Morphine Sulfate Attenuates Hemorrhagic Shock- Induced Hyperpermeability

Charleston, Craig; Puana, Rudolph; McAllister, Russell K.; Hunter, Felicia A.; Childs, Ed W.

doi:10.1213/01.ane.0000221186.64599.78

Cited by 8 publications

(5 citation statements)

References 27 publications

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“…Three 73-m 2 AOIs were assigned inside the venule, with three corresponding 73-m 2 areas just outside it. Leak was expressed as a ratio of fluorescence outside venules (AOIo) compared with that inside venules (AOIi), as previously described with slight modifications and after background subtraction (12): leak ratio ϭ (AOIo/AOIi) ϫ 100.…”

Section: Methodsmentioning

confidence: 99%

Pkd2 mesenteric vessels exhibit a primary defect in endothelium-dependent vasodilatation restored by rosiglitazone

Brookes

Ruff

Upadhyay

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Patients with autosomal dominant polycystic kidney disease have a high prevalence of hypertension and structural vascular abnormalities, such as intracranial aneurysms. Hypertension can develop in childhood and often precedes a significant reduction in the glomerular filtration rate. The major aim of this study was to investigate whether a primary endothelial defect or a vascular smooth muscle (VSM) defect was present in murine polycystic kidney disease (Pkd)2 heterozygous mesenteric vessels before the development of renal failure or hypertension. Using pressure myography, we observed a marked defect in ACh-stimulated endothelium-dependent vasodilatation in Pkd2 arterioles. In contrast, Pkd2 vessels responded normally to sodium nitroprusside, phenylephrine, KCl, and pressure, indicating unaltered VSM-dependent responses. Pretreatment with the peroxisome proliferator-activated receptor-γ agonist rosiglitazone significantly restored ACh-dependent vasodilation in Pkd2 mice. Isolated heterozygous Pkd2 endothelial cells displayed normal ACh-stimulated Ca(2+) and nitric oxide production. However, isolated Pkd2 heterozygous VSM cells displayed basal increases in superoxide and sodium nitroprusside-stimulated peroxynitrite formation, which were both suppressed by rosiglitazone. Furthermore, we observed a defective response of Pkd2 mesenteric venules to ACh in vivo, which was more marked after ischemia-reperfusion injury. In conclusion, the results of our study suggest that the defect in vasodilatation in Pkd2 heterozygous vessels is primarily due to a reduction in nitric bioavailability secondary to increased vascular oxidative stress. The ability of rosiglitazone to correct this phenotype suggests that this defect is potentially reversible in patients with autosomal dominant polycystic kidney disease.

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Section: Methodsmentioning

confidence: 99%

Pkd2 mesenteric vessels exhibit a primary defect in endothelium-dependent vasodilatation restored by rosiglitazone

Brookes

Ruff

Upadhyay

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…Whereas a G(s) inhibitor or PKA inhibitor blocked only chronic effects, a PKC inhibitor blocked only acute effects (888). Morphine attenuated hemorrhagic shockinduced hyper permeability (182). Morphine and naloxone respectively decreased and increased the rate of hemorrhage-induced hypovolemia in sheep (363).…”

Section: B Cardioprotection and Ischemic Preconditioningmentioning

confidence: 97%

Endogenous opiates and behavior: 2009

Bodnar

2010

Peptides

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“…For the remaining studies (see Table, Supplemental Digital Content 6 for individual study details and results, http://links.lww.com/SHK/B319), data was too sparse to categorize the therapeutic agents based on their working mechanism. Charleston et al reported a reduction in hemorrhagic shock-induced microvascular leakage following treatment with morphine sulphate in the intestinal vascular bed (55). Inhibition of complement activation with C1-INH did not affect microvascular leakage (21), while targeting coagulopathy with rFXIII, a fibrin stabilizing factor, reduced pulmonary microvascular leakage (56).…”

Section: Others (N U 5)mentioning

confidence: 99%

Therapeutically Targeting Microvascular Leakage in Experimental Hemorrhagic SHOCK: A Systematic Review and Meta-Analysis

Leeuwen

Borgdorff

Dekker

et al. 2021

Shock

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Background: Microvascular leakage is proposed as main contributor to disturbed microcirculatory perfusion following hemorrhagic shock and fluid resuscitation, leading to organ dysfunction and unfavorable outcome. Currently, no drugs areavailabletoreduceor preventmicrovascular leakageinclinicalpractice.Wethereforeaimedtoprovideanoverviewoftherapeutic agents targeting microvascular leakage following experimental hemorrhagic shock and fluid resuscitation. Methods: PubMed, EMBASE.com, and Cochrane Library were searched in January 2021 for preclinical studies of hemorrhagic shock using any therapeutic agent on top of standard fluid resuscitation. Primary outcome was vascular leakage, defined as edema, macromolecule extravasation, or glycocalyx degradation. Drugs were classified by targeting pathways and subgroup analyses were performed per organ. Results: Forty-five studies, published between 1973 and 2020, fulfilled eligibility criteria. The included studies tested 54 different therapeutics mainly in pulmonary and intestinal vascular beds. Most studies induced trauma besides hemorrhagic shock. Forty-four therapeutics (81%) were found effective to reduce microvascular leakage, edema formation, or glycocalyx degradation in at least one organ. Targeting oxidative stress and apoptosis was the predominantly effective strategy (SMD: À2.18, CI [À3.21, À1.16], P < 0.0001). Vasoactive agents were found noneffective in reducing microvascular leakage (SMD: À0.86, CI [À3.07, 1.36], P ¼ 0.45). Conclusion: Pharmacological modulation of pathways involved in cell metabolism, inflammation, endothelial barrier regulation, sex hormones and especially oxidative stress and apoptosis were effective in reducing microvascular leakage in experimental hemorrhagic shock with fluid resuscitation. Future studies should investigate whether targeting these pathways can restore microcirculatory perfusion and reduce organ injury following hemorrhagic shock. Systematic review registration number: CRD42018095432.

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Morphine Sulfate Attenuates Hemorrhagic Shock- Induced Hyperpermeability

Cited by 8 publications

References 27 publications

Pkd2 mesenteric vessels exhibit a primary defect in endothelium-dependent vasodilatation restored by rosiglitazone

Pkd2 mesenteric vessels exhibit a primary defect in endothelium-dependent vasodilatation restored by rosiglitazone

Endogenous opiates and behavior: 2009

Therapeutically Targeting Microvascular Leakage in Experimental Hemorrhagic SHOCK: A Systematic Review and Meta-Analysis

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