[Ventricular afterload and transmitral Doppler flow profile: effects of the diving test]. / Postcarico ventricolare e profilo Doppler di flusso transmitralico: effetto del diving test.

The influence of loading conditions on mitral flow velocity profile was studies by pulsed wave Doppler echocardiography in 10 normal subjects during diving test (5 min face exposure to iced water). The cold stimulus increased blood pressure (p less than 0.001), peripheral resistances (p less than 0.001), peak-systolic and end-systolic left ventricular (LV) meridional wall stresses (p less than 0.005). No significant change was found in heart rate. LV end-diastolic volume was unchanged, while LV end-systolic volume increased (p less than 0.005). Consequently, LV fractional shortening decreased (p less than 0.001). Thus, in spite of enhanced LV contractility (assessed by a significant increase in LV end-systolic stress to volume ratio, p less than 0.02) LV pump performance fell, because of prevailing afterload as well as lack of acute recruitment of LV preload reserve (afterload-contractility mismatch). Such an increase in LV afterload was associated with remarkable changes in LV diastolic dynamics: isovolumic relaxation time (IRT) was prolonged (p less than 0.001) and ventricular filling was relatively displaced towards late diastole (peak early to peak atrial velocities ratio, pE/pA: 1.5 +/- 0.3 vs 1.9 +/- 0.3 p less than 0.001; peak atrial filling rate: 326 +/- 47 vs 242 +/- 38 ml/s; p less than 0.001; normalized late diastolic velocity: 0.87 +/- 0.10 vs 0.73 +/- 0.06; p less than 0.01). Also, IRT values significantly correlated with pE/pA values (r = -0.75; p less than 0.001). In conclusion, diving test produced important changes in LV hemodynamics which, in turn, influenced LV relaxation and filling pattern. Our results indicate that operative LV loading conditions should be considered when assessing diastolic function by the analysis of transmitral Doppler flow profile.

Effects of ketanserin on transmembrane sodium transport in erythrocytes.

Ketanserin, an antagonist of 5-HT2-serotonergic and alpha 1-adrenergic receptors, has come into use for the therapy of mild to moderate arterial hypertension. Quite recent observations have shown changes in transmembrane sodium (Na) transport after the acute administration of high doses of this drug to normal subjects. It is well known that some of these transport systems have an altered activity in essential hypertension. We evaluated the effects of long-term (3 months) administration of ketanserin (40-80 mg/day) on Na and potassium (K) intracellular concentrations and transmembrane fluxes in red blood cells (RBCs) from 12 essential hypertensive patients. In addition the present study describes the in vitro effects of two different concentrations of the drug (5 x 10(-8) and 5 x 10(-7) M) on erythrocytes in normal subjects. In the first study, both systolic and diastolic blood pressure were significantly lowered by the treatment with ketanserin (from 165/103 to 143/89; p less than 0.001). Na and K intraerythrocyte concentrations fell markedly during ketanserin administration (both p less than 0.001). A marked decrease in Na,K-pump activity (p less than 0.001) and an increase in Na,lithium(Li)-countertransport function (p less than 0.001) were observed. Na outward cotransport, Na leak, and K leak were not modified by the therapy. Direct correlation was found between the fall in mean blood pressure and in Na and K intraerythrocyte concentration (respectively, p less than 0.01 and p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Sublingual and intravenous ketanserin versus sublingual nifedipine in the treatment of severe hypertension: a randomized study.

Thirty-seven patients with severe hypertension were randomly assigned to receive 20 mg of ketanserin sublingually, 10 mg of ketanserin intravenously, or 20 mg of nifedipine sublingually. Systolic and diastolic blood pressures fell significantly after the three treatments. The maximum effects were reached 25 minutes after sublingual ketanserin (with decreases of 7.7% in systolic and 7.1% in diastolic blood pressure), six minutes after intravenous ketanserin (decreases of 9.4% and 9.6%, respectively), and 25 minutes after sublingual nifedipine (decreases of 16.9% and 15.9%, respectively). Blood pressure returned to pretreatment levels 20 minutes after intravenous ketanserin. Heart rate increased significantly in the group receiving nifedipine. No changes in plasma aldosterone, sodium, or potassium levels or in erythrocyte sodium and potassium levels were found after ketanserin. It is concluded that even intravenous ketanserin is inferior to sublingual nifedipine in the control of blood pressure.