Potentiated state contractions in isolated hearts: effects of ischemia and reperfusion
| Autor: | Willem Flameng, H. Van Aken, B F Rusy, M. Mattheussen, Kanigula Mubagwa |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
medicine.medical_specialty
Physiology Ischemia Myocardial Ischemia chemistry.chemical_element Myocardial Reperfusion Calcium In Vitro Techniques Ventricular Function Left Physiology (medical) Internal medicine medicine Pressure Animals Papillary muscle Lagomorpha biology Ryanodine receptor business.industry Ryanodine Myocardium Cardiac Pacing Artificial Heart biology.organism_classification medicine.disease Myocardial Contraction Surgery Sarcoplasmic Reticulum Endocrinology medicine.anatomical_structure chemistry Verapamil Ventricular pressure Rabbits medicine.symptom Cardiology and Cardiovascular Medicine business Muscle contraction medicine.drug |
| Zdroj: | The American journal of physiology. 264(5 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | To investigate mechanisms underlying the contractile dysfunction during myocardial "stunning," potentiated contractions were studied in Langendorff-perfused rabbit hearts paced at 2.5 Hz. Isovolumetric left ventricular pressure (LVP) and the first derivative of LVP (dP/dt) were measured via a balloon. Potentiated contractions, elicited after 3 s of rest (postrest potentiation, PRP) or with paired pulses (paired-pulse potentiation, PPP) were first characterized in nonischemic conditions. Exposure to 5 nM ryanodine changed PRP into postrest depression [control, 134 +/- 1.7% (SE); ryanodine, 65 +/- 3.4%; n = 5] but did not decrease PPP (control, 125 +/- 7.2%; ryanodine, 141 +/- 14.5%). When sarcolemmal Ca2+ influx was decreased by 0.2-2 microM verapamil, PRP increased (control, 136 +/- 3.7%; 1 microM verapamil, 214 +/- 23.8%; n = 5), whereas PPP was maintained (control, 134 +/- 8.0%; 1 microM verapamil, 154 +/- 11.5%). During ischemia, both PRP and PPP were increased above preischemic values (from 128 +/- 1.9 to 355 +/- 60.4% and from 122 +/- 5.4 to 313 +/- 37.4%, respectively, n = 5). Changes of potentiation of dP/dt were qualitatively similar to those of LVP. On reperfusion, rest potentiation transiently decreased (PRP of dP/dt: 127 +/- 6% preischemia vs. 112 +/- 3% at 2 min postischemia; n = 6). However, PPP increased during the first 20 min of reperfusion (PPP of dP/dt: 184 +/- 22% preischemia vs. 236 +/- 34% postischemia; n = 6). This transient depression of PRP during reperfusion suggests an impairment of sarcoplasmic reticulum function in stunned myocardium, at least during the early phase of reperfusion. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|