Validation of the relationship between coagulopathy and localization of hydroxyethyl starch on the vascular endothelium in a rat hemodilution model.

Various anticoagulant properties have been associated with hydroxyethyl starch (HES). However, the mechanism remains unclear and it has not been fully considered whether these properties are beyond the dilutional effect itself. The aim of this study was to reproduce the coagulopathy induced by HES and to test the hypothesis that the coagulopathy is caused by endothelial or glycocalyx damage due to localization of HES on the endothelium, which is caused by the high shear viscosity of dilutional blood. Using a rat model, we compared blood coagulability measured by Sonoclot, levels of endothelial and glycocalyx damage markers and coagulation factors, and blood shear viscosity when hemodilution was performed with physiological saline (PS), 6% HES 130/0.4 in PS, and 10% HES 200/0.5 in PS. We also evaluated the localization rates of fluorescently labeled HES on endothelium in the isolated aorta. HES decreased the fibrin gel formation rate more than did PS. HES was shown to cover the endothelium, possibly due to its high shear viscosity, and this mechanism potentially acted to protect, rather than damage, the endothelium and glycocalyx. However, this covering effect may be the cause of coagulopathy due to inhibition of von Willebrand factor secretion from the endothelium.

Effects of anesthetic agents on contractions of the pregnant rat myometrium in vivo and in vitro.

BACKGROUND: Several anesthetic agents are used in cesarean sections for both regional and general anesthesia purposes. However, there are no data comparing the in vivo effects of propofol, sevoflurane, and dexmedetomidine on the contraction of the myometrium in pregnant rats. The aim of this study was to investigate the effect of these anesthetic agents on myometrial contraction and elucidate the underlying mechanisms. METHODS: Contraction force and frequency changes in response to propofol, dexmedetomidine, or sevoflurane were evaluated in vivo and in vitro. To test the effect of arachidonic acid on myometrial contraction enhanced by dexmedetomidine, changes in myometrial contraction with dexmedetomidine after administration of indomethacin were evaluated. The amount of phosphorylated myosin phosphatase target subunit 1 (MYPT1) in the membrane fraction was expressed as a percentage of the total fraction by Western blot analysis. RESULTS: This study demonstrated that dexmedetomidine enhances oxytocin-induced contraction in the myometrium of pregnant rats, whereas propofol and sevoflurane attenuate these contractions. The dexmedetomidine-induced enhancement of myometrial contraction force was abolished by the administration of indomethacin. Propofol did not affect oxytocin-induced MYPT1 phosphorylation, whereas sevoflurane attenuated oxytocin-induced MYPT1 phosphorylation. CONCLUSIONS: Inhibition of myofilament calcium sensitivity may underlie the inhibition of myometrial contraction induced by sevoflurane. Arachidonic acid may play an important role in the enhancement of myometrial contraction induced by dexmedetomidine by increasing myofilament calcium sensitivity. Dexmedetomidine may be used as a sedative agent to promote uterine muscle contraction and suppress bleeding after fetal delivery.

Sevoflurane Promotes Regeneration of the Endothelial Glycocalyx by Upregulating Sialyltransferase.

BACKGROUND: During ischemia-reperfusion injury, the endothelial glycocalyx is damaged by oxidative stress-induced release of hydrogen peroxide, leading to decreased endothelium-dependent vasodilation. The regenerative effects of sevoflurane on the endothelial glycocalyx and endothelium-dependent vasodilation in oxidative stress remain unclear. Sialic acid, which is a component of the glycocalyx, plays a key role in antioxidant activity and is catalyzed by the sialyltransferase, ST6Gal-I. We hypothesized that ST6Gal-I is involved in the sevoflurane-induced promotion of endothelial glycocalyx restoration and endothelium-dependent vasodilation after oxidative stress. MATERIALS AND METHODS: To assess vasodilation, isometric tension in the rat aorta was measured. Aortic rings were treated with 0.5 mM hydrogen peroxide pre-exposure or post exposure to sevoflurane, with or without an ST6Gal-I inhibitor. The rings were then used for glycocalyx imaging using fluorescein isothiocyanate-labeled lectin staining and for immunohistochemistry for ST6Gal-I. RESULTS: Vasodilation was significantly decreased by treatment with hydrogen peroxide compared to controls. Application of sevoflurane after treatment with hydrogen peroxide revived endothelium-dependent vasodilatation, whereas pretreatment with sevoflurane had no such effect. Sevoflurane after-treatment revived the intensity of fluorescence of the endothelial glycocalyx compared to the hydrogen peroxide group. However, pretreatment with sevoflurane had no such effect. Sevoflurane significantly upregulated the reduced expression of ST6Gal-I induced by hydrogen peroxide treatment. CONCLUSIONS: Sevoflurane exerts regenerative effects on endothelium-dependent vasodilation and the endothelial glycocalyx following oxidative stress in the rat aorta.

Desflurane inhibits endothelium-dependent vasodilation more than sevoflurane with inhibition of endothelial nitric oxide synthase by different mechanisms.

The effects of desflurane on endothelium-dependent vasodilation remain uncertain, whereas sevoflurane is known to inhibit it. Endothelium-dependent vasodilation is mainly mediated by endothelial nitric oxide synthase. The effects of desflurane on endothelium-dependent vasodilation were compared with those of sevoflurane, and inhibition mechanisms, including phosphorylation of endothelial nitric oxide synthase and the calcium pathway, were evaluated for the two anesthetics. We hypothesized that desflurane would inhibit endothelium-dependent vasodilation in a concentration-dependent manner more than sevoflurane, with inhibition of a calcium pathway. Isolated rat aortic rings were randomly assigned to treatment with desflurane or sevoflurane for measurements of the vasodilation ratio. To determine NO production with desflurane and sevoflurane, an in vitro assay was performed with cultured bovine aortic endothelial cells. These cells were also used for measurement of intracellular calcium or Western blotting. For endothelium-dependent vasodilation, the ratio of vasodilation was more significantly inhibited by 11.4% desflurane than by 4.8% sevoflurane. Inhibition did not between 5.7% desflurane and 2.4% sevoflurane. No inhibitory effect of desflurane or sevoflurane was observed in endothelium-denuded aorta. Desflurane inhibited nitric oxide production caused by stimulation of bradykinin significantly more than sevoflurane. Desflurane had a greater suppressive effect on the bradykinin-induced increase in intracellular calcium concentration than did sevoflurane. Sevoflurane, but not desflurane, inhibited phosphorylation of the serine 1177 residue by bradykinin stimulation. Desflurane inhibited endothelium-dependent vasodilation more than sevoflurane through inhibition of a calcium pathway. Sevoflurane inhibited endothelium-dependent vasodilation by inhibition of phosphorylation of the serine 1177 residue of endothelial nitric oxide synthase.

A case of hemothorax due to traumatic bleeding managed effectively by Sonoclot®-guided blood transfusion.

A 71-year-old woman was transported to our hospital due to traumatic bleeding, and an operation was immediately performed for achieving hemostasis. We decided to perform Sonoclot®-guided blood transfusion. When Sonoclot signatures had returned normal values, further bleeding did not occur. We experienced the first case of traumatic bleeding managed effectively by using Sonoclot. We suggest that a Sonoclot analyzer may be useful for the management of severe coagulopathy due to traumatic bleeding like ROTEM and TEG.

[A case report of coronary artery fistula in which perioperative transthoracic and transesophageal echocardiography was useful for surgical decision].

Coronary artery fistula is rare in congenital heart diseases but is the major disease among "coronary" congenital diseases. In a coronary artery fistula, the coronary artery tip connects directly or via an unusual blood vessel to unusual parts, such as the inside of the heart chamber, pulmonary artery or superior vena cava. Left ventricular volume overload and coronary steal phenomenon are serious symptoms. The gold standard of diagnosis has been coronary angiography, but echocardiography using Doppler methods is now useful for its diagnosis. This is a case report of coronary artery fistula for which transthoracic echocardiography (TTE) during anesthetic induction and intraoperative transesophageal echocardiography (TEE) by anesthesiologists provided accurate diagnosis of the shunt position. A 62-year-old female was scheduled to undergo surgery for a coronary artery fistula and aneurysm. Two separate shunts from the coronary artery into the pulmonary artery had been suspected by preoperative TTE. Shunt orientation was reexamined by perioperative TTE and TEE. We confirmed that only one shunt was located at the supra pulmonary valve area, and we consulted the diagnosis to surgeons. As a result, one shunt was found in the surgical view at the same position. Perioperative TTE and TEE are useful for surgical decision.

[Anesthetic management of extracorporeal shock wave lithotripsy: case reports of four young patients with epilepsy].

Four young patients, including a 7-year-old girl with Aicardi syndrome, an 11-year-old boy with Lennox-Gastaut syndrome, a 22-year-old man with epilepsy due to childhood encephalitis, and a 17-year-old girl with Rett syndrome, were scheduled to undergo extracorporeal shock wave lithotripsy (ESWL) for urolithiasis. Epilepsy in all of the patients was well controlled by medication. Series of ESWL treatment were safely performed under general anesthesia with tracheal intubation. We recommend that maintenance of anesthesia be performed by sevoflurane and nitrous oxide, which can increase threshold of epileptic stroke, and controlled ventilation with a muscle relaxant should be performed to prevent lung or renal injury by the shock wave of ESWL.