Daily Anesthesiology Research Analysis
Three impactful studies span perioperative monitoring, pain mechanisms, and organ protection. A Science Advances report introduces an ICU-grade breathable cardiac electronic skin enabling stable intraoperative and postoperative cardiac monitoring. Two Anesthesiology studies reveal (1) ERO1 inhibition reduces sensory neuron excitability and acute pain behaviors, suggesting a non-opioid analgesic target, and (2) cardiopulmonary bypass induces weeks-long renal cortical/medullary hypoxia with histol
Summary
Three impactful studies span perioperative monitoring, pain mechanisms, and organ protection. A Science Advances report introduces an ICU-grade breathable cardiac electronic skin enabling stable intraoperative and postoperative cardiac monitoring. Two Anesthesiology studies reveal (1) ERO1 inhibition reduces sensory neuron excitability and acute pain behaviors, suggesting a non-opioid analgesic target, and (2) cardiopulmonary bypass induces weeks-long renal cortical/medullary hypoxia with histologic injury in sheep, reframing CPB-related kidney risk.
Research Themes
- Wearable perioperative cardiac monitoring
- Non-opioid analgesic mechanisms targeting ER–mitochondria calcium transfer (ERO1)
- Renal hypoxia and injury following cardiopulmonary bypass
Selected Articles
1. An ICU-grade breathable cardiac electronic skin for health, diagnostics, and intraoperative and postoperative monitoring.
This work introduces BreaCARES, a breathable electronic skin that delivers ICU-grade, real-time, wireless cardiac monitoring suitable for outpatient diagnostics, intraoperative stability during cardiac surgery, and continuous postoperative care. It reports superior anti-interference stability, portability, and long-term biocompatibility compared with commonly used clinical/commercial cardiac monitors.
Impact: A wearable demonstrating ICU-grade accuracy across perioperative contexts could transform patient monitoring workflows and enable safer, more comfortable long-term cardiac surveillance. The platform bridges engineering, perioperative monitoring, and digital health.
Clinical Implications: Potential to reduce lead-related artifacts and skin injury, expand monitoring to ambulatory and ward settings with fewer wires, and provide stable intraoperative cardiac signals—especially valuable in cardiac anesthesia and postoperative telemetry.
Key Findings
- Developed a breathable cardiac electronic skin (BreaCARES) enabling real-time, wireless, continuous cardiac monitoring with ICU-grade accuracy.
- Demonstrated stable intraoperative monitoring during heart surgery and continuous, comfortable postoperative monitoring.
- Reported superior anti-interference stability, portability, and long-term on-skin biocompatibility compared with clinical/commercial ICU cardiac monitors.
Methodological Strengths
- Translational engineering-to-clinical demonstration across intraoperative and postoperative use-cases
- Benchmarking against existing clinical/commercial monitors emphasizing anti-interference stability and biocompatibility
Limitations
- Abstract does not provide detailed sample sizes or controlled comparative outcome metrics (e.g., clinical endpoints)
- Lack of randomized clinical trials demonstrating outcome benefits
Future Directions: Conduct randomized or prospective comparative studies to demonstrate reductions in perioperative monitoring failures, skin complications, and to validate signal quality across diverse surgeries and patient populations.
Cardiovascular digital health technologies potentially outperform traditional clinical equipment through their noninvasive, on-body, and portable monitoring with mass cardiac data beyond the confines of inpatient settings. However, existing cardiovascular wearables have difficulty with providing medical-grade accuracy with a chronically comfortable and stable patient/consumer device interface for reliable clinical decision-making. Here, we develop an intensive care unit (ICU)-grade breathable cardiac electronic skin system (BreaCARES) for real-time, wireless, continuous, and comfortable cardiac care. BreaCARES enables a novel digital cardiac care platform for health care, outpatient diagnostics, stable intraoperative monitoring during heart surgery, and continuous and comfortable inpatient postoperative cardiac care, exhibiting ICU-grade accuracy while having superior anti-interference stability, portability, and long-term on-skin biocompatibility to the clinically and commercially available cardiac monitors in cardiovascular ICUs.
2. Inhibition of Endoplasmic Reticulum Oxidoreductin 1 Modulates Neuronal Excitability and Nociceptive Sensitivity in Mice.
In mice, peripheral ERO1 inhibition reduced acute inflammatory and postsurgical pain behaviors and decreased dorsal root ganglion neuron excitability, likely by dampening ER–mitochondria calcium transfer and mitochondrial function. ERO1α is expressed in human DRG, and ERO1 inhibition modulated human sensory neuron excitability in vitro, nominating ERO1 as a non-opioid analgesic target.
Impact: Identifies ERO1 as a modulator of nociceptor excitability across mouse and human DRG, offering a mechanistically grounded, non-opioid analgesic avenue with translational relevance.
Clinical Implications: Potential to develop peripherally acting ERO1 inhibitors for acute pain (e.g., postsurgical) as opioid-sparing strategies; safety profiling must consider mitochondrial function effects.
Key Findings
- ERO1α is expressed across mouse DRG sensory neuron subtypes and in human DRG.
- Peripheral ERO1 inhibition acutely reversed pain-like behaviors in mouse inflammatory and postsurgical pain models.
- In cultured DRG, ERO1 inhibition reduced nociceptor excitability and mitochondrial function, consistent with dampened ER–mitochondria calcium transfer.
- ERO1 inhibition modulated excitability of post-mortem human sensory neurons in vitro.
Methodological Strengths
- Cross-species validation (mouse in vivo behavior, mouse DRG, human post-mortem DRG)
- Convergent behavioral, electrophysiological, and imaging endpoints targeting ER–mitochondria signaling
Limitations
- Predominantly acute pain models; chronic pain efficacy not established
- Specificity and safety of ERO1 inhibitors in vivo require further clarification
Future Directions: Define pharmacology, selectivity, and safety of ERO1 inhibitors; test efficacy in chronic pain models and dosing strategies optimized for peripheral action with minimal mitochondrial compromise.
BACKGROUND: In the peripheral nervous system, nociceptors become hyperexcitable in both acute and chronic pain conditions. This phenotype can be mediated by dysregulated calcium, which occurs if the endoplasmic reticulum and mitochondria fail to buffer it appropriately. The redox enzyme endoplasmic reticulum oxidoreductin 1 (ERO1) regulates calcium transfer at endoplasmic reticulum-mitochondria contact sites (ERMCSs). This study hypothesized that inhibiting ERO1 and thereby dampening ERMCS calcium transfer might lower nociceptor hyperexcitability in sensory neurons and pain-like behaviors in mice. METHODS: C57BL/6 mice were used for histology, behavior, and cell culture experiments. Behavior included thermal tail flick, the formalin hind paw injection model of acute inflammatory pain, and hind paw incision postsurgical pain. Postmortem human dorsal root ganglia (DRGs) were used for immunohistochemistry and in vitro calcium imaging. RESULTS: This study demonstrates that the α isoform of ERO1 is expressed in mouse DRGs across multiple subtypes of mouse sensory neurons. This led us to peripherally administer an ERO1 inhibitor in mice, which acutely reversed nociception in acute inflammatory and postsurgical pain models. The hypothesis was that this may be due to reduced excitability of DRG neurons and tested ERO1 inhibition in vitro. In cultured DRGs, ERO1 inhibition dampened nociceptor excitability and mitochondrial function, suggesting that reduced calcium transfer through ERMCS could be responsible for the behavior observed in vivo . ERO1α expression was also found in human DRGs using immunohistochemistry and previously published single-cell RNA-sequencing data. Finally, the study showed that ERO1 inhibition modulates human sensory neuronal excitability in cultured post-mortem DRGs. CONCLUSIONS: This study found that ERO1 inhibition dampens mitochondrial function, sensory neuron excitability, and acute pain-like behavior in mice. Additionally, ERO1 inhibition decreases sensory neuron excitability in post-mortem human sensory neurons in vitro. The results indicate that targeting ERO1 may be a viable strategy for non-narcotic acute pain relief.
3. Persistent Renal Hypoxia and Histologic Changes at 4 Weeks after Cardiopulmonary Bypass in Sheep.
In a sheep CPB model, renal medullary oxygenation fell during CPB and remained depressed alongside cortical oxygenation for 4 weeks, with 42% developing stage 1 AKI early. Blinded histology at 4 weeks showed increased peritubular inflammation, interstitial fibrosis, and tubular casts compared with healthy controls, indicating prolonged renal injury after CPB.
Impact: Shifts the paradigm from transient to prolonged renal hypoxia and injury after CPB, motivating extended monitoring and renoprotective strategies beyond the immediate perioperative period.
Clinical Implications: Supports consideration of renal oxygenation monitoring and prolonged renoprotective measures post-CPB (e.g., hemodynamic optimization, oxygen delivery, nephrotoxin avoidance) and motivates trials of interventions targeting medullary hypoxia.
Key Findings
- Renal blood flow and medullary tissue oxygenation decreased significantly during CPB.
- Medullary oxygenation continued to decline over 48 h post-CPB with 42% developing stage 1 AKI.
- Medullary and cortical oxygenation remained significantly below baseline at 4 weeks.
- Blinded histology at 4 weeks showed more peritubular inflammation, interstitial fibrosis, and tubular casts vs. healthy controls.
Methodological Strengths
- Longitudinal renal tissue oxygenation measurements up to 4 weeks
- Independent blinded histopathology with healthy control comparison
Limitations
- Large-animal preclinical model; generalizability to humans requires caution
- Modest sample size and subset available for histology
Future Directions: Test renoprotective interventions targeting medullary hypoxia in CPB; translate tissue oxygenation monitoring to clinical settings and correlate with long-term kidney outcomes.
BACKGROUND: The sustained renal effects of exposure to cardiopulmonary bypass are unknown. This study aimed to test whether cardiopulmonary bypass (CPB) is associated with sustained renal tissue hypoxia and whether such hypoxia is associated with histologic injury. METHODS: The study included 12 adult female sheep undergoing CPB with a 2-h aortic cross-clamp. Systemic and renal hemodynamics and oxygen delivery, kidney function, and renal tissue oxygenation were measured before and during CPB, in the 48 h after CPB, and weekly for 4 weeks. The sheep were euthanized at 4 weeks and obtained renal tissue to perform histopathologic assessments for comparison with an independent cohort of five healthy animals that were euthanized without undergoing surgical or experimental interventions. These histologic assessments were performed by an independent, treatment-blinded pathologist. RESULTS: Compared with baseline, renal blood flow and renal medullary tissue oxygenation decreased significantly during CPB. In the first 48 h after CPB, there was a continuing significant decrease in medullary tissue oxygenation (from 39.2 ± 13.8 mmHg at baseline to 21.7 ± 16.2 mmHg at 48 h; Ptime = 0.006) with stage 1 acute kidney injury in 42% of the animals. Moreover, in the following 4 weeks, medullary (16.1 ± 12.9 mmHg at 4 weeks; Ptime = 0.005) and cortical (17.2 ± 6.5 mmHg at 4 weeks; Ptime = 0.005) tissue oxygenation remained significantly lower than baseline. Finally, compared with healthy sheep, at 4 weeks after CPB, sheep kidneys had significantly more peritubular inflammation (8 of 8 vs . 1 of 5; P = 0.007), interstitial fibrosis (6 of 8 vs . 0 of 5; P = 0.021), and tubular casts (8 of 8 vs . 1 of 5; P = 0.007). CONCLUSIONS: Exposure to CPB triggers sustained medullary and cortical tissue hypoxia and is associated with histopathologic renal injury. These findings suggest that the renal effect of exposure to CPB may be more profound and longer lasting than currently appreciated.