Effects of endotoxemia on systemic plasma loss and hematocrit in rats

Endotoxemia in rats increases plasma extravasation but does not result in continuously rising hematocrit. These contradictory observations led us to design a study in anesthetized rats (C, control rats, n = 10; E, endotoxin rats, n = 10) in which we continuously measured in blood hematocrit (conductivity cell) and changes in concentration of 125I-HSA (human serum albumin) and 51Cr-labeled red cell (51Cr-RBC; multichannel analyzer) in an extracorporeal circuit. In two additional series of experiments we measured in blood samples changes in protein concentration (series II, C: n = 7, E: n = 7) and uptake of intraperitoneally injected 125I-HSA and 51Cr-RBC (reflecting lymph flow rate; series III, C: n = 6, E: n = 7). Endotoxemia was induced by infusion (iv, 0.2 ml/100 g.hr) of Escherichia coli endotoxin (20 mg/kg) from t = 0 to t = 60 min; controls received saline. Experiments ended at t = 120 (series I and II) or 150 min (series III). The endotoxemia resulted in a marked rise of serum lactate (by ca 500% at t = 120); heart rate increased and central venous pressure decreased (by ca 20 and -95% at t = 120, respectively). All rats showed characteristic changes in hematocrit during endotoxemia: an increase from t = 20 to t = 45 (by ca 9%) followed by a decrease to preshock values or less at t = 120. The 51Cr activity per microliter blood cells did not change, indicating that there was no red cell mobilization. Protein concentration and 125I-HSA activity also showed a temporary increase during endotoxemia, but 125I-HSA activity per gram protein was decreased. Peritoneal uptake of 125I-HSA and 51Cr-RBC was significantly increased during endotoxemia (by 200%). We conclude that fluid extravasation during endotoxemia is temporary, mainly concerns plasma water, and is compensated by mechanisms like reabsorption and increased lymph flow, resulting in restoration of plasma volume.     

The influence of catecholamines on right ventricular function in septic shock

Catecholamines play an important role in the treatment of septic shock. Not much is known about their effects on right ventricular function. In this paper the available data on the effects of different catecholamines on right ventricular dysfunction complicating septic shock are reviewed.     

Fatal rhinocerebral mucormycosis and diabetic ketoacidosis

The typical features of a fulminating rhinocerebral infection by the fungus Rhizopus in a patient with diabetic ketoacidosis are described. The clinical presentation was characterized by an infection of the face, followed by rapid bilateral visual loss and massive cerebral infarction due to extensive vascular involvement. Early diagnosis is a prerequisite for successful treatment, which consists of control of the underlying disease, surgical debridement and systemic antifungal therapy.     

Correlation of reversion-inducing cysteine-rich protein with kazal motifs (RECK) and extracellular matrix metalloproteinase inducer (EMMPRIN), with MMP-2, MMP-9, and survival in colorectal cancer

mRNA, and latent and active levels MMP-2 and -9 were higher in tumor tissue compared to normal tissue from 63 patients with colorectal cancer, whereas RECK and EMMPRIN levels were lower. Correlations between mRNA, latent, and active MMP were particular high for MMP-2 in tumor tissue (R(s)=0.6-0.8, P<0.001). For active MMP-2, but not for MMP-9, a significant negative partial correlation (R(p)=-0.440, P<0.001) for RECK was found in tumor tissue, which was confirmed by linear regression analysis. In exploratory survival analyses we found that in patients with localized disease the RECK level in normal or tumor tissue had a significant (P=0.017) association with overall survival.     

Facial nerve function in carcinoma of the parotid gland

AimTo analyse, for patients with carcinoma of the parotid gland, the prognostic value for treatment outcome of the function of the facial nerve (NVII), and determining facial nerve dysfunction after treatment.Methods and materialsIn a retrospective study of the Dutch head and Neck cooperative group (NWHHT), data of 324 patients with parotid carcinoma were analysed. The function of N VII before treatment was intact in 77%, partially and completely impaired in 14% and 7%, respectively. Eighty-eight percent of the patients were treated surgically, and 77% of them were treated by a combination of postoperative radiotherapy. In 21% NVII was sacrificed, a reconstruction was performed in one of three.ResultsIndependent risk factors for N VII dysfunction before treatment were tumour localisation, positive neck nodes at presentation, pain, increasing age, and perineural invasion. Regional, not local, control was significantly impaired for complete facial paralysis. N VII dysfunction was an independent factor for disease free survival, and was 69%, 37% and 13% for normal, partially and completely impaired function, respectively. After treatment 22% of the patients experienced a partial paralysis, and 13% of the patients experienced a complete parlysis of N VII.ConclusionFor patients with parotid carcinoma, facial nerve function before treatment is a strong prognostic factor for disease free survival.     

Monoclonal antibody (1116 NS 19-9) defined monosialoganglioside (GICA) in colorectal carcinoma in relation to stage,histopathology and DNA flow cytometry

Immunoreactivity of 1116 NS 19-9 monoclonal antibody defined monosialoganglioside (gastrointestinal cancer-associated antigen, GICA) has been studied in a series of colorectal carcinoma patients of a multicentre prospective controlled trial in order to assess its correlation with parameters such as localization, stage histopathological characteristics and DNA flow cytometry. GICA could be detected in 60% of the carcinomas, but no correlation was observed between its status of immunoreactivity and any of the parameters studied. It is concluded that, though study of the expression of the monosialganglioside may be worth while in relation to fundamental aspects of behaviour of colorectal carcinomas, the significance of its immunohistochemical detection in a diagnostic or prognostic sense is limited.     

Plasma renin activity in haemolytic uraemic syndrome

Plasma renin activity (PRA) was measured in 50 consecutive patients (aged 4 months to 12 years) admitted during the acute phase of the haemolytic uraemic syndrome (HUS). Blood samples were taken as soon as the diagnosis was made and prior to any diuretic, anti-hypertensive or dialysis treatment. Prodromal diarrhoea was present in all but 3 patients, 17 were anuric and 12 were oliguric. PRA ranged from 0.3 to 24.2 ng/ml per hour and was low compared with values in normal infants and children: in 13 HUS patients PRA was above the median and in 37 it was below the median. PRA was significantly, independently and inversely related to age. There was no correlation, however, with blood pressure, urine output, volume status and serum levels of sodium, potassium and creatinine. Moreover, no relationship was found between PRA and the course of the disease. Our findings do not support the idea that renin activation plays a role in the pathophysiology of the haemolytic uraemic syndrome.     

Effects of glucose-insulin-potassium (GIK) on the position of the oxyhemoglobin dissociation curve, 2.3-diphosphoglycerate, and oxygen consumption in canine endotoxin shock

The effects of glucose-insulin-potassium (GIK) on hemodynamics, oxygen transport, P50, 2,3-diphosphoglycerate (2.3-DPG), and adenosine triphosphate (ATP) were evaluated in canine endotoxin shock. Ten dogs were studied under general anesthesia and controlled ventilation. Shock was induced with Escherichia coli endotoxin (1.5 mg/kg body wt). Thereafter two groups of five dogs each were formed by randomization. The one group received GIK (glucose 50%, 2 g/kg, insulin 3 U/kg, and 10 mmole K) in the period between 90 and 120 min after endotoxin. The other group received an equal amount of NaCl infusion and served as a control group. Observations were completed at 180 min after endotoxin. GIK resulted in a significant increase of cardiac output, stroke volume, mean arterial pressure, and oxygen consumption. Serum phosphate levels decreased. No changes were observed of P50 in vitro (at 37 degrees C and pH 7.40) and of P50 in vivo, nor of 2.3-DPG and ATP in the red cells. The data suggest that the increased oxygen consumption after GIK in canine endotoxin shock is caused only by improvement of cardiac output and oxygen availability and not by an effect on oxygen unloading capacity of hemoglobin.