EFFECTS ON IONIZED CALCIUM OF A CORRECTION OF ACIDOSIS WITH ALKALINIZING AGENTS

SUMMARY The effects on the ionized calcium concentration of a correction of various forms of acidosis with sodium bicarbonate or (tris-hydroxymethyl)aminomethane (THAM) were investigated in vitro in human plasma. Calculation of least square regression equations of ionized calcium (m mol) on pH yielded the following regression coefficients: hydrochloric acidosis: —0.65±0.06; lactic acidosis: —0.27±0.05; hydrochloric acidosis corrected with sodium bicarbonate: —0.65±0.02; lactic acidosis corrected with sodium bicarbonate: —0.51±0.03. The results indicate that after correction of lactic acidosis the ionized calcium concentration will be below the control values while pH is restored to the normal range. This effect is even more pronounced when THAM is used. The findings point to the need for calcium administration in cardiac resuscitatio

IONIZED CALCIUM IN ACIDOSIS: DIFFERENTIAL EFFECT OF HYPERCAPNIC AND LACTIC ACIDOSIS

The effects of various forms of acidosis on ionized calcium concentrations were investigated in vivo in rabbits and in vitro in human plasma. Calculation of least square regression equations of ionized calcium (mM) on pH yielded the following regression coefficients in human plasma: hypercapnic acidosis —0.53±0.07; hydrochloric acidosis —0.65±0.06; lactic acidosis —0.27±0.05. These findings in human plasma are roughly paralleled by those in rabbits. From stability constants it was calculated that the formation of Ca-lactate complexes accounts for the difference between lactic and hydrochloric acidosis. It is concluded that differences in the behaviour of ionized calcium between hypercapnic and lactic acidosis might contribute to the known differences in cardiovascular effect

HAEMODYNAMIC EFFECTS OF TRANSIENT ATRIOVENTRICULAR DISSOCIATION IN GENERAL ANAESTHESIA

SUMMARY Isorhythmic atrioventricular dissociation occurs frequently under general anaesthesia but is rarely recognized without continuous electrocardiographic monitoring. Since this arrhythmia was observed in about 50 per cent of the cases during the onset of the neuromuscular blocking action of alcuronium or pancuronium during halothane anaesthesia, the opportunity was taken to investigate the haemodynamic parameters during atrioventricular dissociation. In nine patients the haemodynamic parameters during atrioventricular dissociation as compared to sinus rhythm were characterized by an absence of significant differences in cardiac rate, by a mean lowering in arterial mean pressure of 14 per cent and by a mean decrease in cardiac output of 15 per cent. The calculated peripheral resistance remained unaltere

RHABDOMYOLYSIS INDUCED BY ANAESTHESIA WITH INTRAOPERATIVE CARDIAC ARREST

A 9-year-old boy undergoing anaesthesia including suxamethonium and halothane suffered cardiac arrest on two occasions. Clinical and laboratory examination subsequently showed that the patient had suffered from acute rhabdomyolysis. The eventual recovery was satisfactor

Hemophagocytic syndrome caused by primary herpes simplex virus 1 infection: report of a first case

Introduction: Hemophagocytic syndrome represents a severe hyperinflammatory condition by activated macrophages. Leading viral triggering agents are Epstein-Barr virus (EBV), cytomegalovirus (CMV), and adenovirus. Materials and methods: We present a patient with Wegener's granulomatosis on azathioprine and prednisone medication, who developed a life-threatening hemophagocytic syndrome. Positive plasma polymerase chain reaction (PCR) with negative serology revealed a primary, disseminated infection with herpes simplex virus-1 as the triggering pathogen. After treatment with acyclovir, high-dose steroids, immunoglobulins, and etoposide, the patient recovered. Conclusion: Early diagnosis of potentially underlying infections of hemophagocytic syndrome influences the therapeutic approach. It is important to consider a variety of infectious agents, particularly in immunosuppressed individuals. The reported case emphasizes the importance of screening for herpes simplex virus

Reversal of hemochromatosis by apotransferrin in non-transfused and transfused Hbbth3/+ (heterozygous b1/b2 globin gene deletion) mice

Intermediate beta-thalassemia has a broad spectrum of sequelae and affected subjects may require occasional blood transfusions over their lifetime to correct anemia. Iron overload in intermediate beta-thalassemia results from a paradoxical intestinal absorption, iron release from macrophages and hepatocytes, and sporadic transfusions. Pathological iron accumulation in parenchyma is caused by chronic exposure to non-transferrin bound iron in plasma. The iron scavenger and transport protein transferrin is a potential treatment being studied for correction of anemia. However, transferrin may also function to prevent or reduce iron loading of tissues when exposure to non-transferrin bound iron increases. Here we evaluate the effects of apotransferrin administration on tissue iron loading and early tissue pathology in non-transfused and transfused Hbb(th3/+) mice. Mice with the Hbb(th3/+) phenotype have mild to moderate anemia and consistent tissue iron accumulation in the spleen, liver, kidneys and myocardium. Chronic apotransferrin administration resulted in normalization of the anemia. Furthermore, it normalized tissue iron content in the liver, kidney and heart and attenuated early tissue changes in non-transfused Hbb(th3/+) mice. Apotransferrin treatment was also found to attenuate transfusion-mediated increases in plasma non-transferrin bound iron and associated excess tissue iron loading. These therapeutic effects were associated with normalization of transferrin saturation and suppressed plasma non-transferrin bound iron. Apotransferrin treatment modulated a fundamental iron regulatory pathway, as evidenced by decreased erythroid Fam132b gene (erythroferrone) expression, increased liver hepcidin gene expression and plasma hepcidin-25 levels and consequently reduced intestinal ferroportin-1 in apotransferrin-treated thalassemic mice

Hippocampal volume and declarative memory function in combat-related PTSD

The proposition that declarative memory deficits are systematically related to smaller hippocampal volume was tested in a relatively large sample (n = 95) of U.S. military veterans with and without combat-related posttraumatic stress disorder. This correlative analysis was extended by including multiple measures of verbal and visual declarative memory and multiple memory-relevant regional brain volumes that had been shown to exhibit main effects of PTSD in prior work. Small-to-moderate effects were observed on verbal declarative memory in line with a recent meta-analysis; nevertheless, little or no evidence of systematic linear covariation between memory measures and brain volumes was observed. (JINS, 2009, 15, 830-839.