Chapter 17: Vulnerability of coral reefs of the Great Barrier Reef to climate change

The Great Barrier Reef (GBR) contains the most extensive coral reef ecosystem on earth. It consists of 2900 coral reefs and 900 coral cays that cover approximately 20,000 km2 of the total 345,000 km2 area of the GBR Marine Park. As a consequence of unusually high summer sea surface temperatures, between 42 to 60 percent of the reefs of the GBR experienced mass coral bleaching in 19988. Bleaching was also reported from 31 other nations around the world during 1997–1998. For example, about 50 percent of reefs in the Indian Ocean and south Asia lost much of their coral cover, and an estimated 16 percent of the world’s area of coral reefs was severely damaged. The event coincided with the strongest recorded El Niño-Southern Oscillation event (ENSO) and one of the warmest years on record.This is Chapter 17 of Climate change and the Great Barrier Reef: a vulnerability assessment. The entire book can be found at http://hdl.handle.net/11017/13

Erythropoietin in the critically ill: do we ask the right questions?

Creative Commons Attribution LicensePR received research funding from Polymun Scientific GmbH (Klosterneuburg, Austria), a company involved in the commercial development of cEPO-FC

Microcirculation vs. Mitochondria-What to Target?

Circulatory shock is associated with marked disturbances of the macro- and microcirculation and flow heterogeneities. Furthermore, a lack of tissue adenosine trisphosphate (ATP) and mitochondrial dysfunction are directly associated with organ failure and poor patient outcome. While it remains unclear if microcirculation-targeted resuscitation strategies can even abolish shock-induced flow heterogeneity, mitochondrial dysfunction and subsequently diminished ATP production could still lead to organ dysfunction and failure even if microcirculatory function is restored or maintained. Preserved mitochondrial function is clearly associated with better patient outcome. This review elucidates the role of the microcirculation and mitochondria during circulatory shock and patient management and will give a viewpoint on the advantages and disadvantages of tailoring resuscitation to microvascular or mitochondrial targets

Interaction of the hydrogen sulfide system with the oxytocin system in the injured mouse heart.

This is the final version. Available from the publisher via the DOI in this record.BACKGROUND: Both the hydrogen sulfide/cystathionine-γ-lyase (H2S/CSE) and oxytocin/oxytocin receptor (OT/OTR) systems have been reported to be cardioprotective. H2S can stimulate OT release, thereby affecting blood volume and pressure regulation. Systemic hyper-inflammation after blunt chest trauma is enhanced in cigarette smoke (CS)-exposed CSE-/- mice compared to wildtype (WT). CS increases myometrial OTR expression, but to this point, no data are available on the effects CS exposure on the cardiac OT/OTR system. Since a contusion of the thorax (Txt) can cause myocardial injury, the aim of this post hoc study was to investigate the effects of CSE-/- and exogenous administration of GYY4137 (a slow release H2S releasing compound) on OTR expression in the heart, after acute on chronic disease, of CS exposed mice undergoing Txt. METHODS: This study is a post hoc analysis of material obtained in wild type (WT) homozygous CSE-/- mice after 2-3 weeks of CS exposure and subsequent anesthesia, blast wave-induced TxT, and surgical instrumentation for mechanical ventilation (MV) and hemodynamic monitoring. CSE-/- animals received a 50 μg/g GYY4137-bolus after TxT. After 4h of MV, animals were exsanguinated and organs were harvested. The heart was cut transversally, formalin-fixed, and paraffin-embedded. Immunohistochemistry for OTR, arginine-vasopressin-receptor (AVPR), and vascular endothelial growth factor (VEGF) was performed with naïve animals as native controls. RESULTS: CSE-/- was associated with hypertension and lower blood glucose levels, partially and significantly restored by GYY4137 treatment, respectively. Myocardial OTR expression was reduced upon injury, and this was aggravated in CSE-/-. Exogenous H2S administration restored myocardial protein expression to WT levels. CONCLUSIONS: This study suggests that cardiac CSE regulates cardiac OTR expression, and this effect might play a role in the regulation of cardiovascular function.German Research FoundationIGradUUlm University (Herta-Narthorff-Programm

Metabolic, cardiac and renal effects of the slow hydrogen sulfide-releasing molecule GYY4137 during resuscitated septic shock in swine with pre-existing coronary artery disease

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Published Ahead of Print, 19 January 2017Decreased levels of endogenous hydrogen sulfide (H2S) contribute to atherosclerosis, whereas equivocal data are available on H2S effects during sepsis. Moreover, H2S improved glucose utilization in anaesthetized, ventilated, hypothermic mice, but normothermia and/or sepsis blunted this effect. The metabolic effects of H2S in large animals are controversial. Therefore, we investigated the effects of the H2S donor GYY4137 during resuscitated, fecal peritonitis-induced septic shock in swine with genetically and diet-induced coronary artery disease (CAD). 12 and 18 hours after peritonitis induction, pigs received either GYY4137 (10 mg kg, n = 9) or vehicle (n = 8). Before, at 12 and 24 hours of sepsis, we assessed left ventricular (pressure-conductance catheters) and renal (creatinine clearance, blood NGAL levels) function. Endogenous glucose production and glucose oxidation were derived from the plasma glucose isotope and the expiratory CO2/CO2 enrichment during continuous i.v. 1,2,3,4,5,6-C6-glucose infusion. GYY4137 significantly increased aerobic glucose oxidation, which coincided with higher requirements of exogenous glucose to maintain normoglycemia, as well as significantly lower arterial pH and decreased base excess. Apart from significantly lower cardiac eNOS expression and higher troponin levels, GYY4137 did not significantly influence cardiac and kidney function or the systemic inflammatory response. During resuscitated septic shock in swine with CAD, GYY4137 shifted metabolism to preferential carbohydrate utilization. Increased troponin levels are possibly due to reduced local NO availability. Cautious dosing, the timing of GYY4137 administration and interspecies differences most likely account for the absence of any previously described anti-inflammatory or organ-protective effects of GYY4137 in this model