The dependence of coronary collateral blood flow on regional vascular resistances

Ertl, Georg; Simm, Florence; Wichmann, Jörg; Fuchs, Martin; Lochner, W.

doi:10.1007/bf00501392

Cited by 29 publications

(2 citation statements)

References 16 publications

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“…Temperature (37°C) and pressure at this blood reservoir were maintained as described earlier [17]. The animals were anesthetized with thiobutabarbital (10 mg/kg), alpha-chloralose (40 mg/kg), and urethane (250 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

Deterioration of metabolic coronary regulation in hemorrhagic shock

Ertl¹,

Neubauer²,

Valldorf³

et al. 1985

Res. Exp. Med.

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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 mmHg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 micrograms/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 less than 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 renin-angiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.

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Section: Methodsmentioning

confidence: 99%

Deterioration of metabolic coronary regulation in hemorrhagic shock

Ertl¹,

Neubauer²,

Valldorf³

et al. 1985

Res. Exp. Med.

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“…Recent reports (5,21,28,32) pointed out that collateral flow and its early changes after coronary occlusion are mainly determined by the size and number of preexisting coronary collaterals, the size of the area at risk, the perfusion pressure and the extravascular resistance. In accordance, we found that in the animals with collateral state 0-III (group 3), flow was initially low and changed only slightly, whereas it was clearly higher and increased Basic Research in Cardiology, Vol.…”

Section: Mechanisms Governing the Development Of Coronary Collateral mentioning

confidence: 99%

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

1988

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Coronary collateral blood flow and its changes during the first 30 min of acute coronary artery occlusion were studied in 34 anesthetized dogs to clarify its influence on the vulnerability of the heart in this first arrhythmic phase. Collateral flow was determined with 9-micron tracer microspheres (TM) injected at 1, 10 and 30 min after acute proximal occlusion of the left circumflex (LCX, n = 30) or left anterior descending (LAD, n = 4) coronary artery. The post-mortem selective retrograde coronary angiography was used to evaluate the functional extent of preexisting coronary collaterals. After acute LCX occlusions collateral flow increased significantly (p less than 0.05) from 17.8 +/- 2.7 ml.(min.100 g)-1 (mean +/- SE; n = 13) at 1 min to 29.3 +/- 5.1 ml . (min . 100 g)-1 at 30 min of occlusion in animals with well-formed preexisting coronary collaterals (group 1), whereas it was very low (4.7 +/- 0.6 ml . (min . 100 g)-1; n = 13) and changed only slightly in dogs with poor collaterals (group 2). Most of these animals died by ventricular fibrillation (VF) before a second measurement could be carried out. In four dogs with poor collaterals but an unusually small LCX area (group 3), flow remained almost constant (11.0 +/- 4.7 versus 11.0 +/- 4.4 ml . (min . 100 g)-1) during this period. Similar results were obtained in animals with acute LAD occlusion (group 4). Ventricular extrasystoles (VES) mainly developed in animals with poor collaterals and respective low and almost unchanging collateral flow (group 2,3,4) while none or only a few VES occurred in dogs in which flow initially was clearly higher and increased significantly (group 1). The animals of group 1, 3 and 4 all survived the first arrhythmic phase, whereas all the animals of group 2 died by VF, either in the arrhythmic subphase Ia (n = 7) or Ib (n = 6). The results of the present study show that only the initial magnitude of flow is decisive for the development of VES and VF during the first arrhythmic phase, whereas the subsequent increase in flow is of no importance to the bimodal vulnerability in the first arrhythmic phase (subphases Ia and Ib). The in vivo measured critical minimal collateral flow of about 5 ml . (min . 100 g)-1 corresponds well with the survival limit (border between collateral state III and IV) previously determined by post-mortem retrograde coronary angiography.

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High‐Sensitivity Cardiac Troponin T in Stable Patients Undergoing Pharmacological Stress Testing

Wongpraparut

Piyophirapong

Maneesai

et al. 2015

Clinical Cardiology

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Background: Acute changes in high-sensitivity troponin T (hs-TnT) are induced by myocardial ischemia during exercise stress testing, but there are no reports of pharmacological stress testing. Hypothesis: The pattern of troponin release by myocardial ischemia-induced pharmacological stress testing differs according to the ischemic burden in stable patients. Methods: In total, 250 patients with suspected coronary artery disease underwent pharmacological stress magnetic resonance imaging (MRI). The amount and degree of myocardial ischemia on MRI and ischemic outcomes at 6 months were determined. hs-TnT levels were measured at baseline and 1 and 3 hours after testing. The 6-month clinical outcome was prespecified. Results: Fifty-one patients had moderate to severe myocardial ischemia (group A), and 199 patients had no or mild myocardial ischemia (group B). hs-TnT levels were significantly higher in group A than B at baseline (11 vs 8 pg/mL, P = 0.016) and at 1 hour (12 vs 8 pg/mL, P = 0.009) and 3 hours after testing (12 vs 9 pg/mL, P = 0.012). Baseline hs-TnT levels of ≥14 pg/mL showed a 43% sensitivity and 77% specificity in predicting moderate to severe ischemia by MRI (P = 0.03; area under the curve: 0.608, P = 0.017). Patients administered dobutamine had a higher acute change in hs-TnT levels 3 hours after testing than did those administered adenosine (21 vs 0 pg/mL, P < 0.001). There was a trend toward a higher incidence of myocardial infarction in patients with baseline hs-TnT levels of ≥14 pg/mL. Conclusions: hs-TnT levels are significantly higher in patients with moderate to severe than no or mild myocardial ischemia.

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The dependence of coronary collateral blood flow on regional vascular resistances

Cited by 29 publications

References 16 publications

Deterioration of metabolic coronary regulation in hemorrhagic shock

Deterioration of metabolic coronary regulation in hemorrhagic shock

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

High‐Sensitivity Cardiac Troponin T in Stable Patients Undergoing Pharmacological Stress Testing

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