Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protection of the failing right ventricle (RV) in the surgical treatment of massive pulmonary embolism is a keystone for myocardial recovery. This study evaluated whether cardioplegia should be used or avoided. In a modified Langendorff rat heart model pulmonary embolism was simulated by afterload elevation (20 cm H2O) for 30 min. Hearts were arrested with cardioplegic solutions [St. Thomas Hospital (ST); University of Wisconsin (UW); oxygenated Krebs-Henseleit-Potassium (KHP)] and stored for 10 min or were allowed to beat empty (NoCP) for 15 min. After reestablishing of baseline conditions groups were measured for 60 min. Cardiac index (CI) decreased in all groups to 20% during afterload elevation. Group NoCP showed 68 and Group ST 65% recovery after 10 min and deteriorated after 30 min. After 60 min CI was 37 (ST) and 39% (NoCP). UW and KHP showed a significantly better recovery (KHP 100%; UW 88%). At 60 min CI decreased to 60 (KHP) and 64% (UW), but was still significantly higher than corresponding values of NoCP and ST. Following increased pulmonary afterload cardioplegia with UW or KHP solution is beneficial for RV recovery. The composition of the cardioplegia is obviously important and needs further study.
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PMID:Protection of the right ventricular myocardium during acute right heart failure from pulmonary hypertension. 813 48

Cardiac dysfunction has been documented in vivo after acute massive pulmonary embolism (AMPE). The present study tests whether intrinsic ventricular dysfunction occurs in rat hearts isolated after AMPE. AMPE was induced in spontaneously breathing ketamine-xylazine-anesthetized rats by thrombus infusion until mean arterial blood pressure (MAP) was approximately 40% of basal measurement. A hypotensive control group underwent controlled blood withdrawal to produce MAP approximately 40% of basal levels. Shams underwent identical surgical and anesthesia preparation but without pulmonary embolization. Hearts were perfused in isovolumetric mode, and simultaneous right ventricular (RV) and left ventricular (LV) pressures were measured. AMPE caused arterial hypotension with hypoxemia (PO(2) = 50 +/- 14 Torr), acidemia (pH = 7.26 +/- 0.11), and high lactate concentration (6.9 +/- 1.7 mM). Starling curves from both ventricles demonstrated that AMPE significantly reduced ex vivo systolic contractile function in the RV (P = 0.031) and LV (P = 0.008) compared with both the hypotensive control and sham hearts. AMPE did not alter coronary flow or compliance in either ventricle. Soluble tumor necrosis factor-alpha decreased in the RV (P = 0.043) and LV (P = 0.005) tissue. These data support the hypothesis that AMPE produces intrinsic biventricular dysfunction and suggest that arterial hypotension is not the principal mechanism of this dysfunction.
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PMID:Biventricular cardiac dysfunction after acute massive pulmonary embolism in the rat. 1129 51