular dP/dtmax (74 +/- 12%) and right ventricular contractile force (CF) (104 +/- 10%) after administration of 1.875 mg/kg, i.v. Inotropic activity was dose-dependent and remained elevated for at least 60 min postinfusion. Flosequinan also increased heart rate (HR) (14 +/- 2%) and reduced mean arterial pressure (-9 +/- 3%). The i.v. potency of flosequinan (ED50 = 0.45 mg/kg) and its metabolite (ED50 = 0.38 mg/kg) were similar to that of the inotropic vasodilator amrinone (ED50 = 0.38 mg/kg). Inotropic activity was not significantly altered by pretreatment with propranolol (0.5 mg/kg) and atropine (1.0 mg/kg), further supporting the in vitro data indicating that flosequinan can directly stimulate myocardial contractility independent of beta-adrenergic receptor activation. Additional hemodynamic studies were conducted in an acute heart failure model produced by an overdose of propranolol. Flosequinan (2 mg/kg, i.v.) increased cardiac output (CO) (50 +/- 9%) and stroke volume (SV) (29 +/- 8%) while reducing total peripheral vascular resistance (TPR) (-36 +/- 4%), right atrial pressure (-62 +/- 5%), and left ventricular end-diastolic pressure (LVEDP) (-41 +/- 2%).(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2476620&dopt=Abstract




Acta Obstet Gynecol Scand. 1996 Feb;75(2):120-6.
Central and peripheral hemodynamics in severe preeclampsia.

Yang JM, Yang YC, Wang KG.

Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan, R.O.C.

BACKGROUND: Doppler velocimetry, a new tool for measuring blood flow, vascular resistance, and central hemodynamics can be applied to monitor those patients at risk and provide therapeutic concepts for preeclampsia. This study was designed to use a Doppler velocimetry study to correlate the relationship between central hemodynamics, uteroplacental circulation, and the perinatal outcome in severe preeclampsia. METHODS: Thirty-one patients with severe preeclampsia, not superimposed with any medical disorder and not on antihypertensive treatment prior to admission, were enrolled in this study. On admission, laboratory determination of the maternal blood chemistry and hematogram, together with a Doppler ultrasound study of the maternal hemodynamics, and umbilical and uterine arteries, were performed. Antihypertensive agents including hydralazine, atenolol, and labetolol were given according to the state of the maternal central hemodynamics. Data were collected on the general status of the patients, the results of the Doppler ultrasound study, and the perinatal outcome. RESULTS: Patients were divided into three groups based on the systemic vascular resistance. The left ventricular function and cardiac index declined with increase in vascular resistance. The high-resistance group had a significantly high incidence of infants small for gestational age. Poor fetal growth in the high-resistance group could be attributed to the summation of underperfusion due to decreased uteroplacental blood flow and was frequently associated with maternal hemoconcentration. CONCLUSIONS: Although global vasospasm has been considered to be the basic pathophysiology of preeclampsia, the central hemodynamics varies between, and even in the same, patients. Regional vasospasm in the uteroplacental circulation occurs earlier than in the systemic circulation as a whole. A high cardiac-output in low systemic-vascular-resistance might compensate in those pregnancies with high uterine artery resistance to maintain adequate uteroplacental perfusion.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8604596&dopt=Abstract












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