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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 185 (1985), S. 429-443 
    ISSN: 1433-8580
    Keywords: Myocardial blood flow ; Angiotensin II ; Saralasin ; Nephrectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen (n = 7). A third group of dogs was ventilated with room air and bilaterally nephrectomized 5 h prior to starting the experimental protocol (n = 7). After control data had been obtained, dogs were bled from the femoral arteries into a pressurized reservoir which maintained blood pressure at 45 ± 1 mm Hg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 µg/kg per min). Coronary blood flow was reduced by hemorrhage, and no significant difference existed in coronary flow during hemorrhage among the three groups. Coronary sinus oxygen saturation was diminished in control animals during hemorrhage from 26% ± 1% to 17% ± 1% (P 〈 0.05) but normal in 100% oxygen ventilated animals (30% ± 3%) and in nephrectomized dogs (34% ± 4%). Coronary oxygen extraction was reduced by saralasin in intact but not in nephrectomized dogs. In six additional experiments, in which blood pressure was not artificially held constant during saralasin infusion, saralasin still significantly improved coronary sinus oxygen saturation and thus reduced coronary oxygen extraction. The data suggest that both hypoxia and the reninangiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 78 (1983), S. 518-533 
    ISSN: 1435-1803
    Keywords: renin ; angiotensin ; coronary artery occlusion ; myocardial ischemia ; Captopril ; Saralasin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Studies were carried out in 39 barbiturate-anesthetized dogs to determine whether the renin-angiotensin system is important in control of hemodynamics and coronary flow during myocardial ischemia. Plasma renin activity (PRA) was 2.2±0.4 ng·ml−1·hr−1 immediately before coronary artery occlusion (CAO) and increased to 3.8±0.5 (p〈.005) 15 minutes after CAO. In nephrectomized dogs, PRA was 0.76±0.14 ng·ml−1·hr−1 two hours after nephrectomy and remained unchanged after CAO. In contrast, hemodynamic changes following CAO were similar between nephrectomized and intact dogs: mean arterial pressure fell from 126±4 pre CAO to 116±4 mm Hg post CAO (p〈0.005) in nephrectomized dogs and from 130±11 to 120±11 mm Hg (p〈0.005) in intact dogs. Left atrial pressure rose from 5.4±0.9 pre CAO to 7.7±0.9 mm Hg (p〈0.005) post CAO in nephrectomized dogs and 6.3±1.3 to 9.0±1.8 mm Hg (p〈0.005) in intact dogs. Heart rate remained unchanged in both groups. In sham-operated dogs without CAO, neither the angiotensin II blocker Saralasin nor the converting enzyme inhibitor Captopril had significant effects on systemic (SVR) and coronary (CVR) vascular resistances. In contrast, in dogs with CAO, these drugs reduced CVR from 1.28±0.13 mm Hg·ml−1·min·100 g heart weight (resistance units=RU) to 0.85±0.08 RU (p〈0.05) (Saralasin) 15 minutes after treatment and from 1.17±0.09 to 0.88±0.08 RU (p〈0.025), (Captopril) respectively. However, only Captopril reduced SVR, from 10.7±1.13 to 8.2±0.8 RU (p〈0.025). Both Captopril and Saralasin induced a significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significantly reduced the effect of Captopril on CVR and collateral blood flow while the effect on SVR persisted. Thus the reduction in CVR appears to be an effect of inhibition of the renin-angiotensin system; this system participates in control of CVR during CAO and may limit coronary collateral blood flow.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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