Ringer's lactate solution enhances the inflammatory response during fluid resuscitation of experimentally induced haemorrhagic shock in rats.

INTRODUCTION: Hemorrhagic shock leads to systemic oxygen deficit (hypoxaemia) that results in systemic inflammatory response syndrome (SIRS), a recognised cause of late mortality in this case. The aim of this study was to analyse the impact of fluid resuscitation, using two Ringer solutions, on the microcirculation changes that take place during experimentally induced haemorrhagic shock. MATERIAL AND METHODS: A model of the rat cremaster muscle was used to assess microcirculation in vivo. The experimental groups (n = 10 each) included: control (CTRL); shock (HSG); Ringer's acetate (RAG); and Ringer's lactate (RLG). Microhaemodynamic parameters were measured during the experiment. RESULTS: A statistically significantly higher level of leukocytes, both those attached to the endothelium and those located in the extravascular space (p < 0.05), was reported in the lactate Ringer (LR) group compared with the AR group. There were significant differences in the activity of A3 arterioles compared with A1 and A2 arterioles. Ringer's lactate solution seemed to the inflammation response during fluid resuscitation from haemorrhagic shock. A3 arterioles are likely to play a role as a pre-capillary sphincter in the skeletal muscle. CONCLUSIONS: The present study revealed that fluid resuscitation with Ringer's lactate solution exacerbates inflammation in the skeletal muscle. It is worth noting that Ringer's acetate solution reduces local inflammation and could therefore be recommended as the "first line" crystalloid of the fluid resuscitation during haemorrhagic shock.

Current management of congenital diaphragmatic hernia.

The treatment of congenital diaphragmatic hernia (CDH) still represents a challenge, even for the specialised multidisciplinary teams in centres that provide treatment for CDH. Despite significant progress in the fields of pathophysiology, prenatal diagnosis, surgical techniques and intensive care, CDH is a disease still burdened with a high mortality. Due to the paucity of randomised studies, there are no standard guidelines for treatment. The present review looks at existing diagnostic and therapeutic principles based on the available literature.

Pulsed acoustic cellular expression as a protective therapy against I/R injury in a cremaster muscle flap model.

BACKGROUND: Tissue ischemia and reperfusion (I/R) affects blood flow restoration and oxygen delivery to the damaged tissues contributing to tissue morbidity and microcirculatory compromise. Pulsed acoustic cellular expression (PACE) technology is known to support tissue neovascularization. The aim of this study was to test PACE conditioning mechanism of action on microcirculatory hemodynamics in ischemia-reperfusion injury model. METHODS: 34 rat cremaster muscle flaps were monitored under intravital microscopy system in 4 experimental groups: 1) non-ischemic controls (n=10), 2) 5h ischemia without conditioning (n=8), 3) pre-ischemic (5h) PACE conditioning (n=8), 4) post-ischemic (5h) PACE conditioning (n=8). Standard microcirculatory hemodynamics of RBC velocity, vessel diameters and functional capillary perfusion were recorded for 2h after I/R. Immunohistochemistry assessed expression of proangiogenic factors: VEGF and vWF, whereas real-time PCR assessed proangiogenic (VEGF, eNOS) and proinflammatory factors (iNOS; chemokines: CCL2, CXCL5 and chemokine receptor CCR2). RESULTS: Pre-ischemic PACE conditioning (group 3) resulted in increased RBC velocity of second (A-2) and third order arterioles (A-3) and venule (V-1) by 40%, 15% and 24% respectively comparing to ischemic group without conditioning (p<0.05). Post-ischemic PACE conditioning (group 4) revealed: 1) increase in RBC velocity in second (A-2) and third order arterioles (A-3) by 65% and 31% respectively comparing to ischemia without conditioning (group 2), 2) 33% increase in first order arterioles diameter (A-1) (p<0.05) compared to ischemic controls, 3) 21% increase in number of functional capillaries compared to ischemia without conditioning (group 2) (P<0.05). Immunostaining assays showed that PACE postconditioning up-regulated proangiogenic factors vWF and VEGF protein expression. This correlated with increased gene expression of VEGF (up to 180%). In contrast, gene expression of proinflammatory factors (iNOS, CCL2, CXCL5) decreased compared to ischemic controls. Pre-ischemic PACE conditioning decreased gene expression of proinflammatory chemokines (CCL2 and CXCL5), compared to ischemic controls without conditioning. CONCLUSIONS: As expected 5h ischemia resulted in deterioration of microcirculatory hemodynamics confirmed by decreased vessels diameters and RBC velocities. This was alleviated by pre- and post-ischemic PACE conditioning which improved functional capillary density and stimulated angiogenesis as confirmed by up-regulated VEGF expression. Furthermore, post-ischemic PACE conditioning correlated with decreased expression of early proinflammatory factors (iNOS, CCL2, CXCL5). Both types of PACE conditioning ameliorated deleterious effect of ischemia-reperfusion injury on microcirculatory hemodynamics of muscle flaps.

Long-term follow up of the effects of Extracorporeal Shockwave Therapy (ESWT) on microcirculation in a denervated muscle flap.

UNLABELLED: Extracorporeal Shock Wave Therapy (ESWT) is a golden standard for treatment of kidney and urinary calculi. It is also widely used in a number of orthopedic pathologies and other fields of medicine. Although clinical success the exact mechanism of shock wave technology is not well established. Cremaster muscle model used in our experiment is structurally and functionally similar to other skeletal muscles (striated muscle). The aim of the study was to evaluate influence of ESWT treatment on microcirculation and leukocyte-endothelial interactions after longer time period post ESWT application. MATERIAL AND METHODS: In experiment we used 34 Lewis rats weighting 125-160 grams. Animals were divided into 4 groups--Group 1 (n = 10) control, without ESWT application, group 2 (n = 8), in which measurements were performed 3 days after application of 500 impulses of ESWT; group 3 (n = 8) in which measurements were performed 7 days after application of 500 impulses of ESWT; group 4 (n = 8), in which measurements were performed 21 days after application of 500 impulses of ESWT. RESULTS: The experiment showed a decrease in functional capillaries activity, we also observed the reduction in leukocyte rolling over the endothelium and an increase in flow velocity in V1 venules. CONCLUSIONS: ESWT therapy after 3, 7 and 21 days decreases inflammatory process in the muscle, the other of its effect is weakened. This confirms that the treatment had a positive effect if ESWT is applied repeatedly, because only in this case a wave maintains its beneficial effects.

Pulsed acoustic cellular treatment induces expression of proangiogenic factors and chemokines in muscle flaps.

BACKGROUND: Pulsed Acoustic Cellular Expression (PACE) treatment is a novel technology with potential to improve tissue perfusion, but the mechanism of this action is unknown. We assessed in vivo the effect of PACE therapy on muscle microcirculatory hemodynamics, neovascularization, and proangiogenic and proinflammatory gene expression. METHODS: Cremaster muscles were prepared for standard intravital microscopy in 42 Lewis rats divided into five groups: (1) control (n = 10); acute PACE treatment 15 minutes before surgery with (2) 200 impulses (n = 8) and (3) 500 impulses (n = 8); and PACE treatment 24 hours before surgery with (4) 200 impulses (n = 8) and (5) 500 impulses (n = 8).Microcirculatory hemodynamics of red blood cell velocity and capillary perfusion were recorded for 4 hours. Gene expression levels of proinflammatory (inductible nitric oxide synthase [iNOS]) and proangiogenic factors (endothelial nitric oxide synthase [eNOS], vascular endothelial growth factor [VEGF], chemokine (C-X-C motif) ligand 5 [CXCL5], chemokine (C-C motif) ligand 2 [CCL2], and chemokine (C-C motif) receptor 2 [CCR2] were measured using Taqman real-time Polymerase Chain Reaction (PCR). Immunohistochemistry assessed expression of proangiogenic factors: VEGF, von Willebrand factor (vWF), and vessel density by CD31. RESULTS: PACE treatment resulted in an increase of arteriolar diameters in acute groups 2 and 3 (p < 0.05). In group 5, vessel densities assessed by CD31, VEGF, and vWF expression increased significantly 24 hours after PACE treatment compared with control (p < 0.05). PACE application downregulated proinflammatory iNOS gene expression and upregulated proangiogenic genes expression of eNOS, VEGF, CXCL5, and CCL2. CONCLUSIONS: Application of PACE treatment, applied as short time acting preconditioning and conditioning treatment, resulted in upregulation of proangiogenic chemokines gene expression in the muscle and showed upregulation of expression of proangiogenic factors such as VEGF and vWF on the vessel endothelium.

[Multiple organ failure in a severely malnourished patient with chromosome aberration]. / Skrajne niedoiywienie jako przyczyna niewydolnosci wielonarzadowej u chorej z aberracja chromosomalna.

BACKGROUND: Pneumonia and malnutrition are two of the biggest killers in childhood, as defined by the World Health Organisation. Although common in the developing world, these conditions can also be observed in more advanced countries, as a result of negligence and lack of proper care in disabled children. We describe a case in which severe malnutrition resulted in multiple organ failure. CASE REPORT: A 16-yr-old retarded girl with +14q chromosome aberration, was admitted to hospital because of severe anaemia and dyspnea. She was extremely malnourished. Her body weight was 32 kg with a height of 152 cm (BMI 13.9). Her Hb concentration was 1.12 mmol L(-1), Ht 7%, and RBC 0.93 T L(-1). RBC transfusion resulted in transfusion-related acute lung injury (TRALI) and multiple organ failure. She was treated with mechanical ventilation, inotropic support and parenteral nutrition, complicated by the refeeding syndrome and gastrointestinal haemorrhage. After recovery, a gastrostomy was performed, but due to gastric retention she required a laparotomy for adhesiolysis.The girl recovered and remains under home care. DISCUSSION: In a case of a girl with retardation, multiple organ failure resulting from ten years of malnutrition was observed. She was especially difficult to treat because of a prolonged dysfunction of homeostasis, hypoproteinemia, hypophosphatemia and SIRS. Such patients require careful treatment in ICU settings.