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In experienced hands, complex mitral valve repair can be safely and effectively performed in a totally endoscopic, robotic-assisted manner. We present a technically complex case of a 76-year-old man with severe, symptomatic mitral regurgitation due to Barlow's disease, moderate-to-severe tricuspid regurgitation, and atrial fibrillation., (© The Author 2023. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

We describe our technique for totally endoscopic, robotic-assisted thoracic and pericardial adhesiolysis and redo complex mitral valve repair., (© The Author 2022. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

We describe our technique for totally endoscopic, robotic-assisted tricuspid valve repair with neochords and annuloplasty in a high-risk, obese patient., (© The Author 2022. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

We detail our technique for totally endoscopic, robotic-assisted mitral valve repair with the reimplantation of a ruptured papillary muscle head supported by double papillary muscle relocation and mitral annuloplasty for the treatment of nonacute ischemic mitral regurgitation., (© The Author 2022. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Totally endoscopic, robotic-assisted cardiac surgery has been increasingly utilized for valvular surgery. Peripheral cannulation with endoaortic balloon occlusion offers a safe approach for initiation of cardiopulmonary bypass during such procedures. We present a step-by-step demonstration of unilateral percutaneous femoral cannulation, endoaortic balloon positioning, and decannulation in a patient undergoing totally endoscopic, robotic-assisted mitral valve repair., (© The Author 2022. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Atrial septal defect accounts for 10-15% of congenital heart disease cases. Small-diameter atrial septal defects diagnosed during infancy or early adulthood are prone to spontaneous closure, whereas uncorrected, persistent moderate or large atrial septal defects can induce left-to-right shunting, which causes volume overload, heart failure, atrial arrhythmia, and/or pulmonary hypertension starting between the third and fourth decades of life. We describe in detail our technique for totally endoscopic, robotic-assisted atrial septal defect repair., (© The Author 2021. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Papillary fibroelastoma is a rare, benign tumor that affects males more frequently  than females and that tends to be diagnosed during the fifth or sixth decade of life. It tends to arise on cardiac valves, with the aortic valve being the most frequent location followed by the mitral valve, the tricuspid valve, and the pulmonary valve. We present the case of a robotic-assisted, totally endoscopic excision of a mitral valve papillary fibroelastoma., (© The Author 2021. Published by MMCTS on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Background: Current guidelines support family members' participation in care, but little is known regarding their potential contribution to pain assessment using validated behavioral pain scales., Aims: This study aimed to describe family members' observations of pain behaviors with the Critical-Care Pain Observation Tool and their evaluation of the tool and its use, and to understand their experience and perceptions of their potential role in pain management in the intensive care unit., Design: A mixed methods cross-sectional explanatory design was used., Setting: A medical-surgical intensive care unit in Canada., Participants/subjects: Family members were eligible if they had a loved one admitted in the intensive care unit who was unable to self-report., Methods: Family members identified pain behaviors using the Critical-Care Pain Observation Tool after a brief training, completed a self-administered questionnaire, and participated in a follow-up individual interview regarding their experience and perceived potential role in pain management when their loved one is unable to self-report., Results: Ten family members participated. A 15-minute training appeared sufficient for family members to be comfortable with observing pain behaviors included in the Critical-Care Pain Observation Tool. The tool allowed them to confirm their observations of pain behaviors, to focus more on the patient, and to advocate for better pain management., Conclusions: Future research is needed to explore the views of more family members and to compare their Critical-Care Pain Observation Tool scores to the ones of nurses' for interrater reliability testing., (Copyright © 2019 American Society for Pain Management Nursing. Published by Elsevier Inc. All rights reserved.)

Exercise-induced ischemic preconditioning (IPC) can be assessed by the results of the second of sequential exercise tests. Exercise-induced IPC is quantified by using the time to 1-mm ST-segment depression, the rate-pressure product at 1-mm ST-segment depression, the maximal ST-segment depression, and the rate-pressure product at the peak of exercise. Few studies reported whether exercise-induced IPC could be used in cardiovascular rehabilitation. A systematic review of the literature limited to human studies was performed using electronic databases, and the main key words were ischemic preconditioning, warm-up phenomenon, and exercise. After careful review, 38 articles were included in the systematic review. This review summarizes the molecular pathways of IPC and describes the first window of protection induced by sequential exercise tests, as well as the effect of medication on exercise-induced IPC. A section on the exercise protocol, mode of exercise, and intensity provides understanding as to what is needed for clinicians to induce IPC with sequential stress tests. The final section of the review is a discussion of the potential use of exercise-induced IPC in a cardiovascular rehabilitation setting. Even if exercise-induced IPC is a well-documented phenomenon, additional studies are needed in order to more fully understand its use in rehabilitation.

This review examines the function of calcium-activated chloride currents (I(Cl(Ca))) in the retina with an emphasis on their physiological role in photoreceptors. Although found in a variety of neurons and glial cells of the retina, I(Cl(Ca)) has been most prominently studied in cones, where it activates in response to depolarization-evoked Ca(2+) influx. The slow and complex gating kinetics of the chloride current have been considered to reflect the changing submembrane concentration of intracellular calcium. It is likely that the role of I(Cl(Ca)) is to stabilize the membrane potential of cones during synaptic activity and presynaptic Ca channel modulation. Several candidates in the molecular identification of the channel have been put forward but the issue remains unresolved.

Purpose: The physiological actions of CB(1) cannabinoid receptors (CB(1)Rs) in mammalian retina have yet to be fully described in all cell types. Here we investigate the actions of CB(1)R activation on high-voltage-activated (HVA) Ca(2+) channel currents in purified cultures of rat retinal ganglion cells (RGCs)., Methods: Reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry were used to determine the presence of CB(1)R mRNA and protein in a purified RGC culture generated from neonatal rats using a two-step panning procedure. Ruptured-patch whole-cell voltage clamp was used to test the effect of CB(1)R agonists (WIN 55,212-2) and antagonists (SR141716A, AM281) on HVA Ca(2+) channel currents., Results: RT-PCR analysis confirmed CB(1)R mRNA in cultured RGCs and immunocytochemistry for CB(1)R protein revealed labeling in both the cell body and neurites of isolated RGCs. Patch-clamp recording from cultured rat RGCs showed that the CB(1)R agonist WIN 55,212-2 inhibited HVA Ca(2+) channel currents up to 50% in a concentration-dependent manner (0.5, 1, and 5 muM). The Ca(2+) channel current inhibition by WIN 55,212-2 was blocked by CB(1)R antagonists AM281 and SR141716., Conclusions: Activation of CB(1)Rs in cultured RGCs inhibits HVA Ca(2+) channel currents. These data show that cannabinoids can modify the excitability of RGCs and could affect retinal output. This finding has implications for retinal signal processing as it suggests that endogenous cannabinoids have inhibitory effects on RGCs and that exogenous cannabinoids could modulate retinal function by this pathway as well.

Non-invasive recordings of the retinal activity have an important role to play in the diagnosis of retinal pathologies. The detection of diseases that involve retinal ganglion cells (RGCs), such as optic atrophy and glaucoma, may be improved by isolating the RGC contribution from the multifocal electroretinogram (mfERG). In this study, mfERGs were performed on 20 pigs, 1-6 weeks following unilateral retrobulbar optic nerve section (ONS). The stimuli were 103 non-scaled high-contrast hexagons from which summed and individual mfERG responses were obtained in experimental and control fellow eyes under conditions of ketamine (n = 11) or isoflurane anaesthesia (n = 9). The effect of intravitreal injection of tetrodotoxin (TTX; n = 6) was also investigated. The summed mfERG responses showed a first positive peak (P1) with a short latency (21 ms) followed by two smaller peaks (P2 and P3) of longer latency (46 and 65 ms, respectively). While P2 and P3 amplitude were highly correlated with the time post-optic nerve section (ONS) (P2: r(2) = 0.669; P = 0.007; P3: r(2) = 0.651; P = 0.005), P1 was not (r(2) = 0.193; P = 0.38). P1 and P2 showed no implicit time variation as a function of retinal location, while P3 implicit time varied along the axis of the visual streak, generating a naso-temporal asymmetry. However, the P3 implicit time did not vary consistently with distance away from the optic nerve head. Intravitreal injections of TTX reduced P2 and P3 in the control eyes, consistent with the effect of ONS, and also induced a series of regular oscillations lasting up to 200 ms post stimulus. Under isoflurane anaesthesia, all components of the mfERG ifn experimental and control eyes were, at all time points post-ONS, of similar amplitude and without naso-temporal asymmetry, suggesting a reduced participation of RGCs under these anaesthesic conditions. These data clearly demonstrate that it is possible to isolate the RGC contribution from non-invasive multifocal electroretinography.

Ca(2+)-activated chloride channels were identified with whole-cell patch-clamp recording techniques in salamander retinal Müller cells. Cl(Ca) channels were activated by membrane depolarizations that elicited Ca2+ influx or the application of the Ca2+ ionophore, ionomycin. The Ca channel blocker, Cd2+, abolished the Cl(Ca) channel tail currents. Increasing the duration of the depolarizing pulse resulted in enhancement of the Cl(Ca) channel tail current. Repetitive depolarizations with rapid pulses to +20 mV produced a buildup of I(Cl(Ca)), which reversed at 0 mV in symmetrical [Cl-] and at -40 mV when intracellular [Cl-] was reduced to 10% of the external concentration. I(Cl(Ca)) was blocked by the Cl channel blocker niflumic acid, while niflumic acid had no effect on voltage-gated Ca channels. These results offer the first demonstration of Cl(Ca) channels in a nonastrocytic glial cell and expand our understanding of the functional capacities of retinal glial cells., ((c) 2005 Wiley-Liss, Inc.)

Retinal neural transmission represents a key function of the eye. Identifying the molecular components of this vital process is helped by studies of selected human genetic eye disorders. For example, mutations in the calcium channel subunit gene CACNA1F cause incomplete X-linked congenital stationary night blindness (CSNB2 or iCSNB), a human retinal disorder with abnormal electrophysiological response and visual impairments consistent with a retinal neurotransmission defect. To understand the subcellular basis of this retinal disorder, we generated a mouse with a loss-of-function mutation by inserting a self-excising Cre-lox-neo cassette into exon 7 of the murine orthologue, Cacna1f. Electroretinography of the mutant mouse revealed a scotopic a-wave of marginally reduced amplitude compared with the wild-type mouse and absence of the post-receptoral b-wave and oscillatory potentials. Cone ERG responses together with visual evoked potentials and multi-unit activity in the superior colliculus were also absent. Calcium imaging in Fluo-4 loaded retinal slices depolarized with KCl showed 90% less peak signal in the photoreceptor synapses of the Cacna1f mutant than in wild-type mice. The absence of post-receptoral ERG responses and the diminished photoreceptor calcium signals are consistent with a loss of Ca((2+)) channel function in photoreceptors. Immunocytochemistry showed no detectable Ca(v)1.4 protein in the outer plexiform layer of Cacna1f-mutant mice, profound loss of photoreceptor synapses, and abnormal dendritic sprouting of second-order neurons in the photoreceptor layer. Together, these findings in the Cacna1f-mutant mouse reveal that the Ca(v)1.4 calcium channel is vital for the functional assembly and/or maintenance and synaptic functions of photoreceptor ribbon synapses. Moreover, the outcome of this study provides critical clues to the pathophysiology of the human retinal channelopathy of X-linked incomplete CSNB.

Generation of center-surround antagonistic receptive fields in the outer retina occurs via inhibitory feedback modulation of presynaptic voltage-gated calcium channels in cone photoreceptor synaptic terminals. Both conventional and unconventional neurotransmitters, as well as an ephaptic effect, have been proposed, but the intercellular messaging that mediates the inhibitory feedback signal from postsynaptic horizontal cells (HCs) to cones remains unknown. We examined the possibility that proton concentration in the synaptic cleft is regulated by HCs and that it carries the feedback signal to cones. In isolated, dark-adapted goldfish retina, we assessed feedback in the responses of HCs to light and found that strengthened pH buffering reduced both rollback and the depolarization to red light. In zebrafish retinal slices loaded with Fluo-4, depolarization with elevated K(+) increased Ca signals in the synaptic terminals of cone photoreceptors. Kainic acid, which depolarizes HCs but has no direct effect on cones, depressed the K(+)-induced Ca signal, whereas CNQX, which hyperpolarizes HCs, increased the Ca signals, suggesting that polarization of HCs alters inhibitory feedback to cones. We found that these feedback signals were blocked by elevated extracellular pH buffering, as well as amiloride and divalent cations. Voltage clamp of isolated HCs revealed an amiloride-sensitive conductance that could mediate modulation of cleft pH dependent on the membrane potential of these postsynaptic cells.

Purpose: Although adenosine receptors (A(1)-Rs and A(2)-Rs) have been identified in the mammalian retina, the role of adenosine in this tissue is not fully understood. The purpose of this work was to investigate the action of adenosine on glutamate-induced calcium influx in rat retinal ganglion cells (RGCs) and to determine whether adenosine modulates RGC voltage-gated calcium channels., Methods: Purified RGC cultures were generated from neonatal rats with a two-step panning procedure. Isolated RGCs were loaded with the ratiometric calcium-indicator dye fura-2, and the effect of adenosine (and related agonists and antagonists) on intracellular calcium levels ([Ca(2+)](i)) during exposure to glutamate (10 microM with 10 microM glycine) was assessed. The effect of adenosine on calcium channel currents was also studied in isolated RGCs with whole-cell patch-clamp techniques. In addition, the effect of adenosine on [Ca(2+)](i) was investigated in fura dextran-loaded RGCs in an intact adult rat retina preparation., Results: In isolated RGCs, adenosine (10 and 100 microM) significantly reduced the glutamate-induced increase in [Ca(2+)](i) ( approximately 30%). The effect of adenosine was blocked by the A(1)-R antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), but not by the A(2)-R antagonist 3,7-dimethyl-1-propargylxanthine (DMPX). Adenosine (10 microM) inhibited calcium channel currents by 43%, and again this effect was blocked by DPCPX, but not DMPX. Adenosine (100 microM) also significantly reduced the elevation of [Ca(2+)](i) in RGCs in the intact retina during exposure to N-methyl-d-aspartate (NMDA; 100 microM)., Conclusions: Adenosine can inhibit glutamate-induced calcium influx and voltage-gated calcium currents in rat RGCs through A(1)-R activation. This work supports a role for adenosine as a neuromodulator of mammalian RGCs.

We show that carbenoxolone, a drug used to block hemichannels in the retina to test the ephaptic model of horizontal cell inhibitory feedback, has strong inhibitory effects on voltage-gated Ca channels. Carbenoxolone (100 microM) reduced photoreceptor-to-horizontal cell synaptic transmission by 92%. Applied to patch-clamped, isolated cone photoreceptors, carbenoxolone inhibited Ca channels with an EC(50) of 48 microM. At 100 microM, it reduced cone Ca channel current by 37%, reduced depolarization-evoked [Ca(2+)] signals in fluo-4 loaded retinal slices by 57% and inhibited Ca channels in Müller cells by 52%. A synaptic transfer model suggests that the degree of block of Ca channels accounts for the reduction in synaptic transmission. These results suggest broad inhibitory actions for carbenoxolone in the retina that must be considered when interpreting its effects on inhibitory feedback.