Feasibility of Ultrasound-Guided Percutaneous Axillary Artery Cannulation for Veno-Arterial Extracorporeal Membrane Oxygenation and its Effect on the Recovery of Spontaneous Heartbeat in Patients with ECPR.

Objective: The measurement of the right and left axillary arteries and aortic arch and their vessels by multi-row spiral CT angiography provides the basis for clinical catheter selection and depth for axillary artery placement. This study reported the clinical experience of 7 patients who successfully underwent ultrasound-guided percutaneous axillary artery cannulation for veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Methods: Patients who had CT angiography of the thoracic aorta at our institution between January 2020 and March 2022 were assessed for eligibility and included. The diameters of the cephalic trunk (D1), right common carotid artery (D2), right axillary artery (D3), left common carotid artery (D4), left axillary artery opening (D5), right axillary artery cannulation length (L1), and left axillary artery cannulation length (L2) were measured. The tangential angles α, ß, and γ of the cephalic trunk, left common carotid artery and left subclavian and aorta was measured using an automatic angle-forming tool. The decision to use a 15F cannula for ultrasound-guided percutaneous axillary artery cannulation in veno-arterial extracorporeal membrane oxygenation (VA-ECMO) aims to achieve optimal vascular access. This cannula size strikes a balance, providing sufficient blood flow rates for ECMO support while minimizing the risk of complications associated with larger cannulas. Precise measurements of arterial dimensions, including the cephalic trunk, common carotid arteries, and axillary arteries, play a crucial role in guiding catheter selection and determining the depth of axillary artery placement. These measurements allow for tailored approaches based on individual patient characteristics, enhancing the safety and efficacy of the intervention. Additionally, measuring tangential angles (α, ß, and γ) provides insights into arterial alignment, optimizing the cannula trajectory for efficient blood flow. The use of an automatic angle-forming tool enhances measurement precision, contributing to procedural accuracy, minimizing complications, and ensuring the success of ultrasound-guided percutaneous axillary artery cannulation. In summary, the choice of a 15F cannula and precise measurements are essential components of the methodology, emphasizing safety, efficacy, and personalized approaches in VA-ECMO. From March to June 2022, 7 patients (6 males and 1 female) in our intensive care medicine department underwent successful ultrasound-guided percutaneous axillary artery cannulation for VA-ECMO with 15F cannula, including 3 cases with extracorporeal cardiopulmonary resuscitation (ECPR) and 4 cases with circulatory collapse. Results: 292 patients met the study criteria, 215 males and 77 females, with a mean age of 67.2±14.2 years. The measurements showed that D1 was (13.1±2.0) mm, D2 was (8.8±2.5) mm, D3 was (6.1±1.2) mm, D4 was (8.3±3.5) mm, D5 was (6.1±1.1) mm, L1 was (114.1±17.8) mm, and L2 was (128.4±20.2) mm. The tangential angles α of the cephalic trunk left common carotid artery and left subclavian artery to the aorta were (43.8°±17.1°), ß was (50.7°±14.8°), and γ was (62.4°±19.1°). Males had significantly wider D3 and D5, longer L1 and L2, and smaller gamma angles than females (P < .05). Three ECPR cases showed no recovery of the spontaneous heartbeat with femoral artery cannulation for VA-ECMO but recovered spontaneous heartbeat after axillary artery cannulation for VA-ECMO was adopted. The measurements in this study have important implications for veno-arterial extracorporeal membrane oxygenation (VA-ECMO) procedures. They provide crucial information about arterial dimensions, including the cephalic trunk, common carotid arteries, and axillary arteries. This information guides clinicians in selecting catheters and determining the ideal depth for percutaneous axillary artery cannulation during ECMO interventions. Notable gender differences in arterial dimensions highlight the need for personalized approaches in ECMO procedures. Customizing catheter choices and cannulation depth based on individual patient characteristics, informed by these measurements, improves the safety and effectiveness of the intervention. The measured tangential angles (α, ß, and γ) offer insights into arterial alignment, crucial for optimizing cannula trajectory and ensuring proper alignment for efficient blood flow. The use of an automatic angle-forming tool enhances measurement precision, contributing to procedural accuracy and minimizing the risk of complications during ECMO procedures. In summary, these measurements directly enhance the precision and safety of VA-ECMO procedures, underscoring the importance of personalized approaches based on individual anatomical variations and improving overall intervention success and outcomes. Conclusion: Ultrasound-guided percutaneous axillary artery cannulation for VA-ECMO with a 15F cannula is clinically feasible. Axillary artery cannulation for VA-ECMO contributes to the restoration of spontaneous heartbeat in ECPR patients more than femoral artery cannulation, and the possible mechanism is a better improvement of coronary blood flow. However, the study has limitations, including a modest sample size and a single-center, retrospective design, impacting its generalizability. To validate and extend these findings, further research with larger and diverse cohorts, including prospective investigations, is necessary to ensure their applicability across various clinical settings and patient demographics in VA-ECMO.

α7 Nicotinic Acetylcholine Receptor Mediates the Neuroprotection of Remote Ischemic Postconditioning in a Rat Model of Asphyxial Cardiac Arrest.

BACKGROUND: Remote ischemic postconditioning (RIPost) has been shown to reduce the ischemia-reperfusion injury of the heart and brain. However, the protection mechanisms have not yet been fully elucidated. We have observed that RIPost could alleviate the brain injury after cardiac arrest (CA). The aim of this study was to explore whether α7 nicotinic acetylcholine receptor (α7nAChR) mediates the neuroprotection of RIPost in a rat model of asphyxial CA. MATERIALS AND METHODS: Asphyxial CA model was induced by occlusion of the tracheal tube for 8 min and resuscitated later. RIPost produced by three cycles of 15-min occlusion and 15-min release of the right hind limb by a tourniquet was performed respectively at the moment and the third hour after restoration of spontaneous circulation. The α7nAChR agonist PHA-543613 and the antagonist methyllycaconitine (MLA) were used to investigate the role of α7nAChR in mediating neuroprotective effects. RESULTS: Results showed that α7nAChR was decreased in hippocampus and cortex after resuscitation, whereas RIPost could attenuate the reduction. The use of PHA-543613 provided neuroprotective effects against cerebral injury after CA. Furthermore, RIPost decreased the levels of neuron-specific enolase, inflammatory mediators, the number of apoptotic cells, and phosphorylation of nuclear factor-κB while increased the phosphorylation of signal transducer and activator of transcription-3. However, the above effects of RIPost were attenuated by α7nAChR antagonist methyllycaconitine. CONCLUSIONS: Neuroprotection of RIPost was related with the activation of α7nAChR, which could suppress nuclear factor-κB and activate signal transducer and activator of transcription-3 in a rat asphyxial CA model.

Spinal astrocytic activation is involved in a virally-induced rat model of neuropathic pain.

Postherpetic neuralgia (PHN), the most common complication of herpes zoster (HZ), plays a major role in decreased life quality of HZ patients. However, the neural mechanisms underlying PHN remain unclear. Here, using a PHN rat model at 2 weeks after varicella zoster virus infection, we found that spinal astrocytes were dramatically activated. The mechanical allodynia and spinal central sensitization were significantly attenuated by intrathecally injected L-α-aminoadipate (astrocytic specific inhibitor) whereas minocycline (microglial specific inhibitor) had no effect, which indicated that spinal astrocyte but not microglia contributed to the chronic pain in PHN rat. Further study was taken to investigate the molecular mechanism of astrocyte-incudced allodynia in PHN rat at post-infection 2 weeks. Results showed that nitric oxide (NO) produced by inducible nitric oxide synthase mediated the development of spinal astrocytic activation, and activated astrocytes dramatically increased interleukin-1ß expression which induced N-methyl-D-aspartic acid receptor (NMDAR) phosphorylation in spinal dorsal horn neurons to strengthen pain transmission. Taken together, these results suggest that spinal activated astrocytes may be one of the most important factors in the pathophysiology of PHN and "NO-Astrocyte-Cytokine-NMDAR-Neuron" pathway may be the detailed neural mechanisms underlying PHN. Thus, inhibiting spinal astrocytic activation may represent a novel therapeutic strategy for clinical management of PHN.

Histologic distribution, fragment cloning, and sequence analysis of g protein couple receptor 30 in rat submaxillary gland.

Recent studies indicated that G protein couple receptor 30 (GPR30), a nongenomic estrogen receptor, is widely expressed in many organ systems inducing many quick reaction of estrogen. However, there was rare report about the expression of GPR30 in the salivary gland. In the present study, we investigated the distribution of GPR30 in rat submaxillary gland by means of immunohistochemistry and in situ hybridization. GPR30 core sequences were amplified by RT-PCR with total RNA extracted from rat submaxillary gland and were analyzed by sequencing with Sanger's method. The results showed that the epithelial cells of serous alveoli and granular convoluted duct in rat submaxillary gland displayed GPR30-immunoreactivity on the plasma membrane and cytoplasm. Moreover, GPR30 mRNA hybridization signals were also detected in the cytoplasm of the above cells. GPR30 cDNA sequence cloned from rat submaxillary gland is identical to that of GPR30 from rat paraventricular and supraoptic nucleus. In conclusion, the expression of GPR30 in the serous and granular epithelial cells of submaxillary gland indicates that submaxillary gland could also be a target organ rapidly responding to estrogen stimulus, and estrogen may be involved in the functional regulation of submaxillary gland.

Spinal astrocytic activation contributes to mechanical allodynia in a mouse model of type 2 diabetes.

Diabetic neuropathic pain (DNP) plays a major role in decreased life quality of type 2 diabetes patients, however, the molecular mechanisms underlying DNP remain unclear. Emerging research implicates the participation of spinal glial cells in some neuropathic pain models. However, it remains unknown whether spinal glial cells are activated under type 2 diabetic conditions and whether they contribute to diabetes-induced neuropathic pain. In the present study, using a db/db type 2 diabetes mouse model that displayed obvious mechanical allodynia, we found that spinal astrocyte but not microglia was dramatically activated. The mechanical allodynia was significantly attenuated by intrathecally administrated l-α-aminoadipate (astrocytic specific inhibitor) whereas minocycline (microglial specific inhibitor) did not have any effect on mechanical allodynia, which indicated that spinal astrocytic activation contributed to allodynia in db/db mice. Further study aimed to identify the detailed mechanism of astrocyte-induced allodynia in db/db mice. Results showed that spinal activated astrocytes dramatically increased interleukin (IL)-1ß expression which may induce N-methyl-D-aspartic acid receptor (NMDAR) phosphorylation in spinal dorsal horn neurons to enhance pain transmission. Together, these results suggest that spinal activated astrocytes may be a crucial component of mechanical allodynia in type 2 diabetes and "Astrocyte-IL-1ß-NMDAR-Neuron" pathway may be the detailed mechanism of astrocyte-induced allodynia. Thus, inhibiting astrocytic activation in the spinal dorsal horn may represent a novel therapeutic strategy for treating DNP.

The effects of intravenous hyperoxygenated solution infusion on systemic oxygenation and intrapulmonary shunt during one-lung ventilation in pigs.

BACKGROUND: Many anesthetic methods have been applied to maintain acceptable oxygenation during one-lung ventilation (OLV). However, the optimal management has not been definitely determined. The aim of this study was to investigate whether intravenous hyperoxygenated solution (HOS) infusion would improve systemic oxygenation and reduce intrapulmonary shunt during OLV. MATERIALS AND METHODS: Sixteen pigs (25-35 kg) were anesthetized, tracheally intubated, and mechanically ventilated. After placement of femoral artery and pulmonary artery catheters, a left-sided double-lumen tube (DLT) was placed via tracheotomy. The animals were allocated randomly to one of the two study groups (n = 8 each); control group (C group) and hyperoxygenated solution group (H group). Animals in H group received intravenous HOS infusion immediately after the beginning of OLV via internal right jugular vein with an infusion pump, and the rate of infusion was 15 mL.kg(-l).h(-l); and in C group, the same amount of lactate Ringer's solution (LRS) was used in place of HOS. Arterial and venous blood gases analysis were recorded in three phases: during two-lung ventilation just before beginning OLV (TLV), 30 min after beginning OLV (OLV + 30), and 60 min after beginning OLV (OLV + 60). We measured arterial oxygen saturation (SaO(2)), mixing venous oxygen saturation (S(V)O(2)), partial pressure of arterial oxygen (PaO(2)), partial pressure of mixing venous oxygen (PvO(2),) oxygen contents in systemic arterial and mixed venous blood (CaO(2), CvO(2)), and venous admixture percentage (Qs/Qt%). Heart rate (HR), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), and cardiac output (CO) were also recorded. RESULTS: After 30 and 60 min OLV, there was a significant decrease in PaO(2), SaO(2), PvO(2), SvO(2), CaO(2), and CvO(2), and a significant increase of Qs/Qt% in both groups (P < 0.01). The values of PaO(2), SaO(2), PvO(2), SvO(2), and CvO(2) in H group at both OLV + 30 and OLV + 60 were significantly higher than those in C group (P < 0.05, P < 0.01). Although the values of CaO(2) in H group were higher than those in C group at OLV + 30 and OLV + 60, there were no significant differences. Comparing the values of Qs/Qt% between the two groups at OLV + 30 and OLV + 60, there were also no significant differences. CONCLUSIONS: Intravenous HOS infusion led to minimal changes in intrapulmonary shunt, nevertheless, it could ameliorate arterial oxygenation obviously during OLV. This might be a new strategy to improve systemic oxygenation during OLV.

Debittering effect of Actinomucor elegans peptidases on soybean protein hydrolysates.

Effects of the enzymes in Actinomucor elegans extract and the enzyme Alcalase 2.4L on debittering the soybean protein hydrolysates were investigated. When the protein was treated only with the latter, a strong bitterness formed; but it decreased if the protein was treated with both the enzymes. The more the enzymes were used, weaker was the bitterness tasted. SDS-PAGE profile and ESI-MS spectrum of the hydrolysates evidenced that the Alcalase could convert the protein into peptides rapidly, while the enzymes in the A. elegans extract were able to further degrade some peptides which were difficult or unable to be hydrolyzed by the Alcalase. Further systematic analysis of the peptidases showed that the Alcalase exhibited a significant endopeptidase activity towards NBZ-Phe-pNA substrate (p < 0.01), whereas many exopeptidases in the A. elegans extract had the carboxypeptidase activity towards N-CBZ-Ile-Leu (p < 0.01). It is concluded that those exopeptidases presented in the A. elegans extract can benefit by decreasing the bitterness of the soybean protein hydroysate. They are also capable of being used with the Alcalase in a single-step enzymatic reaction to prepare the bitterless protein hydrolysate, which may be an efficient application for food industry.

Hyperoxygenated solution preconditioning attenuates lung injury induced by intestinal ischemia reperfusion in rabbits.

BACKGROUND: The current study was undertaken to elucidate the possible therapeutic effects of hyperoxygenated solution (HOS) preconditioning on lung injury induced by intestinal ischemia/reperfusion (I/R) in rabbits. MATERIALS AND METHODS: Eighty rabbits were randomly divided into four groups (n = 20 each) as follows: (1) control group in which sham operation was performed (sham group), (2) HOS pretreatment group and sham operation (HOS + sham group), (3) ischemia/reperfusion group (I/R group), (4) HOS pretreatment and ischemia/reperfusion group (HOS + I/R group). Intestinal I/R model was produced by clamping superior mesenteric artery with an atraumatic vascular clamp for 1 h, and followed by reperfusion for 2 h. Animals in HOS + sham group and HOS + I/R group received intravenous HOS infusion (20 mL/kg, 10 mL/kg.h for 2 h) every day for 5 d before operation, and animals in sham group and I/R group received the same amount of normal saline in the same way. At the end of reperfusion, 8 animals from every group were sacrificed and histopathological changes of lung were observed; pulmonary edema, lung myeloperoxidase activity, superoxide dismutase activity, and malondialdehyde levels in lung tissues were also detected. The rest 12 animals in every group underwent 60 min of intestinal ischemia followed by 72 h of reperfusion, and effects of HOS pretreatment on survival in rabbits with lung injury induced by intestinal I/R was observed. RESULTS: When rabbits were subjected to 60 min of intestinal ischemia, a high incidence of mortality was observed within 24 h. In this situation, HOS preconditioning before the start of ischemia/reperfusion significantly reduced the mortality. HOS preconditioning also decreased lung wet/dry ratio, neutrophil infiltration, lipid membrane peroxidation, and increased superoxide dismutase activity in the lungs after intestinal I/R compared with the I/R-treated rabbit lungs without HOS treatment. Histopathological analysis also indicated the effectiveness of HOS pretreatment. CONCLUSIONS: HOS preconditioning could preserve superoxide dismutase activity, decrease lipid membrane peroxidation and neutrophil infiltration in the lungs, then ameliorate the deleterious changes in pulmonary injury induced by intestinal I/R.

Protective effects of hyperoxygenated solution preconditioning on intestinal ischemia-reperfusion injury in rabbits.

BACKGROUND: The aim of this study was to investigate the protective effects of hyperoxygenated solution (HOS) preconditioning on intestinal ischemia-reperfusion (IR) injury in rabbits. MATERIALS AND METHODS: Thirty-two rabbits were randomly divided into four groups as follows: (1) control group in which sham operation was performed (Sham group); (2) sham operation and HOS treatment group (sham+H group); (3) ischemia-reperfusion group (IR group); (4) ischemia-reperfusion and HOS treatment group (H group). Intestinal IR model was produced by clamping superior mesenteric artery with an atraumatic vascular clamp for 1 h, followed by reperfusion for 2 h. Animals in H group received intravenous HOS infusion (20 mL/kg) every day for 5 days before ischemia-reperfusion; animals in the sham+H group received the same amount of HOS before sham operation, and animals in IR group received the same amount of normal saline in the same way. At the end of reperfusion, histopathological changes of intestine were observed, and malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities in intestinal tissues were also detected. Intestinal barrier function was assessed by blood d-lactate levels and bacterial translocation (BT). RESULTS: The H group showed significantly lower MDA levels and higher activities of SOD, CAT, and GSH-Px in the intestinal tissue compared with the IR group. Furthermore, the mean d-lactate levels and incidence of BT in the H group were significantly lower than those in the IR group. Histopathological analysis also indicated that there were significant histological improvements in the H group compared with the IR group. CONCLUSIONS: HOS preconditioning at an appropriate dose ameliorates the deleterious changes in intestinal mucosal injury and barrier function associated with IR by effectively preventing a decrease in the intestinal antioxidant defense system, which is another simple and effective measure to protect intestine from IR injury.

Amelioration of intestinal ischemia-reperfusion injury with intraluminal hyperoxygenated solution: studies on structural and functional changes of enterocyte mitochondria.

BACKGROUND: The aim of this study was to investigate the effects of intraluminal hyperoxygenated solution (HOS) on enterocyte mitochondrial structure and respiratory function after intestinal ischemia-reperfusion (IR) in rabbits. MATERIALS AND METHODS: Thirty-two rabbits were divided randomly into four groups: control group in which sham operation was performed (Sham group), ischemia-reperfusion group (IR group), and two HOS treatment groups (H1 group and H2 group). Intestinal IR model was produced by clamping superior mesenteric artery (SMA) with an atraumatic vascular clamp for 1 h, followed by reperfusion for 2 h. Animals in the H1 group and H2 group received intraluminal HOS infusion for 1 h immediately after occlusion of SMA, and the rates of infusion were 10 and 20 mL/kg.h, respectively. After 2 h of reperfusion, enterocyte mitochondria morphological quantitative analysis was made with electron microscopy and biogenetics stereology, and the following parameters, including mitochondrial respiratory control ratio (RCR), intestinal O(2) extraction ratio (ER), and mucosal ATP contents, were measured, respectively. RESULTS: After IR, the mitochondria was severely swollen with broken cristae, and mean transaction area, diameter, surface density, and volume density of the mitochondria increased significantly. Meanwhile, specific surface and numeral density of the mitochondria decreased significantly. The mitochondrial RCR, intestinal O(2) ER, and mucosal ATP contents were all decreased significantly. There were no differences in all parameters between the IR group and H1 group. In the H2 group, the mitochondria were slightly swollen, and mean transaction area, diameter, surface density, and volume density of the mitochondria were all significantly lower, with the specific surface and numeral density of the mitochondria significantly higher compared with the IR group. The mitochondrial RCR, intestinal O(2) ER and mucosal ATP contents in H2 group were all significantly higher than those in IR group. CONCLUSIONS: Intraluminal HOS infusion at 20 mL/kg.h during ischemia ameliorates structural and functional changes of enterocyte mitochondria associated with intestinal IR injury, which is a safe, simple, and effective measure to protect the intestine from IR injury.