Top PDF Remifentanil ameliorates intestinal ischemia-reperfusion injury

Remifentanil ameliorates intestinal ischemia-reperfusion injury

Remifentanil ameliorates intestinal ischemia-reperfusion injury

Opioids have been used as analgesics for centuries but it is only in the last decade or so that they have been discovered to also play a significant role in immunomodulation. Although the immunomodulatory effects of remifentanil are not as well studied as those of morphine and fentanyl, current data suggest that its receptor-mediated effects are not different from other μ-opioid agonists [46]. Immune cells express functionally active opioid receptors on their surface, and opioids have been shown to exert their effect directly via these receptors [47,48]. Such effects include the inhibition of the activity of nuclear factor-kappaB (NF-κB), the prototyp- ical upstream facilitator of IL-6 production [49]. For ex- ample, chronic morphine treatment significantly impaired the translocation of the NF-κB p65 and p50 transcription fac- tors into the nuclear compartment of a variety of cells in a model of lung infection [50]. Moreover, the opioid-induced preconditioning signaling cascade has been reported to acti- vate the phosphatidylinositol-3-kinase/Akt and the three mitogen-activated protein kinase (MAPK) pathways c-Jun N-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK) 1/2. Activation of these signaling cascades in preconditioning has been linked to pro-survival and anti-apoptotic effects [51-57]. Fur- thermore, it is possible that such mild stimulation of inflammatory pathways induces counter-regulatory mechanisms such as the release of anti-inflammatory cytokines and preconditions cells to reduce the impact of a stronger consecutive stimulus. Such conditioning cascades have been described for low doses of LPS that protect against subsequent IRI [58,59].
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<p>Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation</p>

<p>Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation</p>

From Figure 4, the ultrastructural changes among sham, I/R, high-dose deltonin, and high-dose deltonin+LY294002 showed that deltonin reduced autophagy activities during cerebral I/R injury. Figure 5A demonstrated that anisomycin (activator of p38/MAPK) decreased the neurological scores than deltonin group (P<0.05). Figure 5B showed that delto- nin reduced the infarct volume, but anisomycin attenuated the effect. Figure 5C showed the protein expressions of TLR4, p-38, p-p38, and IL-1. No signi fi cant difference was found in the expressions of p38 in all groups (P>0.05), but TLR4, p-p38, and IL-1 were elevated greatly in I/R (P<0.01). Reversely, TLR4, p-p38, and IL-1 reduced by deltonin
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Protective Effect of Trigonella foenum graecum (fenugreek) Seed Extract on Experimental Intestinal Ischemia/Reperfusion Injury in Rats

Protective Effect of Trigonella foenum graecum (fenugreek) Seed Extract on Experimental Intestinal Ischemia/Reperfusion Injury in Rats

The histopathological findings showed that the injury scores in the mucosa 1 h after reperfusion was significantly lower in the fenugreek group than in the I/R group and suggested that the small intestinal mucosa in the fenugreek and VitC group was better preserved than in the I/R group. In the current study, we demonstrated that I/R in the aorta artery is associated with significant histopathological damages in the mucosa of the jejunum. Yasar, et al. (2010) reported that doxycycline was associated with improved recovery from I/R injury through attenuating the response of cytokines after 1-hour reperfusion period. 31 Sato, et al. (2011) showed that lutein, an antioxidant, significantly reduced oxidative injury. 35 Appropriate accumulation of antioxidants in tissues probably leads to protective effects against oxidative injury.
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<p>Edaravone Ameliorates Renal Warm Ischemia-Reperfusion Injury by Downregulating Endoplasmic Reticulum Stress in a Rat Resuscitation Model</p>

<p>Edaravone Ameliorates Renal Warm Ischemia-Reperfusion Injury by Downregulating Endoplasmic Reticulum Stress in a Rat Resuscitation Model</p>

During ischemia, multiple signalling pathways, which are closely relative with in fl am- matory and metabolic, play pro-apoptosis roles in cells. 1 However, the subsequent blood perfusion restoration may course more severe injury known as ischemia- reperfusion injury (IRI). Renal ischaemia-reperfusion injury (IRI) is known as one of the most common causes of acute kidney injury (AKI) and secondary to various clinical conditions, such as kidney grafting and resuscitation. 2,3 Reactive oxygen species (ROS) play an important role in the development of IRI. It has been reported that
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<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

<p>Ginkgolide B ameliorates myocardial ischemia reperfusion injury in rats via inhibiting endoplasmic reticulum stress</p>

23. Teng X, Song J, Zhang G, et al. Inhibition of endoplasmic reticulum stress by intermedin (1-53) protects against myocardial injury through a PI3 kinase-Akt signaling pathway. J Mol Med. 2011;89(12):1195–1205. 24. Santos-Gallego CG, Vahl TP, Goliasch G, et al.Sphingosine-1-phosphate receptor agonist fingolimod increases myocardial salvage and decreases adverse postinfarction left ventricular remodeling in a porcine model of ischemia/reperfusion. Circulation. 2016;133(10):954–966. 25. Chen C, Nong Z, Meng M, et al. Toxicological evaluation of Yulangsan

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Peptide binding to cleaved CD31 dampens ischemia/reperfusion-induced intestinal injury

Peptide binding to cleaved CD31 dampens ischemia/reperfusion-induced intestinal injury

In conclusion, our data shows that a peptide able to bind to truncated membrane-anchored CD31, such as P8RI, holds a promising therapeutic potential to reduce the intestinal damage inflicted by I/R. The action of the peptide is likely exerted on cells of the innate immunity, which are in the first line of defense against acute tissue injury. Notably, all the cells of the innate immune system express high levels of CD31 [8], and the most abundant population of such cells is represented by neutro- phils. Altogether, the present work suggests that P8RI could reduce the extent of intestinal I/R injury by modulating both the local and systemic response of neutrophils.
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Protective Effect of Crataegus Hydroalcoholic Extract on Intestinal Ischemia-Reperfusion Injury in a Rat Model

Protective Effect of Crataegus Hydroalcoholic Extract on Intestinal Ischemia-Reperfusion Injury in a Rat Model

In this study, the effect of orally administered CHE at the doses of 25, 50, and 100 mg/kg for 10 consecutive days was evaluated on intestinal I/R injury. The results showed that administration of CHE at dose of 25 mg/kg improved necrohemorrhagic inflammation and villi destruction. No pathologic lesion was observed other than mild hyperemia in the 50 mg/kg of CHE. Although hyperemia and necrohemorrhagic inflammation were greater in the dose of 100 mg/kg, the intensity of hemorrhage and villi destruction was significantly lower than the control group. However, the intensity of these parameters was significantly higher than the sham group. So, it can be said that the protective effect of CHE decreased at the dose of 100 mg/kg. Contrary to expectations, this study did not find a dose-dependent effect in Crataegus extract against intestinal I/R injury, despite the effect of the extract was dose-dependent up to the dose of 50 mg/kg. In contrast to our study results, hawthorn extract produced dose- dependent gastroprotective activity in ethanol-induced acute stress ulcer model in rat. 20 In another study, the
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Qingkailing injection ameliorates cerebral ischemia reperfusion injury and modulates the AMPK/NLRP3 Inflammasome Signalling pathway

Qingkailing injection ameliorates cerebral ischemia reperfusion injury and modulates the AMPK/NLRP3 Inflammasome Signalling pathway

Cerebral ischemia diminishes the oxygen supply, which damages the brain cells leading to neurological dysfunction and cerebral infarction. Challenges still exist in the management of cerebral ischemia, and more efficient agents to treat cerebral ischemia have yet to be identified. QKL is a famous CFDA approved Chinese medicine that has been clinically used throughout China for over 30 years. Understanding of biological mechanism of QKL from experimental studies may help developing potential clinical strat- egies of QKL to treat cerebral ischemia. The present study showed that QKL injection protected the brain against cerebral ischemia-reperfusion injury, including improved rCBF, decreased neurological deficits and brain infarct volumes, inhibited BBB injuries and sup- pressed post-stroke inflammatory responses. Using Nissl staining and TUNEL analysis, we found that QKL suppressed brain cell apoptosis, which is the biological mechanism leading to the clinical symp- toms of cerebral ischemia. In line with our study, other studies indicated that QKL injection improves neurological function, suppresses BBB dysfunction, and inhibits inflammatory responses [19, 25]. How- ever, the underlying mechanism of the QKL anti-
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Simvastatin nanoparticles attenuated intestinal ischemia/reperfusion injury by downregulating BMP4/COX-2 pathway in rats

Simvastatin nanoparticles attenuated intestinal ischemia/reperfusion injury by downregulating BMP4/COX-2 pathway in rats

immersed in 0.3% H 2 O 2 for 20 min and washed with PBS. The parts were then incubated in rabbit anti-COX-2, anti-BMP4, and anti-p38MAPK polyclonal antiserum (Abcam, UK) for 1 h (1:100 dilution). After the primary incubation and three rinses in PBS, parts were incubated in biotinylated goat anti-rabbit IgG (Invitrogen, CA, USA) for 15 min (1:2,000 dilution). Following the incubation in substrate chromagen solution for 15 min, all parts were washed in PBS and distilled water, mounted in glycerol, and checked later under the microscope. The small intestinal parts stained positively for COX-2, BMP4, and p38MAPK were evaluated and compared among groups.
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Antioxidant and anti-inflammatory effects of selenium in oral buccal mucosa and small intestinal mucosa during intestinal ischemia-reperfusion injury

Antioxidant and anti-inflammatory effects of selenium in oral buccal mucosa and small intestinal mucosa during intestinal ischemia-reperfusion injury

Among the internal organs, the small intestine is the most vulnerable organ to ischemia-reperfusion (IR) in- jury [3]. IR injury in the small intestine breaks mucosal barrier, which results in occurrence of systemic inflam- matory response syndrome (SIRS). Then, SIRS can in- duce secondary injuries to the distant organs leading to multiple organ failure (MOF) or even to death [4]. The mechanisms of the initiation and progression of SIRS during small intestinal IR injury are ROS formation, ROS-dependent inhibitor κB-α (IκB-α) phosphorylation in cytoplasm, and subsequent nuclear factor κ B (NF- κ B) activation in nucleus. Recent in vitro studies have shown that ROS enhances cytoplasmic signaling pathways lead- ing to NF- κ B nuclear translocation [5-7]. Therefore, the antioxidant therapy can be considered as a therapeutic strategy to attenuate inflammatory responses induced by
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AICAR Attenuates Organ Injury and Inflammatory Response after Intestinal Ischemia and Reperfusion

AICAR Attenuates Organ Injury and Inflammatory Response after Intestinal Ischemia and Reperfusion

IL-6 in LPS-stimulated neutrophils (44). Moreover, administration of AICAR in vivo resulted in decreased severity of LPS-induced lung injury, suggesting that the antiinflammatory effects of AICAR is caused by downregulation of the NF-κB pathway and subsequent decreases in TNF-α and IL-6 (44). In this regard, our study showed that AICAR treatment at- tenuated gut I/R-induced lung levels of TNF-α and IL-6, suggesting a similar mo- lecular mechanism of action of AICAR in gut I/R injury. Inflammatory mediators such as lung iNOS and COX-2 also were attenuated with AICAR treatment, indi- cating a potential role of these factors in gut I/R-induced lung injury. Impairment in the lung epithelium and endothelium barrier function plays a major role in the development of acute respiratory distress syndrome, and a key feature of this fail- ure is the loss of cells through apoptosis (45). The modulation of apoptosis could prevent lung fibrosis, and the progression into acute lung injury (24,45–47). AICAR attenuated lung apoptosis in gut I/R-as- sociated lung injury as indicated by the reduction of apoptotic cells in the lung parenchyma after treatment. In addition to the lung, AICAR treatment also signifi- cantly reduced gut apoptosis.
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Original Article Propofol ameliorates ischemia/reperfusion induced cerebral injury by upregulation of microRNA-206 expression

Original Article Propofol ameliorates ischemia/reperfusion induced cerebral injury by upregulation of microRNA-206 expression

Ischemia-reperfusion (I/R) injury that caused by ischemia and perfusion is a common patho- physiological process during operations, which has been paid more and more attention. MiR- 206 is a recently identified miRNA that play important roles in the differentiation of myo- cytes as well as tumor metastasis and apopto- sis. Dey et al. reported that miR-206 promoted myogenesis and accelerated myogenic differ- entiation by inhibiting Pax7 expression [15]. Studies of Fu et al. demonstrated that miR-206 could repress tumor proliferation and invasion in breast cancer by targeting Cx43 [16]. In addi-
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The Protective Effect of Orally Administered Amlodipine against Intestinal Ischemia-Reperfusion Injury in Rats

The Protective Effect of Orally Administered Amlodipine against Intestinal Ischemia-Reperfusion Injury in Rats

Finally, the findings of this study suggest that amlodipine has a preventive activity on I/R-induced intestine injury. The observed preventive effects of amlodipine in the present study can possibly be mediated by means of its well-known antioxidant and anti-inflammatory potential. Therefore, we suggest that amlodipine may be a novel approach to therapy for protective intestinal I/R injury. Nonetheless, there is a need for further studies to examine the mechanism by which amlodipine performs these functions.

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The effect of melatonin on bacterial translocation following ischemia/reperfusion injury in a rat model of superior mesenteric artery occlusion

The effect of melatonin on bacterial translocation following ischemia/reperfusion injury in a rat model of superior mesenteric artery occlusion

rigidity [6]. Moreover, it has recently reported that deriva- tives of melatonin that are formed when the indoleamine functions as a scavenger may actually be more effective than melatonin itself in neutralizing the peroxyl radicals [18]. In our study, we observed a significantly reduced incidence of bacterial translocation to the blood, liver, spleen, and mesenteric lymph nodes in animals pre- treated with melatonin in an acute mesenteric ischemia/ reperfusion model. Furthermore, melatonin treatment provided a statistically significant reduction in ileal bacter- ial overgrowth. It was previously shown that mesenteric ischemia/reperfusion not only produces mucosal damage but also induces alterations of intestinal motor activity with a delay in gastrointestinal transit time [19]. These alterations can be the result of structural and neur- onal changes occurring within the enteric nervous sys- tem which may play a role in the progress of bacterial overgrowth with subsequent translocation due to inad- equate bacterial clearance [20]. In addition to its prop- erties against I/R oxidative injury, melatonin has been suggested to act as a local regulator of gastrointestinal motility [21].
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YiQiFuMai powder injection ameliorates blood&ndash;brain barrier dysfunction and brain edema after focal cerebral ischemia&ndash;reperfusion injury in mice

YiQiFuMai powder injection ameliorates blood&ndash;brain barrier dysfunction and brain edema after focal cerebral ischemia&ndash;reperfusion injury in mice

findings indicate that the potential targets or pathways of YQFM in the treatment of ischemic stroke are related to PAR-1, MMP-9, NF- κ B, etc. In addition, a combination of four active compounds derived from Sheng-Mai-San was reported to alleviate cerebral I/R injury, correlating with the inhibition of autophagy and modulation of the adenosine monophosphate-activated protein kinase/mTOR and Jun kinase pathways and to inhibit H 2 O 2 -induced PC12 cell apoptosis in vitro. 20,62 Ginsenoside Rg1 can also improve

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Influence of Ketotifen, Cromolyn Sodium, and Compound 48/80 on the survival rates after intestinal ischemia reperfusion injury in rats

Influence of Ketotifen, Cromolyn Sodium, and Compound 48/80 on the survival rates after intestinal ischemia reperfusion injury in rats

Another 0.5 cm intestinal segment cut 5 cm from the ter- minal ileum were immersed and fixed in 2.5% glutaralde- hyde overnight at 4°C and washed three times in PBS. They were then postfixed in aqueous 1% OsO 4 and 1% K 3 Fe (CN) 6 for 1 hour. Following three times of PBS wash- ing, the tissue was dehydrated through a graded series of 30 to 100% ethanol and 100% propylene oxide and immersed in 1:1 mixture of propylene oxide and Polybed 812 epoxy resin for 1 hour. The infiltration solution was then changed to 100% resin. After 24 hours of infiltration, the tissue was embedded in molds and cured at 37°C overnight, followed by additional hardening at 65°C for 2 days. Ultrathin (70 nm) sections were collected on 200- mesh copper grids and stained with 2% uranyl acetate in 50% methanol for 10 minutes, followed by 1% lead cit- rate for 7 minutes. Sections were photographed using a Hitachi H-600 transmission electron microscope (TOSHIBA, Japan) at 80 kV onto electron microscope film.
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Targeted complement inhibition by C3d recognition ameliorates tissue injury without apparent increase in susceptibility to infection

Targeted complement inhibition by C3d recognition ameliorates tissue injury without apparent increase in susceptibility to infection

Intestinal IRI. Adult male BALB/c and C57BL/6 mice (National Cancer Insti- tute) aged 8 weeks and weighing 20–25 g were anesthetized with 10 mg/kg ketamine and 6 mg/kg xylazine by i.p. injection. Animals were breath- ing spontaneously, and body temperature for the entire experiment was maintained with a heat mat. A medial laparotomy was performed, and the intestines were carefully moved, allowing access to the superior mes- enteric artery. The superior mesenteric artery was clamped using a micro- surgical clamp (Fine Surgical Instruments Inc.). Ischemia was confirmed by pallor of the small intestine. Sham-operated mice underwent lapa- rotomy without clamping of the superior mesenteric artery. After 30 min- utes of ischemia, the arterial clamp was removed, allowing reperfusion of the mesenteric vasculature. Animals were sutured using 6.0 ethicon suture and allowed to reperfuse for 2 hours. Animals were randomized into CR2-Crry– and Crry-Ig–treatment groups and given 0.012, 0.025, 0.05, 0.1, or 0.2 mg CR2-Crry and 0.1, 0.2, 0.5, or 1.0 mg Crry-Ig (n = 4–7). Inhibitors were administered i.v. 30 minutes after reperfusion, and ani- mals were sacrificed 90 minutes later following 2 hours of reperfusion. Animal procedures were approved by the Medical University of South Carolina Animal Care and Use Committee.
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Original Article Glutamine ameliorates intestinal ischemia-reperfusion Injury in rats by activating the Nrf2/Are signaling pathway

Original Article Glutamine ameliorates intestinal ischemia-reperfusion Injury in rats by activating the Nrf2/Are signaling pathway

GLN is the most important and most available energy source in intestinal epithelial cells, lym- phocytes, and macrophages [18-20], as well as a precursor of nucleotide synthesis and gluta- thione in the important antioxidant defense system. Luo et al show that GLN supplementa- tion maintains gut glutathione levels during I/R [21]. Further, Wu and Ban’s studies demon- strate that GLN treatment has a protective effect during intestinal mucosal I/R injury, can reduce endotoxins elevation in I/R, and reduc- es bacterial translocation [22-24]. However, it is unclear whether GLN is protective for the intestinal mucosa against oxidative stress. Therefore, we established a rat I/R injury model to investigate the effects of GLN on I/R and its mechanism of action. Our results demonstrat- ed that the GLN pretreated I/R rats had a great- er villous height and a lower degree of intestinal permeability compared to the I/R rats. This suggests that GLN pretreatment plays an important role in the maintenance of the intes- tinal structure and barrier function in I/R- injured rats. Furthermore, we found that I/R leads to oxidative stress. Villi are rich in ROS- related enzymes, and I/R activates adenine- hypoxanthine metabolic pathways that produce abnormal increases in oxygen free radicals. Phospholipids are made of polyunsaturated fatty acids, which have a plurality of unsaturat- ed bonds, and oxygen radicals have high affini- ty for these unsaturated bonds and can stimu- late excessive lipid peroxidation chain reac- tions. This results in cell membrane lipid peroxi- dation, inhibition of mitochondrial activity, and increased membrane permeability of the cell and lysosome, leading to cell swelling/rupture. Our results indicate that GLN pretreatment inhibited lipid peroxidation, improved the body’s ability to scavenge oxygen free radicals, and thus, inhibited membrane disintegration. The potential protective mechanisms may include upregulation of endogenous antioxidant factors (i.e., SOD, Nrf2, and HO-1) and downregulation of MDA levels by the Nrf2/ARE signaling pathway.
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Agent-based dynamic knowledge representation of Pseudomonas aeruginosa virulence activation in the stressed gut: Towards characterizing host-pathogen interactions in gut-derived sepsis

Agent-based dynamic knowledge representation of Pseudomonas aeruginosa virulence activation in the stressed gut: Towards characterizing host-pathogen interactions in gut-derived sepsis

In the traditional laboratory setting, effluent from the lumen of intestinal segments fol- lowing ischemia reperfusion injury was used in in vitro experiments to study the effects of endogenous opioids and ischemia byproducts on virulence expression in P. aerugi- nosa [9,26]. The GMABM was used to simulate 30 minutes of segmental intestinal ischemia followed by reperfusion injury. Immune activation and phosphate depletion were initially excluded from the execution of the ischemia/reperfusion simulation. Pre- sently, there are no published data evaluating Pseudomonas virulence expression and host survival using an animal model of non-lethal transient intestinal ischemia. How- ever, the GMABM simulations demonstrated that exposure to select microenvironment changes in the gut subsequent to transient ischemia/reperfusion injury produced signif- icant barrier dysfunction (Figure 15), setting the stage for potential host morbidity. This condition has clinical relevance, as often the onset of critical illness and systemic inflammation is associated with transient hypotension and hypoperfusion prior to onset of resuscitative measures [36]. This simulation data also suggests that an in vivo experiment to confirm this type of behavior should focus its sample collection in the 6-12 hour time frame post -ischemia, and that higher frequency measurements in this time frame would be substantially more informative as opposed to collections beyond
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Does remifentanil attenuate renal ischemia&ndash;reperfusion injury better than dexmedetomidine in rat kidney?

Does remifentanil attenuate renal ischemia&ndash;reperfusion injury better than dexmedetomidine in rat kidney?

were randomly separated into five groups, each containing six rats. Following anesthesia induction, the abdomen of rats was dissected and right nephrectomy was performed. In the control group (group C, n = 6), the rats were sacrificed after taking blood samples and removal of right kidneys without any infusion. In the saline group (group S, n = 6), normal saline infusion was started after anesthesia induction and the right kidney was harvested without left renal ischemia and reperfusion. In the sham group (group Sh, n = 6), following anesthesia induction and right nephrectomy, normal saline infusion was started as in group S but left renal ischemia was also performed by occlusion of the left renal artery for 30 minutes. Then, the arterial clamp was removed and reperfusion of the kidney was observed for 30 minutes. In dexmedetomidine-treated group (group DEX, n = 6), right nephrectomy and left renal I/R were performed, but in addi- tion to these, Precedex (dexmedetomidine hydrochloride 100 µ g/2 mL; Abbott Laboratories, North Chicago, IL, USA) was infused at 3 µ g ⋅ kg -1 ⋅ h -1 ⋅ following a bolus of 3 µ g.kg -1
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