BACKGROUND:Zinc-based alloy medical implant materials have excellent mechanical properties,complete degradability and good biocompatibility,and are mainly used in orthopedic implants,cardiovascular stents,bile duct stents,tracheal stents,nerve catheters,etc. OBJECTIVE:To review the research progress of biodegradable zinc-based alloys in bone defect repair and prospect the promising research direction and achievements of zinc-based materials. METHODS:After searching PubMed,Web of Science,WanFang Data,and CNKI databases from the establishment of the database to June 2023,various relevant articles on biodegradable zinc-based alloys for bone implant material research were collected.The basic characteristics of biodegradable zinc based alloys were summarized,and the role of zinc-based alloys in promoting bone tissue repair was sorted and summarized.The current research hotspots and shortcomings were discussed. RESULTS AND CONCLUSION:(1)Zinc-based alloys have good biocompatibility.Using zinc-based alloys as the matrix material,with the help of scaffold structure construction technology and coating optimization process,the bone conductivity of zinc-based alloys will be effectively improved,and their degradation products will have efficient bone induction to regulate the gene expression of osteoblasts and osteoclasts,thereby promoting the repair and reconstruction of bone defects.(2)However,in the research on optimizing zinc-based alloys,the coating process is relatively insufficient,and additive loading technology is still lacking.(3)Zinc-based alloys have excellent mechanical and biological properties.Through special processes,their bone conductivity and osteoinductivity can be increased to effectively improve their ability to promote bone repair and reconstruction,and it is expected to further achieve the development of personalized transplant materials.Further research and development are needed to optimize the integration of coating and additive loading technologies into zinc-based alloys.

ObjectiveTo explore the construction and evaluation methods of a rat model of acute myocardial infarction（AMI） with Qi and Yin deficiency syndrome established by sleep deprivation combined with coronary artery ligation. MethodsThirty-six SD rats were randomly divided into a normal group（n=6）， a myocardial infarction group（model A group， n=10）， an acute sleep deprivation+myocardial infarction group（model B group， n=10）， and a chronic sleep deprivation+myocardial infarction group（model C group， n=10） according to body weight. Rats in the normal group were not treated， rats in the model A group underwent only ligation of the left anterior descending coronary artery， rats in the model B group were sleep deprived for 96 h and then underwent ligation of the left anterior descending coronary artery， and rats in the model C group were sleep deprived for an additional 48 h each week with a 24 h rest period as one cycle for three weeks on the basis of the model B group. After coronary artery ligation in the model C group， the first week was defined as the starting point of the first sleep deprivation cycle， and indexes were tested weekly for rats in each group for 3 weeks. Electrocardiogram was used to determine the ligation of the left anterior descending coronary artery in rats， and small animal echocardiography was used to evaluate the cardiac function. The levels of serum creatine kinase（CK）， creatine kinase isoenzyme（CK-MB）， lactate dehydrogenase（LDH）， cardiac troponin T（cTnT）， interleukin-18（IL-18）， and tumor necrosis factor-α（TNF-α） were detected by biochemical assays， and hematoxylin-eosin（HE） staining was used to evaluate the pathological changes of myocardial tissue in rats. The syndrome indicators of Qi and Yin deficiency were evaluated by general state and body weight， grip strength， facial temperature， paw temperature， rectal temperature， salivary flow rate， open field test， tongue color［red（R）， green（G）， and blue（B）］ values， pulse amplitude changes， and enzyme-linked immunosorbent assay（ELISA） for the detection of expression levels of cyclic adenosine monophosphate（cAMP）， cyclic guanosine monophosphate（cGMP）， rat serum corticotropin-releasing factor（CRF）， adrenocorticotropic hormone（ACTH）， triiodothyronine（T3）， tetraiodothyronine（T4）， and corticosterone（CORT） in serum. ResultsIn terms of disease indicators， compared with the normal group， the ST segment of the electrocardiogram in each model group was significantly elevated， the echocardiographic parameters were decreased， the contents of myocardial enzymes and inflammatory factors were increased（P<0.01）， and the myocardial tissue in the infarcted area was significantly damaged. In terms of syndrome indicators， compared with the normal group， the body weight of rats in the model B and C groups decreased at each time point， the grip strength of each model group decreased， the total distance traveled and the number of entries into the center in the open field test decreased， the immobility time increased， the facial and rectal temperatures of rats in the model B and C groups increased， the salivary flow rate of each model group decreased， the tongue color was bright red or light， the tongue body was dry or smooth like a mirror， lacking of moisture sensation， the R， G and B values of the tongue surface increased， the pulse amplitude changes decreased， and the contents of T3 and T4 increased， while the expressions of cAMP， CRF， ACTH and CORT in the model B and C groups increased（P<0.05， P<0.01）. ConclusionContinuous sleep deprivation for 96 h in a multi-platform method combined with coronary artery ligation can construct a rat model of AMI with Qi and Yin deficiency syndrome， and the syndrome manifestations can be maintained for 3 weeks.

ObjectiveTo explore the feasibility， evaluation methods and metabolic differences of high-fat diet（HFD） combined with myocardial ischemia-reperfusion injury（MIRI） to establish a rat model of myocardial ischemia-reperfusion with phlegm and blood stasis blocking collaterals syndrome（PBSBCS）. MethodsThirty-two SD rats were randomly divided into the sham operation， HFD， MIRI， and MIRI+HFD groups. Rats in the sham operation and MIRI groups were fed a standard diet（regular chow）， while the HFD and MIRI+HFD groups received a HFD for 10 weeks. Rats in the MIRI and MIRI+HFD groups underwent myocardial ischemia-reperfusion surgery， while the sham operation group underwent only thread placement without ligation. Cardiac function was assessed via small-animal echocardiography， including left ventricular ejection fraction（EF）， left ventricular fractional shortening（FS）， cardiac output（CO）， and stroke volume（SV）. Serum levels of creatine kinase（CK）， CK-MB， triglyceride（TG）， total cholesterol（TC）， high-density lipoprotein cholesterol（HDL-C）， low-density lipoprotein cholesterol（LDL-C）， lactate dehydrogenase（LDH）， endothelin-1（ET-1）， endothelial nitric oxide synthase（eNOS）， tumor necrosis factor-α（TNF-α）， interleukin-18（IL-18）， oxidized LDL（ox-LDL）， and cardiac troponin T（cTnT） were measured by biochemical assays and enzyme-linked immunosorbent assay（ELISA）. Myocardial histopathology was evaluated via hematoxylin-eosin（HE） staining， while myocardial infarction and no-reflow area were assessed using 2，3，5-triphenyltetrazolium chloride（TTC）， Evans blue， and thioflavin staining. Changes in syndrome characteristics［body weight， tongue surface red-green-blue ［RGB］ values， and pulse amplitude］ of PBSBCS were recorded. Serum differential metabolites were analyzed by ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）. ResultsCompared with the sham operation group， the HFD and MIRI+HFD groups showed significant increases in body weight（P<0.01）， RGB values and pulse amplitude decreased in the HFD， MIRI and MIRI+HFD groups， TC， TG， LDL-C and ox-LDL levels increased in the HFD and MIRI+HFD groups， while HDL-C decreased. Blood perfusion peak time and myocardial no-reflow area increased， serum eNOS level decreased， and CK-MB， LDH， and cTnT activities increased in the HFD， MIRI and MIRI+HFD groups（P<0.05， P<0.01）. Whole blood viscosity was increased in the HFD group at medium shear rate， and in the MIRI and MIRI+HFD groups at low， medium and high shear rates（P<0.05， P<0.01）. Platelet aggregation rate increased in the MIRI and MIRI+HFD groups， accompanied by elevated ET-1， TNF-α， and IL-18 levels， reduced cardiac function indices， expanded myocardial no-reflow and infarction areas， and increased serum CK， CK-MB， LDH， and cTnT activities（P<0.05， P<0.01）. Compared with the MIRI group， the HFD and MIRI+HFD groups showed significant increase in body weight， TC， TG， LDL-C and ox-LDL levels， and significant decrease in HDL-C content（P<0.01）. The MIRI+HFD group showed decrease in RGB values and pulse amplitude， and an increase in whole blood viscosity， platelet aggregation， blood perfusion peak time， myocardial no-reflow and infarction areas， elevated ET-1， TNF-α and IL-18 levels， decreased eNOS content， EF and SV， increased serum CK， CK-MB and cTnT activities， and worsened myocardial pathology（P<0.05）. Compared with the HFD group， the MIRI+HFD group showed similar aggravated trends（P<0.05， P<0.01）. Metabolomics results showed that 34 potential biomarkers involving 13 common metabolic pathways were identified in the MIRI+HFD group compared with the sham operation group. ConclusionThe MIRI group resembles blood stasis syndrome in hemodynamics and myocardial injury， and the HFD group mirrors phlegm-turbidity syndrome in lipid profiles and tongue characteristics. While the MIRI+HFD group aligns with PBSBCS in comprehensive indices， effectively simulating clinical features of coronary heart disease（CHD）， which can be used for the evaluation of the pathological mechanism and pharmacodynamics of CHD with PBSBCS.

ObjectiveTo investigate the preparation method of a mouse model of cerebral infarction with Qi and Yin deficiency syndrome induced by streptozotocin（STZ） combined with the photochemical method， and to evaluate the biological basis of the established model. MethodsForty C57B6/J mice were randomly divided into the normal and model groups， with 20 mice in each group. The normal group received no treatment， while the model group was injected intraperitoneally with 55 mg·kg^-1 of STZ once a day for 5 days. Fourteen days post-STZ induction， 10 mice from the normal group were randomly taken into the photochemical group， while 10 mice from the model group were randomly taken into the STZ+photochemical group. Rose Bengal solution injection combined with 520 nm laser irradiation was used to cause thrombosis and induce cerebral infarction in mice. Syndrome indexes for Qi and Yin deficiency were assessed by general state observation， body weight， grip strength， rectal temperature， behavioral experiments， energy metabolism， tongue color［red（R）， green（G）， blue（B）］ values， adenosine triphosphate（ATP） content， corticotropin-releasing factor（CRF） and triiodothyronine（T3） levels. The pathological changes of cerebral infarction in mice were evaluated by detecting serum superoxide dismutase（SOD）， interleukin-1β（IL-1β）， IL-6， and tumor necrosis factor-α（TNF-α） levels in combination with Bederson score. Finally， the endogenous metabolites in mice were detected by ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）， and multivariate statistical analysis was performed by partial least squares-discriminant analysis（PLS-DA） and orthogonal partial least squares-discriminant analysis（OPLS-DA）. The data filtering criteria were set as variable importance in the projection（VIP） value> 1， fold change（FC）<0.8 or FC>1.2， P<0.05， to obtain differential metabolites. Then MetaboAnalyst 3.0 was utilized for pathway enrichment analysis of the differential metabolites， aiming to explore the metabolic profile changes and biological basis of mice with Qi and Yin deficiency syndrome of cerebral infarction. ResultsRegarding the syndrome indicators， compared with the normal group， the mice in the model group had lower body weight， higher rectal temperature， lower limb motor ability and energy metabolism efficiency， lower ATP content， lower R， G and B values of the tongue surface， and lower speed of blood glucose regression（P<0.05， P<0.01）. As for the disease indicators， compared with the normal group， the Bederson scores of the photochemical group and the STZ+photochemical group increased， the grip strength decreased， the SOD level decreased， and the levels of inflammatory factors increased（P<0.05）. The results of metabolomics showed that a good separation pattern of components was observed among mice in each group， with significant differences in components. Identification of MS data revealed a total of 44 differential metabolites in mice with Qi and Yin deficiency syndrome of cerebral infarction. Among them， 32 metabolites were up-regulated， mainly including triglycerides， diglycerides， phospholipids， and ceramides. And 12 metabolites were down-regulated， mainly including amino acid and phosphate metabolites. Pathway enrichment analysis of the above differential metabolites indicated that the metabolic pathways were mainly enriched in folate biosynthesis， terpenoid skeleton biosynthesis， glycerophospholipid metabolism， vitamin B₆ metabolism， glycerolipid metabolism and sphingolipid metabolism. These pathways were involved in multiple processes such as lipid transport， insulin resistance， and energy metabolism. ConclusionThe method of STZ injection combined with photochemical induction can successfully establish a mouse model of cerebral infarction with Qi and Yin deficiency syndrome， and intervene in vivo processes such as folate biosynthesis， glycerophospholipid metabolism， and glycerolipid metabolism.

ObjectiveTo explore the construction and evaluation methods of a rat model of acute myocardial infarction（AMI） with Qi and Yin deficiency syndrome established by sleep deprivation combined with coronary artery ligation. MethodsThirty-six SD rats were randomly divided into a normal group（n=6）， a myocardial infarction group（model A group， n=10）， an acute sleep deprivation+myocardial infarction group（model B group， n=10）， and a chronic sleep deprivation+myocardial infarction group（model C group， n=10） according to body weight. Rats in the normal group were not treated， rats in the model A group underwent only ligation of the left anterior descending coronary artery， rats in the model B group were sleep deprived for 96 h and then underwent ligation of the left anterior descending coronary artery， and rats in the model C group were sleep deprived for an additional 48 h each week with a 24 h rest period as one cycle for three weeks on the basis of the model B group. After coronary artery ligation in the model C group， the first week was defined as the starting point of the first sleep deprivation cycle， and indexes were tested weekly for rats in each group for 3 weeks. Electrocardiogram was used to determine the ligation of the left anterior descending coronary artery in rats， and small animal echocardiography was used to evaluate the cardiac function. The levels of serum creatine kinase（CK）， creatine kinase isoenzyme（CK-MB）， lactate dehydrogenase（LDH）， cardiac troponin T（cTnT）， interleukin-18（IL-18）， and tumor necrosis factor-α（TNF-α） were detected by biochemical assays， and hematoxylin-eosin（HE） staining was used to evaluate the pathological changes of myocardial tissue in rats. The syndrome indicators of Qi and Yin deficiency were evaluated by general state and body weight， grip strength， facial temperature， paw temperature， rectal temperature， salivary flow rate， open field test， tongue color［red（R）， green（G）， and blue（B）］ values， pulse amplitude changes， and enzyme-linked immunosorbent assay（ELISA） for the detection of expression levels of cyclic adenosine monophosphate（cAMP）， cyclic guanosine monophosphate（cGMP）， rat serum corticotropin-releasing factor（CRF）， adrenocorticotropic hormone（ACTH）， triiodothyronine（T3）， tetraiodothyronine（T4）， and corticosterone（CORT） in serum. ResultsIn terms of disease indicators， compared with the normal group， the ST segment of the electrocardiogram in each model group was significantly elevated， the echocardiographic parameters were decreased， the contents of myocardial enzymes and inflammatory factors were increased（P<0.01）， and the myocardial tissue in the infarcted area was significantly damaged. In terms of syndrome indicators， compared with the normal group， the body weight of rats in the model B and C groups decreased at each time point， the grip strength of each model group decreased， the total distance traveled and the number of entries into the center in the open field test decreased， the immobility time increased， the facial and rectal temperatures of rats in the model B and C groups increased， the salivary flow rate of each model group decreased， the tongue color was bright red or light， the tongue body was dry or smooth like a mirror， lacking of moisture sensation， the R， G and B values of the tongue surface increased， the pulse amplitude changes decreased， and the contents of T3 and T4 increased， while the expressions of cAMP， CRF， ACTH and CORT in the model B and C groups increased（P<0.05， P<0.01）. ConclusionContinuous sleep deprivation for 96 h in a multi-platform method combined with coronary artery ligation can construct a rat model of AMI with Qi and Yin deficiency syndrome， and the syndrome manifestations can be maintained for 3 weeks.

ObjectiveTo explore the feasibility， evaluation methods and metabolic differences of high-fat diet（HFD） combined with myocardial ischemia-reperfusion injury（MIRI） to establish a rat model of myocardial ischemia-reperfusion with phlegm and blood stasis blocking collaterals syndrome（PBSBCS）. MethodsThirty-two SD rats were randomly divided into the sham operation， HFD， MIRI， and MIRI+HFD groups. Rats in the sham operation and MIRI groups were fed a standard diet（regular chow）， while the HFD and MIRI+HFD groups received a HFD for 10 weeks. Rats in the MIRI and MIRI+HFD groups underwent myocardial ischemia-reperfusion surgery， while the sham operation group underwent only thread placement without ligation. Cardiac function was assessed via small-animal echocardiography， including left ventricular ejection fraction（EF）， left ventricular fractional shortening（FS）， cardiac output（CO）， and stroke volume（SV）. Serum levels of creatine kinase（CK）， CK-MB， triglyceride（TG）， total cholesterol（TC）， high-density lipoprotein cholesterol（HDL-C）， low-density lipoprotein cholesterol（LDL-C）， lactate dehydrogenase（LDH）， endothelin-1（ET-1）， endothelial nitric oxide synthase（eNOS）， tumor necrosis factor-α（TNF-α）， interleukin-18（IL-18）， oxidized LDL（ox-LDL）， and cardiac troponin T（cTnT） were measured by biochemical assays and enzyme-linked immunosorbent assay（ELISA）. Myocardial histopathology was evaluated via hematoxylin-eosin（HE） staining， while myocardial infarction and no-reflow area were assessed using 2，3，5-triphenyltetrazolium chloride（TTC）， Evans blue， and thioflavin staining. Changes in syndrome characteristics［body weight， tongue surface red-green-blue ［RGB］ values， and pulse amplitude］ of PBSBCS were recorded. Serum differential metabolites were analyzed by ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）. ResultsCompared with the sham operation group， the HFD and MIRI+HFD groups showed significant increases in body weight（P<0.01）， RGB values and pulse amplitude decreased in the HFD， MIRI and MIRI+HFD groups， TC， TG， LDL-C and ox-LDL levels increased in the HFD and MIRI+HFD groups， while HDL-C decreased. Blood perfusion peak time and myocardial no-reflow area increased， serum eNOS level decreased， and CK-MB， LDH， and cTnT activities increased in the HFD， MIRI and MIRI+HFD groups（P<0.05， P<0.01）. Whole blood viscosity was increased in the HFD group at medium shear rate， and in the MIRI and MIRI+HFD groups at low， medium and high shear rates（P<0.05， P<0.01）. Platelet aggregation rate increased in the MIRI and MIRI+HFD groups， accompanied by elevated ET-1， TNF-α， and IL-18 levels， reduced cardiac function indices， expanded myocardial no-reflow and infarction areas， and increased serum CK， CK-MB， LDH， and cTnT activities（P<0.05， P<0.01）. Compared with the MIRI group， the HFD and MIRI+HFD groups showed significant increase in body weight， TC， TG， LDL-C and ox-LDL levels， and significant decrease in HDL-C content（P<0.01）. The MIRI+HFD group showed decrease in RGB values and pulse amplitude， and an increase in whole blood viscosity， platelet aggregation， blood perfusion peak time， myocardial no-reflow and infarction areas， elevated ET-1， TNF-α and IL-18 levels， decreased eNOS content， EF and SV， increased serum CK， CK-MB and cTnT activities， and worsened myocardial pathology（P<0.05）. Compared with the HFD group， the MIRI+HFD group showed similar aggravated trends（P<0.05， P<0.01）. Metabolomics results showed that 34 potential biomarkers involving 13 common metabolic pathways were identified in the MIRI+HFD group compared with the sham operation group. ConclusionThe MIRI group resembles blood stasis syndrome in hemodynamics and myocardial injury， and the HFD group mirrors phlegm-turbidity syndrome in lipid profiles and tongue characteristics. While the MIRI+HFD group aligns with PBSBCS in comprehensive indices， effectively simulating clinical features of coronary heart disease（CHD）， which can be used for the evaluation of the pathological mechanism and pharmacodynamics of CHD with PBSBCS.

ObjectiveTo investigate the preparation method of a mouse model of cerebral infarction with Qi and Yin deficiency syndrome induced by streptozotocin（STZ） combined with the photochemical method， and to evaluate the biological basis of the established model. MethodsForty C57B6/J mice were randomly divided into the normal and model groups， with 20 mice in each group. The normal group received no treatment， while the model group was injected intraperitoneally with 55 mg·kg^-1 of STZ once a day for 5 days. Fourteen days post-STZ induction， 10 mice from the normal group were randomly taken into the photochemical group， while 10 mice from the model group were randomly taken into the STZ+photochemical group. Rose Bengal solution injection combined with 520 nm laser irradiation was used to cause thrombosis and induce cerebral infarction in mice. Syndrome indexes for Qi and Yin deficiency were assessed by general state observation， body weight， grip strength， rectal temperature， behavioral experiments， energy metabolism， tongue color［red（R）， green（G）， blue（B）］ values， adenosine triphosphate（ATP） content， corticotropin-releasing factor（CRF） and triiodothyronine（T3） levels. The pathological changes of cerebral infarction in mice were evaluated by detecting serum superoxide dismutase（SOD）， interleukin-1β（IL-1β）， IL-6， and tumor necrosis factor-α（TNF-α） levels in combination with Bederson score. Finally， the endogenous metabolites in mice were detected by ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS）， and multivariate statistical analysis was performed by partial least squares-discriminant analysis（PLS-DA） and orthogonal partial least squares-discriminant analysis（OPLS-DA）. The data filtering criteria were set as variable importance in the projection（VIP） value> 1， fold change（FC）<0.8 or FC>1.2， P<0.05， to obtain differential metabolites. Then MetaboAnalyst 3.0 was utilized for pathway enrichment analysis of the differential metabolites， aiming to explore the metabolic profile changes and biological basis of mice with Qi and Yin deficiency syndrome of cerebral infarction. ResultsRegarding the syndrome indicators， compared with the normal group， the mice in the model group had lower body weight， higher rectal temperature， lower limb motor ability and energy metabolism efficiency， lower ATP content， lower R， G and B values of the tongue surface， and lower speed of blood glucose regression（P<0.05， P<0.01）. As for the disease indicators， compared with the normal group， the Bederson scores of the photochemical group and the STZ+photochemical group increased， the grip strength decreased， the SOD level decreased， and the levels of inflammatory factors increased（P<0.05）. The results of metabolomics showed that a good separation pattern of components was observed among mice in each group， with significant differences in components. Identification of MS data revealed a total of 44 differential metabolites in mice with Qi and Yin deficiency syndrome of cerebral infarction. Among them， 32 metabolites were up-regulated， mainly including triglycerides， diglycerides， phospholipids， and ceramides. And 12 metabolites were down-regulated， mainly including amino acid and phosphate metabolites. Pathway enrichment analysis of the above differential metabolites indicated that the metabolic pathways were mainly enriched in folate biosynthesis， terpenoid skeleton biosynthesis， glycerophospholipid metabolism， vitamin B₆ metabolism， glycerolipid metabolism and sphingolipid metabolism. These pathways were involved in multiple processes such as lipid transport， insulin resistance， and energy metabolism. ConclusionThe method of STZ injection combined with photochemical induction can successfully establish a mouse model of cerebral infarction with Qi and Yin deficiency syndrome， and intervene in vivo processes such as folate biosynthesis， glycerophospholipid metabolism， and glycerolipid metabolism.

Background: Intraoperative hypercapnia reduces the time to emergence from volatile anesthetics, but few clinical studies have explored the effect of hypercapnia on the emergence time from intravenous (IV) anesthesia. We investigated the effect of inducing mild hypercapnia during the recovery period on the emergence time after total IV anesthesia (TIVA). Methods: Adult patients undergoing transurethral lithotripsy under TIVA were randomly allocated to normocapnia group (end-tidal carbon dioxide [ETCO2] 35–40 mmHg) or mild hypercapnia group (ETCO2 50-55 mmHg) during the recovery period. The primary outcome was the extubation time. The spontaneous breathing-onset time, voluntary eye-opening time, and hemodynamic data were collected. Changes in the cerebral blood flow velocity in the middle cerebral artery were assessed using transcranial Doppler ultrasound. Results: In total, 164 patients completed the study. The extubation time was significantly shorter in the mild hypercapnia (13.9 ± 5.9 min, P = 0.024) than in the normocapnia group (16.3 ± 7.6 min). A similar reduction was observed in spontaneous breathing-onset time (P = 0.021) and voluntary eye-opening time (P = 0.008). Multiple linear regression analysis revealed that the adjusted ETCO2 level was a negative predictor of extubation time. Middle cerebral artery blood flow velocity was significantly increased after ETCO2 adjustment for mild hypercapnia, which rapidly returned to baseline, without any adverse reactions, within 20 min after extubation. Conclusions Mild hypercapnia during the recovery period significantly reduces the extubation time after TIVA. Increased ETCO2 levels can potentially enhance rapid recovery from IV anesthesia.

Background: Intraoperative hypercapnia reduces the time to emergence from volatile anesthetics, but few clinical studies have explored the effect of hypercapnia on the emergence time from intravenous (IV) anesthesia. We investigated the effect of inducing mild hypercapnia during the recovery period on the emergence time after total IV anesthesia (TIVA). Methods: Adult patients undergoing transurethral lithotripsy under TIVA were randomly allocated to normocapnia group (end-tidal carbon dioxide [ETCO2] 35–40 mmHg) or mild hypercapnia group (ETCO2 50-55 mmHg) during the recovery period. The primary outcome was the extubation time. The spontaneous breathing-onset time, voluntary eye-opening time, and hemodynamic data were collected. Changes in the cerebral blood flow velocity in the middle cerebral artery were assessed using transcranial Doppler ultrasound. Results: In total, 164 patients completed the study. The extubation time was significantly shorter in the mild hypercapnia (13.9 ± 5.9 min, P = 0.024) than in the normocapnia group (16.3 ± 7.6 min). A similar reduction was observed in spontaneous breathing-onset time (P = 0.021) and voluntary eye-opening time (P = 0.008). Multiple linear regression analysis revealed that the adjusted ETCO2 level was a negative predictor of extubation time. Middle cerebral artery blood flow velocity was significantly increased after ETCO2 adjustment for mild hypercapnia, which rapidly returned to baseline, without any adverse reactions, within 20 min after extubation. Conclusions Mild hypercapnia during the recovery period significantly reduces the extubation time after TIVA. Increased ETCO2 levels can potentially enhance rapid recovery from IV anesthesia.

Background: Intraoperative hypercapnia reduces the time to emergence from volatile anesthetics, but few clinical studies have explored the effect of hypercapnia on the emergence time from intravenous (IV) anesthesia. We investigated the effect of inducing mild hypercapnia during the recovery period on the emergence time after total IV anesthesia (TIVA). Methods: Adult patients undergoing transurethral lithotripsy under TIVA were randomly allocated to normocapnia group (end-tidal carbon dioxide [ETCO2] 35–40 mmHg) or mild hypercapnia group (ETCO2 50-55 mmHg) during the recovery period. The primary outcome was the extubation time. The spontaneous breathing-onset time, voluntary eye-opening time, and hemodynamic data were collected. Changes in the cerebral blood flow velocity in the middle cerebral artery were assessed using transcranial Doppler ultrasound. Results: In total, 164 patients completed the study. The extubation time was significantly shorter in the mild hypercapnia (13.9 ± 5.9 min, P = 0.024) than in the normocapnia group (16.3 ± 7.6 min). A similar reduction was observed in spontaneous breathing-onset time (P = 0.021) and voluntary eye-opening time (P = 0.008). Multiple linear regression analysis revealed that the adjusted ETCO2 level was a negative predictor of extubation time. Middle cerebral artery blood flow velocity was significantly increased after ETCO2 adjustment for mild hypercapnia, which rapidly returned to baseline, without any adverse reactions, within 20 min after extubation. Conclusions Mild hypercapnia during the recovery period significantly reduces the extubation time after TIVA. Increased ETCO2 levels can potentially enhance rapid recovery from IV anesthesia.