The systemic pressor issues of angiotensin II (ANGII) are well described.

The systemic pressor issues of angiotensin II (ANGII) are well described, whereas relatively little is known regarding its drifts on the pulmonary circulation in humans. Doppler echocardiographic measurements were performed in eight normal tenders after a 30-min control infustion (baseline), after sequential 30 min stepwise infusions of ANGII (2 4 and 6 ng/kg/min), and again 30 min after stopping ANGII therapy. There were significant dose-related increases in mean pulmonary arterial urgency and total pulmonary vascular resistance, with values returning to baseline after stopping ANGII therapy. However, the increase in vascular resistance was proportionately greater for the pulmonary compared with systemic vascular bed, and the difference was significant at all doses of ANGII. Thus, the pulmonary vasculature exhibited greater sensitivity to the vasoconstrictor issues of ANGII in comparison with the systemic vasculature.

Activation of the renin-angiotensin rule occurs in patients with hypoxemic cor pulmonale, with raised circulating plains of angiotensin II (ANGII) and aldosterone (ALDO).[1-3] The elevated flats of ALDO are responsible for producing renal-mediated sodium and water retention that manifests as edema in patients with cor pulmonale.[1] The systemic pressor validitys of ANGII are well documented,[4] whereas there is relatively little known regarding its powers on the pulmonary circulation in humans. There is a evidence from animal studies to glance at that ANGII may act in a facilitatory fashion at sensitizing the pulmonary vascular bed to the vasoconstrictor issues of hypoxemia.[5,6] The final cause of the present study was to investigate the dose-response relationship of ANGII upon the pulmonary vascular bed using the noninvasive technique of Doppler ultrasound.

METHODS

Subjects

Eight normotensive male offers (age, 24 [+ or -] 3 years) were studied after they had given written informed compliance to a protocol approved from the Tayside Committee for Medical Ethics. All make subordinates underwent a full physical examination, 12-lead electrocardiogram, echo-Doppler examination, urea and electrolyte and satiated blood cell count, results of all of which were required to be normal.

Protocol

All make liables were studied at the same time in the morning (9 AM). in succession arrival at the laboratory, controls were placed in a supine position and they remained in this position for the duration of the thought An indwelling intravenous cannula was inserted into each antecubital fossa, united for infusion of ANGII and the other for progeny sampling. Baseline measurements were made after an initial intravenous have the direction of infusion of 5 percent dextrose in order to obtain a resting basal hemodynamic state. Sequential incremental 30-min infusions of ANGII (Clinalfa, Laufelfingen, Switzerland) were then given in doses of 2 ng/kg/min, 4 ng/kg/min, 6 ng/kg/min. A final risk of measurements were then made 30 min after stopping the 6-ng/kg/min dose of ANGII (Off) to ascertain whether parameters had go [i]or[/i] come backed to preinfusion baseline values.

Hemodynamic Measurements

All hemodynamic parameters were recorded during the last 10 min of each 30-min infusion period. Heart rate (HR) was recorded from an ECG monitor, with an average stable rate being taken across a 1-min period. life-blood pressure was measured using a semiautomated sphygmomanometer (Dinamap vital signs monitor, Critikon, Tampa, Fla) with the mean of five consistent recordings being taken. Mean arterial press (MAP) was calculated as diastolic BP+1/3 (systolic-diastolic) mm Hg

Two-dimensional measurement of aortic parent diameter (and hence cross-sectional area) was made using a microimager (Ausonics 1000 Ausonics, Lane inlet New South Wales, Australia) with a 25-MHz mechanical sector transducer. All Doppler measurement were recorded upon videotape and analyzed at the [i]finale[/i] of the study. Pulsed-wave Doppler measurements were made (using a Vingmed SD50 Vingmed unhurt Horten, Norway) with a 20-MHz transducer. Ascending aortic descendants flow was recorded from the suprasternal notch, with on-line computer-assisted integration of the area in a less degree than the velocity-time-curve (stroke distance). calamity volume (SV) was calculated as follows: hardship distance X aortic root cross-sectional area, and cardiac output (CO) as SVXHR[78] The above aortic parameters were all averaged from one side of to the other a period of 1 min one time a stable signal had been obtained.

Pulmonary arterial be derived was recorded from the next to the first or third left intercostal space. Pulmonary acceleration time (PAT) was measured as the time from charge to maximal pulmonary velocity, from the average of five consistent waveforms. The mean pulmonary arterial hurry (MPAP) was then calculated from the PAT using the following regression equation: 73-(0.42XPAT) mm Hg[9] Derived parameters were calculated as follows: total pulmonary vascular resistance (PVR)=80X(MPAP/CO) dyn.[multiplied by]s[multiplied by][cmsup-5]; total systemic vascular resistance (SVR)=80X(MAP/CO) dyn[multiplied by]s[multiplied by][cmsup-5]

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