42 research outputs found
Central venous to arterial carbon dioxide gap as an indicator of oxygen debt in isovolemic anemia
Effect of melatonin on the severity of l-arginine-induced experimental acute pancreatitis in rats
AIM: To determine the effect of melatonin pre- and post-treatment on the severity
of L-arginine (L-Arg) -induced experimental pancreatitis in rats. METHODS: Male
Wistar rats (25) were divided into five groups. Those in group A received two
injections of 3.2g/kg body weight L-Arg i.p. at an interval of 1h. In group MA,
the rats were treated with 50 mg/kg body weight melatonin i.p. 30 min prior to
L-Arg administration. In group AM, the rats received the same dose of melatonin
1h after L-Arg was given. In group M, a single dose of melatonin was administered
as described previously. In group C the control animals received physiological
saline injections i.p. All rats were exsanguinated 24 h after the second L-Arg
injection. RESULTS: L-Arg administration caused severe necrotizing pancreatitis
confirmed by the significant elevations in the serum amylase level, the
pancreatic weight/body weight ratio (pw/bw), the pancreatic IL-6 content and the
myeloperoxidase activity, relative to the control values. Elevation of the serum
amylase level was significantly reduced in rats given melatonin following L-Arg
compared to rats injected with L-Arg only. The activities of the pancreatic
antioxidant enzymes (Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and catalase (CAT))
were significantly increased 24 h after pancreatitis induction. Melatonin given
in advance of L-Arg significantly reduced the pancreatic CAT activity relative to
that in the rats treated with L-Arg alone. In the liver, L-Arg significantly
increased the lipid peroxidation level, and the glutathione peroxidase and
Cu/Zn-SOD activities, whereas the Mn-SOD activity was reduced as compared to the
control rats. Melatonin pre-treatment prevented these changes. CONCLUSION:
Melatonin is an antioxidant that is able to counteract some of the L-Arg-induced
changes during acute pancreatitis, and may therefore be helpful in the supportive
therapy of patients with acute necrotizing pancreatitis
The Role of Endothelin-1 and Endothelin Receptor Antagonists in Inflammatory Response and Sepsis
Changes in Plasma Kynurenic Acid Concentration in Septic Shock Patients Undergoing Continuous Veno-Venous Haemofiltration
Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU
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Pulmonary mechanical responses to intestinal ischaemia-reperfusion and endotoxin preconditioning
During intestinal ischaemia-reperfusion, endotoxin can be translocated. Pretreatment with sublethal doses of endotoxin develops tolerance to ischaemia-reperfusion in different organs; however, the tolerance to intestinal ischaemia-reperfusion in the lung has rarely been investigated. Our aim was to study the role of endotoxin pretreatment in the mechanical responses and inflammatory activation induced by intestinal ischaemia-reperfusion in the lung. Wistar rats were preconditioned with a sublethal dose of endotoxin on day −3 or −1. On day 0, anesthetized, paralyzed and mechanically ventilated rats were subjected to a 60-min occlusion of the superior mesenteric artery and a subsequent 240-min reperfusion. The low-frequency forced oscillation technique was employed to characterize the separate mechanical responses of the airways and respiratory tissues. Intestinal ischaemia-reperfusion caused a significant decrease in airway resistance and increases in tissue resistance and elastance, nitric oxide synthase and myeloperoxidase activities. Pretreatment with endotoxin modified both the pulmonary mechanical responses and the inflammatory markers in the lung during intestinal ischaemia-reperfusion. We conclude that endotoxin or the endotoxin-induced processes (and humoral mediators) have significant roles in the pathomechanism of the remote pulmonary effect of intestinal ischaemia-reperfusion
Monitoring microcirculatory blood flow with a new sublingual tonometer in a porcine model of haemorrhagic shock
Circulatory consequences of reduced endogenous nitric oxide production during small-volume resuscitation
Hypertonic small-volume resuscitation transiently restores the cardiovascular function during various circulatory disturbances. Nitric oxide (NO) is an important mediator of flow-induced peripheral and central hemodynamic changes, and therefore, we hypothesized that a decreased endogenous NO production could influence the consequences and the effectiveness of hypertonic fluid therapy. The main goal of this study was to outline and compare the circulatory effects small volume hypertonic saline-dextran (HSD, 7.5% NaCl-10% dextran; 4 ml/kg iv) infusion with (n=7) or without (n=7) artificially diminished NO production in normovolemic anesthetized dogs. HSD administration significantly increased cardiac index (CI), coronary flow (CF) and myocardial contractility, and elevated plasma nitrite/nitrate (NOx) and endothelin-1 (ET-1) levels. However, the late (2 h) postinfusion period was characterized by significantly decreased myocardial NO synthase (NOS) and enhanced myeloperoxidase activities. Pre-treatment with the non-selective NOS inhibitor N-nitro-L-arginine (NNA, 4 mg/kg) immediately increased cardiac contractility, and the HSD-induced CI and CF elevations and the positive inotropy were absent. Additionally, plasma ET-1 levels increased and NOx levels were significantly decreased. In conclusion, our results demonstrate that HSD infusion leads to preponderant vasoconstriction when endogenous NO synthesis is diminished, and this could explain the loss of effectiveness of HSD resuscitation in NO-deficient states
Modulation of cardiac contractility through endothelin-1 release and myocardial mast cell degranulation
The aim of this study was to outline the consequences of a hypertonic saline-dextran-40 (HSD) infusion-induced peripheral flow stimulus on the ventricular function in closed-chest, pentobarbital-anesthetized dogs. We hypothesized that HSD-induced elevation in endothelin-1 (ET-1) and nitric oxide (NO) release can have a role in myocardial contractile responses; and that cardiac mast cells (MC) degranulation may be involved in this process. The consequences of disodium cromoglycate (a MC stabilizer) or ETR-p1/fl peptide (an endothelin-A receptor antagonist) treatment were evaluated. A 4 ml/kg iv HSD40 infusion significantly increased cardiac index and myocardial contractility, and resulted in a decreased peripheral resistance. The postinfusion period was characterized by significant plasma NO and ET-1 elevations, these hemodynamic and biochemical changes being accompanied by a decreased myocardial ET-1 content, NO synthase activity and enhanced myocardial MC degranulation. Disodium cromoglycate treatment inhibited the HSD40-induced elevations in myocardial contractility and MC degranulation, and similar hemodynamic changes were noted after treatment with ETR-p1/fl peptide, together with a normalized myocardial myocardial ET-1 content, NO synthesis and a significant reduction in MC degranulation. These results indicate that peripheral NO and ET-1 release modulates the cardiac contractility through myocardial ET-A receptor activation and MC degranulation