Photoacclimation in Dunaliella tertiolecta reveals a unique NPQ pattern upon exposure to irradiance

Highly time-resolved photoacclimation patterns of the chlorophyte microalga Dunaliella tertiolecta during exposure to an off–on–off (block) light pattern of saturating photon flux, and to a regime of consecutive increasing light intensities are presented. Non-photochemical quenching (NPQ) mechanisms unexpectedly responded with an initial decrease during dark–light transitions. NPQ values started to rise after light exposure of approximately 4 min. State-transitions, measured as a change of PSII:PSI fluorescence emission at 77 K, did not contribute to early NPQ oscillations. Addition of the uncoupler CCCP, however, caused a rapid increase in fluorescence and showed the significance of qE for NPQ. Partitioning of the quantum efficiencies showed that constitutive NPQ was (a) higher than qE-driven NPQ and (b) responded to light treatment within seconds, suggesting an active role of constitutive NPQ in variable energy dissipation, although it is thought to contribute statically to NPQ. The PSII connectivity parameter p correlated well with F′, Fm′ and NPQ during the early phase of the dark–light transients in sub-saturating light, suggesting a plastic energy distribution pattern within energetically connected PSII centres. In consecutive increasing photon flux experiments, correlations were weaker during the second light increment. Changes in connectivity can present an early photoresponse that are reflected in fluorescence signals and NPQ and might be responsive to the short-term acclimation state, and/or to the actinic photon flux

A Rare Case of Carcinoid Constrictive Pericarditis.

We describe a case of atypical carcinoid heart disease. A 62-year-old woman with well-differentiated neuroendocrine tumor metastatic to the liver and lymph nodes presented with recurrent unilateral pleural effusions and lower extremity edema. Multimodality imaging and workup resulted in the diagnosis of carcinoid-related constrictive pericarditis, a rare form of carcinoid heart disease. (Level of Difficulty: Intermediate.)

Role of controlled cardiac reoxygenation in reducing nitric oxide production and cardiac oxidant damage in cyanotic infantile hearts.

Cardiopulmonary bypass (CPB) is used increasingly to correct cyanotic heart defects during early infancy, but myocardial dysfunction is often seen after surgical repair. This study evaluates whether starting CPB at a conventional, hyperoxic pO2 causes an "unintentional" reoxygenation (ReO2) injury. We subjected 2-wk-old piglets to ventilator hypoxemia (FIO2 approximately 0.06, pO2 approximately 25 mmHg) followed by 5 min of ReO2 on CPB before instituting cardioplegia. CPB was begun in hypoxemic piglets by either abrupt ReO2 at a pO2 of 400 mmHg (standard clinical practice) or by maintaining pO2 approximately 25 mmHg on CPB until controlling ReO2 with blood cardioplegic arrest. The effects of abrupt vs. gradual ReO2 without surgical ischemia (blood cardioplegia) were also compared. Myocardial nitric oxide (NO) production (chemiluminescence measurements of NO2- + NO3-) and conjugated diene (CD) generation (spectrophotometric A233 measurements of lipid extracts) using aortic and coronary sinus blood samples were assessed during cardioplegic induction. 30 min after CPB, left ventricular end-systolic elastance (Ees, catheter conductance method) was used to determine cardiac function. CPB and blood cardioplegic arrest caused no functional or biochemical change in normoxic (control) hearts. Abrupt ReO2 caused a depression of myocardial function (Ees = 25 +/- 5% of control). Functional depression was relatively unaffected by gradual ReO2 without blood cardioplegia (34% recovery of Ees), and abrupt ReO2 immediately before blood cardioplegia caused a 10-fold rise in cardiac NO and CD production, with subsequent depression of myocardial function (Ees 21 +/- 2% of control). In contrast, controlled cardiac ReO2 reduced NO production 94%, CD did not rise, and Ees was 83 +/- 8% of normal. We conclude ReO2 injury is related to increased NO production during abrupt ReO2, nullifies the cardioprotective effects of blood cardioplegia, and that controlled cardiac ReO2 when starting CPB to correct cyanotic heart defects may reduce NO production and improve myocardial status postoperatively

Simultaneous arterial and coronary sinus cardioplegic perfusion: an experimental and clinical study

The existence of inhomogeneous distribution of coronary flow with antegrade or retrograde perfusion alone has led to alternating between these delivery routes to maximize their individual benefits. Concern over myocardial damage prevented the simultaneous application of antegrade and retrograde cardioplegic blood delivery. Based upon the predominance of retrograde drainage via Thebesian veins, and evidence that pressure-controlled intermittent coronary sinus occlusion during antegrade cardioplegic delivery enhances its distribution and protective properties, this study tests (a) the hypothesis that simultaneous aortic and coronary sinus perfusion is safe during aortic clamping, and (b) reports initial clinical application of this combined strategy in 174 patients. Five minipigs (25-30 kg) underwent 1 hr of aortic clamping with simultaneous aortic (antegrade) and coronary sinus (retrograde) perfusion at 200 ml/min with normal blood (37 degrees C) before and after 30 minutes of perfusion with either warm (37 degrees C) or cold (4 degrees C) blood cardioplegia (BCP). Furthermore, the combined strategy was used in 174 high-risk patients (NYHA class III-IV) at 3 university hospitals to perform myocardial protection during CABG or valve replacement, or a combination of both. Included were 16 patients in cardiogenic shock and 24 undergoing reoperation. In both the clinical and the experimental studies the coronary sinus pressure was always < 40 mmHg in beating or arrested hearts. Compared to control values (81.4 +/- 0.4% tissue water content), no right-ventricular (80.8 +/- 0.8%) or left-ventricular (79.5 +/- 0.3%) edema developed, no lactate was produced (control: -1.0 +/- 0.5 mg/100 g/min, empty beating: -0.64 +/- 5, and BCP arrest: -8.6 +/- 6.6)