Whether and how pulmonary hypertension (PH) impacts perioperative outcome in non-cardiac surgery is incompletely understood. From November 1999, all patients undergoing non-cardiac, non-local anaesthetic surgery and ever examined by echocardiography within 30 days before surgery were screened. Those having echocardiographic pulmonary artery systolic pressure >70 mm Hg were enrolled provided they were not already intubated. Case-matched peers with normal pulmonary pressures served as controls. Perioperative outcomes were compared between the two groups, and predictors of adverse perioperative outcomes were investigated by multivariate logistic regression analysis. From November 1999 to August 2004, a total of 62 patients (male 38, mean age 67 yr) with PH were found. Compared with the case-matched controls, patients with PH experienced equivalently smooth operative courses, but significantly more frequent postoperative heart failure (9.7 vs 0%, P = 0.028), delayed tracheal extubation (21 vs 3%, P = 0.004), and in-hospital deaths (9.7 vs 0%, P = 0.028). Multivariate regression analysis identified emergency surgery [odds ratio (OR), 44.738; P = 0.028], coronary artery disease (CAD; OR, 9.933; P = 0.042), and systolic pulmonary artery pressure (OR, 1.101; P = 0.026) as independent predictors of postoperative mortality and surgery-specific cardiac risk level (OR, 6.791; P = 0.033) and CAD (OR 6.546, P = 0.017) as predictors of morbidity. PH is an important predictor of adverse cardiopulmonary outcome in non-cardiac surgery as reflected by markedly increased postoperative complications, especially in patients with coexistent high-risk clinical and surgical characteristics.

Background and purpose:  Doxorubicin evokes oxidative stress and precipitates cell apoptosis in testicular tissues. The aim of this study was to investigate whether the Ginkgo biloba extract 761 (EGb), a widely used herbal medicine with potent anti‐oxidant and anti‐apoptotic properties, could protect testes from such doxorubicin injury.Experimental approach:  Sprague‐Dawley male rats (8 weeks old) were given vehicle, doxorubicin alone (3 mg kg⁻¹ every 2 days for three doses), EGb alone (5 mg kg⁻¹ every 2 days for three doses), or EGb followed by doxorubicin (each dose administered 1 day after EGb). At 7 days after the first drug treatment oxidative and apoptotic testicular toxicity was evaluated by biochemical, histological and flow cytometric analyses.Key results:  Compared with controls, testes from doxorubicin‐treated rats displayed impaired spermatogenesis, depleted haploid germ cell subpopulations, increased lipid peroxidation products (malondialdehyde), depressed antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and glutathione), reduced antioxidant enzyme expression (superoxide dismutase) and elevated apoptotic indexes (pro‐apoptotic modulation of Bcl‐2 family proteins, intensification of p53 and Apaf‐1, release of mitochondrial cytochrome c, activation of caspase‐3 and increase of terminal deoxynucleotidyl transferase nick‐end labelling/sub‐haploid cells), while EGb pretreatment effectively alleviated all of these doxorubicin‐induced abnormalities in testes.Conclusions and implications:  These results demonstrate that EGb protected against the oxidative and apoptotic actions of doxorubicin on testes. EGb may be a promising adjuvant therapy medicine, potentially ameliorating testicular toxicity of this anti‐neoplastic agent in clinical practice.

The objective of this study was to investigate whether a cytoprotective herb-derived agent, Ginkgo biloba extract (EGb) 761, could have a beneficial effect on doxorubicin-induced cardiac toxicity in vitro and in vivo. Primary cultured neonatal rat cardiomyocytes were treated with the vehicle, doxorubicin (1 µM), EGb761 (25 µg/mL), or EGb761 plus doxorubicin. After 24 h, doxorubicin upregulated p53 mRNA expression, disturbed Bcl-2 family protein balance, disrupted mitochondrial membrane potential, precipitated mitochondrion-dependent apoptotic signalling, induced apoptotic cell death, and reduced viability of cardiomyocytes, whereas EGb761 pretreatment suppressed all the actions of doxorubicin. Similarly, rats treated with doxorubicin [3 mg/kg intraperitoneally (i.p.) three doses every other day] displayed retarded growth of body and heart as well as elevated apoptotic indexes in heart tissue at both 7 and 28 days after exposure, whereas EGb761 pretreatment (5 mg/kg i.p. 1 day before each dose of doxorubicin) effectively neutralized the aforementioned gross and cellular adverse effects of doxorubicin. Doxorubicin impairs viability of cardiomyocytes at least partially by activating the p53-mediated, mitochondrion-dependent apoptotic signalling. EGb761 can effectively and extensively counteract this action of doxorubicin, and may potentially protect the heart from the severe toxicity of doxorubicin.