Octreotide: a new approach to the management of acute abdominal hypertension

Kaçmaz, Ayhan; Polat, Ali; User, Yılmaz; Tilki, Metin; Özkan, Sevil; Şener, Göksel

doi:10.1016/j.peptides.2003.09.004

Cited by 23 publications

(14 citation statements)

References 34 publications

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“…So, GSH is accepted as an indicator of post-ischemic tissue injury (10). Other studies also showed that renal MDA level increases, indicating the presence of enhanced lipid peroxidation due to the I/R injury (21) and other authors showed that some cytokines such as IL1-β and IL-6 were increased after renal ischemia reperfusion injury, but treatment with trasylol, which has anti-inflammatory effect like doxycycline decreased these levels (18).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of doxycycline in ischemia/reperfusion injury on kidney

et al. 2009

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Renal ischemia and reperfusion injury is the major cause of acute renal failure and may also be involved in the development and progression of some forms of chronic kidney disease. The aim of this study was to evaluate whether doxycycline, a member of the tetracycline family of antibiotics, protects kidney tissue or not. 36 Sprague-Dawley rats (200-250 g) were used. The animals were divided into three groups: control, ischemia/reperfusion and ischemia/reperfusion+doxycycline group. Rats were subjected to renal ischemia by clamping the left pedicle for 1 h, and then reperfused for 1 h. The ischemia/reperfusion+doxycycline group were pretreated intraperitoneally with doxycycline suspension (10 mg/kg) 2 h before the induction of ischemia. Our results indicate that malondialdehyde, matrix-metalloproteinase-2, interleukin-2, interleukin-6, interleukin-10, interleukin 1-beta and tumor necrosis factor-alpha levels were significantly higher in the ischemia/reperfusion group than those in the control group. Doxycycline administration significantly decreased these parameters. Tissue inhibitor of metalloproteinases-1 levels also increased after ischemia/reperfusion and decreased with doxycycline pretreatment, but these changes were not significantly different. Glutathione levels significantly decreased after ischemia/reperfusion injury when compared with the control group and doxycycline pretreatment significantly increased glutathione levels when compared with the ischemia/reperfusion group. Apoptotic cells and p53 positive cells were significantly decreased in doxycycline treated group. These results suggest that doxycycline reduces renal oxidative injury and facilitates repair. Doxycycline may play a role in a renoprotective therapeutic regimen.

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Section: Discussionmentioning

confidence: 99%

Protective effects of doxycycline in ischemia/reperfusion injury on kidney

et al. 2009

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“…Oxidative stress is known to be a result of the imbalance between the production of reactive oxygen species (ROS), antioxidants and repair processes (2). Lipid peroxidation, mediated by ROS, is believed to be an important cause of destruction and damage to cell membranes during oxidative stress (3). Tissue levels of malondialdehyde (MDA) are used as indicators of lipid peroxidation (4,5).…”

Section: Introductionmentioning

confidence: 99%

“…Glutathione (GSH) also provides major protection in oxidative injury by participating in the cellular system of defense against oxidative damage. Several reports have indicated that various stimuli, such as I/R injury, cause GSH depletion (3). However, ROS also activates nuclear factor-κB (NF-κB).…”

Section: Introductionmentioning

confidence: 99%

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Kinaci

Erkasap

Küçük

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxy nucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by realtime polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and antiapoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

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“…This has been coupled with an insignificant increase in functional lung volume in animal studies although this effect is counterbalanced by a slight reduction in chest wall compliance and a commensurate increase in pleural pressure imposed by the device. Octreotide, 170,171 melatonin 172 and high-dose diuretics in haemodynamically stable patients can reduce IAP with an unproven value of early dialysis and ultra-filtration, each of which is administered often with relatively high-dose inotropic support. 173 These approaches may be supplemented in the absence of prospective randomized data with gastric suctioning, 174 enemata, concentrated albumin, 175 gastric pro-kinetic therapy and colo-pro-kinetic administration but there are no proven advantages of these medical therapies.…”

Section: Medical Managementmentioning

confidence: 99%

Primary Intra-Abdominal Hypertension and Abdominal Compartment Syndrome: Pathophysiology and Treatment

Ap¹,

Wun²,

Chiappa³

et al. 2015

Emerg Med Open J

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Abdominal Compartment Syndrome (ACS) is a potentially lethal condition caused by various events that produce intra-abdominal hypertension. The most common cause is blunt abdominal trauma. Increasing intra-abdominal pressure causes progressive hypoperfusion and ischemia of the intestines and other peritoneal and retroperitoneal structures. Pathophysiological effects include release of cytokines, production of oxygen free radicals, and decreased cellular formation of adenosine triphosphate. These processes may lead to translocation of bacteria from the gut and intestinal edema, predisposing patients to multiorgan dysfunction syndrome. The consequences of abdominal compartment syndrome are profound and affect many vital body systems. Respiratory, hemodynamic, cardiovascular, renal, and neurological abnormalities are signs of abdominal compartment syndrome. Medical management of critically ill patients with raised intra-abdominal pressure should be instigated early to prevent further organ dysfunction and to avoid progression to ACS. Many treatment options are available and are often part of routine daily management in the ICU (nasogastric, rectal tube, prokinetics, enema, sedation, body position). Some of the newer treatments are very promising options in specific patient populations with raised IAP. Nursing care involves vigilant monitoring for early detection, including serial measurements of intra-abdominal pressure.KEYWORDS: Intra-abdominal hypertension; Abdominal compartment syndrome; Damage control laparotomy; Laparostomy; Open abdomen. DEFINITIONS, INCIDENCE AND MEASUREMENT STRATEGIES IN INTRA-ABDOMINAL HY-PERTENSION (IAH) AND ABDOMINAL COMPARTMENT SYNDROME (ACS)The concept of the Abdominal Compartment Syndrome (ACS) has been rediscovered as a final common pathway of the physiologic sequelae of increased Intra-Abdominal Pressure In each case if the graph shifts to the right, higher IAP and lower APP values may not be associated with significant end-organ dysfunction creating a degree of "ACS-resistance." Shifts to the left would create "ACS-sensitivity" where lower values of IAP (higher APP values) may still be associated with organ dysfunction which might not occur normally. This results in difficulty for broader acceptance of critical IAP and APP levels for individual cases. ACS-sensitivity may potentially occur in patients where there is pre-existing partial end-organ failure, morbid obesity or following fluid hyper-resuscitation in patients with severe burns, haemorrhagic pancreatitis, massive blood loss, widespread intra-peritoneal sepsis and high-output intestinal fistulae. 6-8There is no strict definition of what represents abnormal IAP, but there is a general acceptance that measured pressures >12 mmHg when recorded 1-6 hours apart are considered to represent IAH, where Sugrue, et al. have shown that this represents up to 40% of cases admitted to a surgical Intensive Care Unit (ICU). 9 Although there are biases in the prospective assessment of a selective population admitted to an ICU who ...

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Octreotide: a new approach to the management of acute abdominal hypertension

Cited by 23 publications

References 34 publications

Protective effects of doxycycline in ischemia/reperfusion injury on kidney

Protective effects of doxycycline in ischemia/reperfusion injury on kidney

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Primary Intra-Abdominal Hypertension and Abdominal Compartment Syndrome: Pathophysiology and Treatment

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