Arterial Duct Stenting Versus Modified Blalock-Taussig Shunt in Patient with Ductal-Dependent Pulmonary Circulation: Systematic Review & Meta-Analysis

Objective:Patients with ductal-dependent pulmonary circulation require alternative bloodflow to provide and maintain adequate oxygenation.Modified Blalock-Taussig Shunt(MBTS)has been the standard for providing such a result.Currently,less invasive methods such as Arterial Duct(AD)stenting have been performed as alter-natives.This study aims to compare the outcome of AD stenting and MBTS.Method:Systematic research was performed in online databases using the PRISMA protocol.The outcomes measured were 30-day mortality,com-plication,unplanned intervention,oxygen saturation,duration of hospital,and ICU length of stay.Any compara-tive study provided with full text is included.The outcome of each study was analyzed using a trandom effects model with relative risk and mean difference as the effect size.Bias risk assessment was conducted using the New-castle-Ottawa Scale.All analyses were performed using Review Manager 5.4.1.Result:A total of 11 studies with 3154 samples included in this study.There is no significant difference in 30-day mortality between the two groups(p-value=0.10).However,there is significantly less complication(RR 0.53[0.35,0.82];p-value=0.004)and unplanned intervention(RR 0.59[0.38,0.92];p-value=0.02)in the AD stent group.Comparison of the Nakata index showed no significant difference(p-value=0.88).Post-operative oxygen saturation was measured signifi-cantly higher in the AD stenting(MD 1.80[0.85,2.74];p-value=0.0002).However,AD stent group shows sig-nificantly lower long-term oxygen saturation(MD-8.43[-14.38,-2.48];p-value=0.005).Both hospital and ICU length of stay was significantly shorter in the AD stent group(MD-8.30[-11.13,-5.48];p-value<0.00001;MD-5.09[-7.79,-2.38];p-value=0.0002).Conclusion:AD stenting provides comparable outcomes relative to MBTS as it provides less complication and unplanned intervention and higher post-procedural O2 saturation.However,MBTS proved its superiority in maintaining higher long-term oxygen saturation and still became the preferred option to manage complex cases where stenting is either challenging or unsuccessful.

Effect of Simulated Microgravity and its Associated Mechanism on Pulmonary Circulation in Rats

Objective To study the effect of Simulated Microgravity and its Associated Mechanism on Pulmonary Circulation in Rats. Methods Rat tail-suspension model was used to simulate the physiological effects of microgravity and changes in pulmonary blood vessel morphology, pulmonary arterial and venous blood pressure, pulmonary vascular resistance, pulmonary vasomotoricity, as well as the regulation of pulmonary circulation by cytokines produced and released by the lung of rats were measured. Results The walls of pulmonary blood vessels of rats were thickened, and the pulmonary artery was reconstructed with increased pulmonary vascular resistance. The pulmonary blood vessels of rats became more prone to dilation as contractions increased. Rat epithelial Adrenomedulin gene transcription and protein expression were upregulated. The level of basic fibroblast growth Factor of rat was also elevated. Conclusion Findings from the present study on rats revealed that the microgravity can affect pulmonary blood vessel structure, pulmonary arterial pressure, and pulmonary blood vessel self-regulation and cytokine production.

Hypoxia in the pulmonary vein increases pulmonary vascular resistance independently of oxygen in the pulmonary artery

Introduction:Hypoxic pulmonary vasoconstriction(HPV)can be a challenging clinical problem.It is not fully elucidated where in the circulation the regulation of resistance takes place.It is often referred to as if it is in the arteries,but we hypothesized that it is in the venous side of the pulmonary circulation.Methods:In an open thorax model,pigs were treated with a veno-venous extra corporeal membrane oxygenator to either oxygenate or deoxygenate blood passing through the pulmonary vessels.At the same time the lungs were ventilated with extreme variations of inspired air from 5%to 100%oxygen,making it possible to make combinations of high and low oxygen content through the pulmonary circulation.A flow probe was inserted around the main pulmonary artery and catheters in the pulmonary artery and in the left atrium were used for pressure monitoring and blood tests.Under different combinations of oxygenation,pulmonary vascular resistance(PVR)was calculated.Results:With unchanged level of oxygen in the pulmonary artery and reduced inspired oxygen fraction lowering oxygen tension from 29 to 6.7 kPa in the pulmonary vein,PVR was doubled.With more extreme hypoxia PVR suddenly decreased.Combinations with low oxygenation in the pulmonary artery did not systematic influence PVR if there was enough oxygen in the inspired air and in the pulmonary veins.Discussion:The impact of hypoxia occurs from the alveolar level and forward with the blood flow.The experiments indicated that the regulation of PVR is mediated from the venous side.

Effects of Prostaglandins and Leukotrienes on Hypoxic Pulmonary Vasoconstriction in Rats

To investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV), in vivo rats experiment and in vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB 2 and 6 keto PGF 1α in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (P pa ) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB 2 and 6 keto PGF 1α and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin) in vivo and in vitro , HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY 171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.

Effects of 3，4－Dihydroxyacetophenone （3，4－DHAP） on Hypoxic Pulmonary and Systemic Vascular Response in Dogs

The effects of 3,4-DHAP on hypoxic pulmonary and systemic vascular responses were studied in anaesthetized dogs. The percentage change in pulmonary vascular resistance(△PVR%)and that in systemic vascular resistance(△SVR%)induced by 5 min hypoxia decreased significantly.3,4-DHAP in doses of 1 mg/kg,3mg/kg,and 10 mg/kg i.v caused a decrease in b PVR% from the control value of 47.27±22.27% to 24.62±21.76%,18.15±18.73%,and 24.10±19.76% respectively, and a decrease in △SVR% from the control value of 12.91±7.39% to -0.34±12.7%,-2.11±12.76%,and -2.37±15.52% respectively.The results showed that 3,4-DHAP could decrease the hypoxic responses of pulmonary and systemic blood vessels.But it did not change △PVR% or △SVR% in dose of 30mg/kg,neither did it influence the heart rate,cardiac output or cerebral blood flow during hypoxia in all the doses used.

Factors Accounting for Different Responses of Pulmonary and Cerebral Vessels to Hypoxia

The roles of sympathicus, sensory neuropeptides (SNP),cyclooxygenase metabolites (COX-M), lipoxygenase metabolites (LOX-M), endothelium derived relaxing factor (EDRF),reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were investigated in intact rats, rabbits and dogs. The results showed that during hypoxia,the excitation of sympathicus caused a constriction of both pulmonary and cerebral vessels,while SNP, EDRF and the opening of voltage sensitive PC caused the dilation of both of them; LOX-M mediated HPV and HCVD, COX-M might serve as their modulators; the blockade of ATP sensitive PC induced by hypoxia mediated HPV, but had no effect on HCVD; the reduction of O_2￣- in the lung might potentiate HPV, however, O_2￣- remained unchanged in brain during hypoxia. It is suggested that the alterations of LOX-M,ROS and the ATP sensitive PC are the factors accounting for the difference in the response of pulmonary and cerebral vessels to hypoxia.

Acute respiratory distress syndrome:focusing on secondary injury

Acute respiratory distress syndrome(ARDS)is one of the most common severe diseases seen in the clinical setting.With the continuous exploration of ARDS in recent decades,the understanding of ARDS has improved.ARDS is not a simple lung disease but a clinical syndrome with various etiologies and pathophysiological changes.However,in the intensive care unit,ARDS often occurs a few days after primary lung injury or after a few days of treatment for other severe extrapulmonary diseases.Under such conditions,ARDS often progresses rapidly to severe ARDS and is difficult to treat.The occurrence and development of ARDS in these circumstances are thus not related to primary lung injury;the real cause of ARDS may be the“second hit”caused by inappropriate treatment.In view of the limited effective treatments for ARDS,the strategic focus has shifted to identifying potential or high-risk ARDS patients during the early stages of the disease and implementing treatment strategies aimed at reducing ARDS and related organ failure.Future research should focus on the prevention of ARDS.