Risk factors for recurrence in colorectal cancer: a retrospective analysis in a regional Australian hospital.

Background: Colorectal cancer is the third most commonly diagnosed malignancy in Australia. Up to a third of patients who have undergone surgery with curative intent for colorectal cancer will have a recurrence of disease leading to significant morbidity and mortality. Regional Australians have disproportionately worse outcomes.

A case of splenic artery pseudoaneurysm rupture presenting as rectal bleeding in a regional hospital.

Splenic artery pseudoaneurysm is a rare phenomenon most associated with chronic pancreatitis or previous trauma. Complications can include erosion and rupture into local structures, a situation that carries a reported mortality of 10-40%. A 58-year-old male with chronic alcoholic pancreatitis and a known splenic artery pseudoaneurysm presented to the emergency department of a regional hospital with rectal bleeding and sepsis.

Caseload distribution of general surgeons in regional Australia: is there a role for a rural surgery sub-specialization?

Background: Rural and regional Australia presents a unique challenge in the delivery of surgical services by virtue of its geographical vastness and low population density. While up to 33% of Australians live in rural or regional areas, only 14.8% of surgeons work in a rural or regional area.

Myocardial mitochondrial injury induced by pulmonary exposure to particulate matter in rats.

Exposure to air pollution has been associated with acute myocardial ischemia, impaired myocardrial function, and ST-segment depression. Particulate matter (PM)-associated metals, especially vanadium and nickel, have been implicated in observed cardiovascular impairments. We aimed to assess the effect of single intratracheal pulmonary exposure to vanadium-rich respirable oil combustion PM (HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats.

Blood pressure modulation following activation of mast cells by cationic cell penetrating peptides.

Short cell penetrating peptides (CPP) are widely used in vitro to transduce agents into cells. But their systemic effect has not been yet studied in detail. We studied the systemic effect of the cell penetrating peptides, penetratin, transportan and pro-rich, on rat hemodynamic functions.

Pseudoaneurysm of the hepatic artery.

Introduction: Hepatic artery pseudoaneurysms are a rare complication of biliary tract surgery and have an associated mortality that approaches 50%.

Case Report: A case of massive haemobilia caused by a hepatic artery pseudoaneurysm several months following laparoscopic cholecystectomy is described.

Discussion: It was successfully managed by angiographic embolisation, with the patient making a complete recovery.

Mast cell activation by fibrinogen-related homologous c-terminal peptides (haptides) modulates systemic blood pressure.

Background: Haptides are a family of short peptides homologous to C-termini sequences of fibrinogen chains β and γ (haptides Cβ and preCγ, respectively) which were previously shown to penetrate and bind cells.

Objectives: This work investigates the systemic effect of the haptides with possible clinical implications.

Methods: Intra-arterial monitoring in rats recorded the haptides' effects on systemic blood pressure.

Short homologous peptides based on C-terminal sequences of fibrinogen β- and γ-chains (Haptides) affect cardiovascular function by eNOS inhibition.

Haptides are a family of 19-21-mer cell-binding and permeating peptides homologous to sequences in the C termini on both fibrinogen β- and γ-chain (Cβ and preCγ, respectively). The effect of the Haptides on the cardiovascular system was studied by different assays, including the activity of isolated perfused rat heart and blood vessels in the organ bath. Haptides (50-80 μg/ml) decreased the hemodynamic functions of perfused rat hearts by up to 60% (p < 0.

Occult cardiotoxicity--toxic effects on cardiac ischemic tolerance.

The outcome of cardiac ischemic events depends not only on the extent and duration of the ischemic stimulus but also on the myocardial intrinsic tolerance to ischemic injury. Cardiac ischemic tolerance reflects myocardial functional reserves that are not always used when the tissue is appropriately oxygenated. Ischemic tolerance is modulated by ubiquitous signal transduction pathways, transcription factors and cellular enzymes, converging on the mitochondria as the main end effector.

Successful restoration of function of frozen and thawed isolated rat hearts.

Objective: Long-term organ preservation for transplantation may allow optimal donor-recipient matching with potential reduction in the incidence and severity of rejection. Complete cessation of metabolism may be obtained by freezing. Previous attempts to freeze intact mammalian hearts were limited to -3.

Ozone administration reduces reperfusion injury in an isolated rat heart model.

Background: Accumulating clinical experience with ozone administration for conditions associated with ischemia has been encouraging. The aim of our study was to determine the effect of ozone on reperfusion injury in an isolated rat heart model.

Methods: Isolated rat hearts were perfused with modified Krebs-Henseleit buffer solution via ascending aorta cannulation.

Occult cardiotoxicity: subtoxic dosage of Bis(2-chloroethoxy)methane impairs cardiac response to simulated ischemic injury.

The effect of Bis(2-chloroethoxy)methane (CEM) on myocardial response to ischemia was tested in rats. CEM was dermally applied for 3 days to F344/N male rats, at 0, 100, 400, or 600 mg/kg/d. Subsequently, left ventricular sections were prepared from each rat heart.

Dexrazoxane prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart.

Introduction: Dexrazoxane (Dex), used clinically to protect against anthracycline-induced cardiotoxicity, possesses iron-chelating properties. The present study was designed to examine whether Dex could inhibit the ischemia/reperfusion (I/R) induced damage to the rat heart.

Materials And Methods: Isolated perfused rat hearts were exposed to global ischemia (37 degrees C) and 60 min reperfusion.

Apomorphine-induced myocardial protection is due to antioxidant and not adrenergic/dopaminergic effects.

Apomorphine (Apo), a dopaminergic agonist used for treatment of Parkinson disease, is a potent antioxidant. In addition to its antioxidative effects, the dopaminergic and adrenergic effects of Apo were studied. Isolated perfused rat hearts were exposed to 25 min of no-flow global ischemia (37 degrees C) and 60 min of reperfusion (I/R, control).

Oxidized and ubiquitinated proteins may predict recovery of postischemic cardiac function: essential role of the proteasome.

This study examined the hypothesis that postischemic levels of oxidized and/or ubiquitinated proteins may be predictive of functional recovery as they may be indicative of activity of the 20S and/or 26S proteasomes, respectively. Subjecting isolated rat hearts to 15 min of ischemia had no effect on 20S- and 26S-proteasome activities; however, both were significantly (p < 0.05) decreased by 70% and 54%, respectively, following 30 min of ischemia and 60 min of reperfusion, changes associated with increased levels of protein carbonyls and ubiquitinated proteins.

Impaired mitochondrial response to simulated ischemic injury as a predictor of the development of atrial fibrillation after cardiac surgery: in vitro study in human myocardium.

Objective: Atrial fibrillation occurs in 20% to 40% of patients after cardiac surgery, but its pathophysiology remains unclear. Recent studies demonstrated preexisting histologic markers that portend the development of postoperative atrial fibrillation. In this prospective study, we focused on mitochondrial dysfunction in response to ischemic stress as a potential predictor for postoperative atrial fibrillation.

Apomorphine prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart.

This study examined the hypothesis that low-concentration apomorphine improves postischemic hemodynamic and mitochondrial function in the isolated rat heart model by attenuating oxidation of myocardial proteins. Control and apomorphine-treated hearts were subjected to 35 min of perfusion, 25 min of normothermic global ischemia, and 60 min of reperfusion. Apomorphine (2 microM) was introduced into the perfusate for 20 min starting from the onset of reperfusion.

Preconditioning improves postischemic mitochondrial function and diminishes oxidation of mitochondrial proteins.

This study examines the hypothesis that ischemic or pharmacologic preconditioning improves postischemic mitochondrial function by attenuating oxidation of mitochondrial proteins. Isolated rat hearts were perfused for 38 min preischemia, followed by 25 min global ischemia and then 60 min reperfusion. Hearts were preconditioned by two episodes of 3 min global ischemia, followed by 2 min of reflow (IP), or by perfusion with 50 micromol/l nicorandil (Nic) for 10 min, followed by 10 min washout.

Protection of myocardium by cyclosporin A and insulin: in vitro simulated ischemia study in human myocardium.

Background: The efficacy of myocardial protection by cyclosporin A (CSA) and insulin was tested in human right atrial myocardial slices subjected to simulated ischemia and reoxygenation.

Methods: Slices of right atrial trabeculae were obtained from patients undergoing elective cardiac surgery. Trabeculae were incubated with oxygenated glucose containing phosphate buffered saline (O(2), G-PBS).

Effect of nitric oxide and nitroxide SOD-mimic on the recovery of isolated rat heart following ischemia and reperfusion.

Nitric oxide synthesized from L-arginine in cells has important salutary physiological roles, but can also exert deleterious effects. Nitric oxide (NO) can ameliorate post-ischemic reperfusion myocardial injury, yet formation from NO and O(2)z*(-) of peroxynitrite and its downstream toxic products, such as *OH, *NO(2) and CO(3)*(-), can ultimately exacerbate reperfusion damage. Nitroxide stable radicals, such as 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TPL), unlike SOD, readily penetrate cells and catalytically remove intracellular O(2)*(-).

Cardioprotective and antioxidant effects of apomorphine.

Apomorphine is a potent antioxidant that infiltrates through biological membranes. We studied the effect of apomorphine (2 microM) on myocardial ischemic-reperfusion injury in the isolated rat heart. Since iron and copper ions (mediators in formation of oxygen-derived free radicals) are released during myocardial reperfusion, apomorphine interaction with iron and copper and its ability to prevent copper-induced ascorbate oxidation were studied.

Glucose metabolism, energetics, and function of rat hearts exposed to ischemic preconditioning and oxygenated cardioplegia.

We examined changes induced during ischemia-reperfusion on myocardial metabolism and function by oxygenated warm cardioplegia (CP) and ischemic preconditioning (IP). The postischemic hemodynamic recovery was comparable and significantly better in IP and CP groups, than in untreated hearts (e.g.

The effect of ionizing irradiation on vasomotor reactivity in the rat thoracic aorta in vitro.

Purpose: Ionizing irradiation inhibits restenosis in animal models and human. Vasomotor tone preservation during and after radiation therapy is of clinical importance. We therefore investigated vascular reactivity following radiation therapy.

Nicorandil decreases postischemic actin oxidation.

This study examined the hypothesis that preconditioning can decrease postischemic oxidative protein damage. Isolated rat hearts were subjected to 25 min of normothermic global ischemia followed by 45 min of reperfusion. These were compared with hearts pretreated with 20 microM nicorandil or preconditioned with two cycles of ischemia.