Inhibition of COX pathway in experimental myocardial infarction.

Release of inflammatory mediators within the ischemic myocardium has long been thought to contribute to myocardial damage and dysfunction. Myocardial infarction (MI) and congestive heart failure (CHF) were induced in rats by ligating the left coronary artery. Animals were treated with the selective cyclooxygenase-2 (COX-2) inhibitor-5,5-dimethyl-3-(3-fluorophenyl1)-4-(4-methyl-sulphonyl-2(5H)-fluranone (DFU), low-, high-dose acetyl salicylic acid (aspirin), or vehicle for 3 months.

Cyclooxygenase-2 (COX-2) in acute myocardial infarction: cellular expression and use of selective COX-2 inhibitor.

Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery.

Cyclooxygenase-2 and nuclear factor-kappaB in myocardium of end stage human heart failure.

Over the past three decades, numerous studies have shown diverse functional and morphological effects for prostanoids on cardiac myocytes with levels of prostanoids elevated in congestive heart failure. We examined the expression of cyclooxygenase-2 (COX-2) and activation of nuclear factor-kappaB (NF-kappaB) in failing human hearts. Expression of COX-2 and activation of NF-kappaB were examined in myocardial tissues from 27 patients with end stage heart failure, 2 septic patients, and 8 normal control subjects.

Inhibition of NOS II prevents cardiac dysfunction in myocardial infarction and congestive heart failure.

Strong expression of the inducible form of nitric oxide synthase (NOS II) has been shown in the myocardium of patients with myocardial infarction (MI). We hypothesized that NOS II plays an important role in the development of MI and subsequent heart failure and that inhibition of NOS II may beneficially alter the course of the disease. Long-term administration (2 mo) of the selective NOS II inhibitor S-methylisothiourea (SMT) to rats with MI significantly improved cardiac function.

Successful retrieval and function of lungs from non-heart-beating donors.

Background: Lung transplantation has been used effectively as a therapeutic tool in end-stage pulmonary diseases, but organ shortages have restricted its use. There is growing interest in alternative organ sources such as organs from circulation-arrested cadavers, so called non-heart-beating donors.

Methods: We examined the effects of postmortem rapid in situ cadaver lung cooling by bilateral chest cavity flushing (group 2) and by pulmonary artery flush through right heart catheterization followed by pleural cavity flushing (group 3) on pulmonary function and morphology in a rabbit non-heart-beating donor model.

Endothelin receptor antagonist improves pulmonary hemodynamics during lung ischemia/reperfusion injury.

Background: We have previously shown that elevated release of endothelin-1 is associated with increased pulmonary vascular resistance (PVR) immediately after reperfusion of the transplanted lung. In the present study, we investigated the effect of ET receptor blockage on pulmonary hemodynamics and function in an ex vivo lung reperfusion model after 6 hr of cold ischemia.

Methods: Eighteen rabbits were divided into three groups: no ischemia followed by 3 hr of reperfusion (group I) and 6 hr of cold ischemia followed by 3 hr of reperfusion with either blood (group II) or blood + SB209670 (mixed ETA/ETB receptor antagonist) (group III).

Heterogeneous expression and activity of endothelial and inducible nitric oxide synthases in end-stage human heart failure: their relation to lesion site and beta-adrenergic receptor therapy.

Background: Recent reports have suggested that excessive amounts of endogenous NO may contribute to the myocardial dysfunction and injury in heart failure. In the present report, we investigate the cellular expression and activity of endothelial (eNOS) and inducible (iNOS) NO synthase in failing human hearts with special reference to the underlying lesion and drug therapy.

Methods And Results: Myocardial tissues were obtained from 28 failing human hearts with various pathogeneses and 4 nonfailing hearts as controls.

Induction of cyclooxygenase-2 and activation of nuclear factor-kappaB in myocardium of patients with congestive heart failure.

Background: Chronic heart failure is associated with induction of secondary inflammatory mediators, including prostanoids. The latter exert diverse functional and morphological effects on cardiac myocytes. Induction of cyclooxygenase (COX), the enzyme responsible for generating prostanoids, requires activation of nuclear factor-kappaB (NF-kappaB).

Application of the lectin-dependent cell-mediated cytotoxicity assay to bronchoalveolar lavage fluid and venous blood samples collected from canine lung allografts.

One of the major obstacles in postoperative management of lung transplant recipients is differentiating between rejection and infection episodes. In addition, there are no reliable methods routinely to monitor lung allografts to ascertain that they are well tolerated by the host. Conventional noninvasive methods such as chest roentgenographs, radio nuclide perfusion scans, and pulmonary function tests used in conjunction with clinical assessment have been shown to be nonspecific (1,2).

The incidence of awareness, and amnesia for perioperative events, after cardiac surgery with lorazepam and fentanyl anesthesia.

One hundred patients (mean age 59 +/- 10 years) were premedicated with morphine, 0.15 mg/kg, and scopolamine, 0.008 mg/kg.