Reduced High Density Lipoproteins as a Risk Factor after Acute Myocardial Infarction

ABSTRACT. FranzÉn J, Johansson BW, Gustafson A (Department of Internal Medicine, University Hospital, Lund and Section of Cardiology, Department of Internal Medicine, MalmÖ General Hospital, MalmÖ, Sweden). Reduced high density lipoproteins as a risk factor after acute myocardial infarction. In a group of normocholesterolemic, non-diabetic middle-aged males surviving an acute myocardial infarction for 4±2 years (mean ± SD), we have previously described a low apolipoprotein A-1 and a deficient fibrinolytic activity as two major characteristics. In the present study we have followed morbidity and mortality risk factors for five years in these males. Mortality was 40% in a hypertensive group and 16% in a normotensive group. In the normotensive group mortality was related to reinfarction. Furthermore, patients with a poor prognosis in the normotensive group had lower high density lipoprotein (HDL) cholesterol and lower apolipoprotein A-I concentration in plasma than patients with a good prognosis. Unexpectedly, in the hypertensive group death was related to a low (p<0.05) cortisol concentration in urine. It is concluded that a low HDL level may be a bad prognostic sign in males who have sustained an acute myocardial infarction and show no evidence of other risk factors, such as diabetes, hypercholesterolemia or hypertension.     

Thermogenetic response to mild hypothermia in anaesthetized infants and children

Metabolic correlates were related to room, core body and skin temperatures in 66 anaesthetized infants and children. Forty-one who had normal cardiorespiratory function were undergoing minor lower abdominal surgical procedures and were spontaneously breathing O₂/air mixture and halothane (body weight, 3.4–25.3 kg). Twenty-five had congenital heart malformations; 14 were cyanotic (weight, 3.4–24.3 kg) and 11 were acyanotic (weight, 3.7–20 kg). These 25 had balanced anaesthesia with halothane and their lungs were mechanically ventilated. Oxygen consumption (V?o₂), i. e. heat production, and CO₂ elimination (V?co₂) were measured by mass spectrometry. Indirect calorimetry was used for calculation of energy consumption. Temperatures were recorded in the lower third of the oesophagus (core temperature), at the mammillary level along the anterior axillary line (skin temperature), and in room air. Oesophageal temperatures ranged from 34.0°C to 38.1°C and skin temperatures from 32.1°C to 37.4°C (mean ± SD, 34.5°C ± 1.2°C). Heat production (V?o₂) was not related to body, skin or room temperatures. In concordance V?co₂ and energy expenditure were unrelated to the measured temperatures. Thermogenesis is thus eliminated in infants as well as in children, by the anaesthetic techniques used in the current study. This emphasizes the importance of prevention of heat loss in paediatric anaesthesia. Since the reduced skin and body temperatures in this study did not increase oxygen consumption, temperature regulation via an enhanced V?o₂ does not appear as a factor that aggravates hypoxaemia in cyanotic infants and children with congenital heart malformations.     

Ventilation and ventilatory CO2 response in children during halothane anaesthesia after nonopioid (midazolam) and opioid (papaveretum) premedication

The influence of non-opioid (NO) and opioid (O) premedication on ventilation and ventilatory CO2 response was studied in 18 spontaneously breathing children during halothane anaesthesia. Eight patients in Group NO and 10 in Group O were comparable in age, body weight and type of surgery performed. The sedative effect was evaluated and measurements by pneumotachography and in-line capnography were made immediately after induction of sleep, just before the start of surgery, during surgery and after surgery both before and after 3 min of about 2% CO2 inhalation. Immediately after induction the mean value (+/- s.e. mean) of end-tidal CO2 concentration (ETCO2) was 4.86 +/- 0.21% in Group NO and 5.28 +/- 0.22% in Group O. Before and during surgery, minute ventilation (VE) was higher in Group NO (P less than 0.05) mainly due to higher respiratory rates. ETCO2 was similar in the two groups before, during and after surgery. The ratio of VE to CO2 elimination (VCO2) and of dead space (VD) to tidal volume (VT) was higher in Group NO, but ventilatory response to CO2 inhalation immediately before the postoperative period was similar in both groups. It was concluded that opioid premedication resulted in more efficient ventilation during anaesthesia and surgery, and that CO2 response at the end of surgery was maintained in both groups.     

Insulin and C-peptide Secretory Responses to Glucagon in Man: Studies on the Dose-Response Relationships

ABSTRACT. The present study investigated the insulin and C-peptide secretory responses to glucagon in non-diabetic humans. Glucagon induced a transient increase in plasma insulin and C-peptide concentrations. At the dose level of 0.5 mg, glucagon elicited more efficient responses than at the dose level of 0.25 mg (p<0.05). However, the responses were not further potentiated by glucagon at 1.0 mg. Plasma glucose levels did not change during the first 2 min after glucagon injection, when already a marked increase in plasma insulin and C-peptide levels were observed. Thereafter, however, plasma glucose levels increased, to be maximal at 20 min after glucagon injection. Calculations of the minute-to-minute increase of plasma insulin and C-peptide levels revealed that plasma insulin levels increased by 32±7% of the increase in plasma C-peptide levels during the first 2 min, and by 36±6% of the increase in plasma C-peptide levels during the 3rd and 4th min after injection; the difference being the liver extraction of insulin. We conclude from this study in man 1) that glucagon stimulates insulin secretion through both direct and indirect effects, 2) that following glucagon injection, approximately 65% of the secreted insulin is extracted by the liver, and 3) that the dose level of 0.5 mg glucagon is the optimal dose level for the stimulation of insulin secration.     

Production of Interferon-α/β by Murine Dendritic Cell Lines Stimulated by Virus and Bacteria

The interferon-α and -β (IFN-α/β) producing ability of the two murine dendritic cell (DC) lines D2SC/1 and FSDC was studied. The D2SC/1 cells produced IFN-α and -β when stimulated by herpes simplex virus (HSV), Sendai virus (SV) or by the bacteria Escherichia coli or Staphylococcus aureus Cowan I. Precultivating (priming) D2SC/1 cells with recombinant IFN-β or a combination of IFN-β and granulocyte–macrophage colony-stimulating factor increased production of IFN-α/β induced by HSV or the bacteria, but not by SV. Also, the kinetics of IFN-α/β responses were different for SV compared to HSV and the bacteria, suggesting different induction mechanisms. The FSDC cells differed from the D2SC/1 cells mainly in that predominantly IFN-β was produced, that little or no IFN-α/β production was induced by the bacteria, and that the IFN-α/β responses were most efficiently primed by IFN-γ. Priming the DC lines with tumour necrosis factor-α, interleukin-10 (IL-10) or IL-4 did not affect the IFN-α/β response induced by HSV. The results show that the two DC lines provide a convenient tool to study the induction and control of the IFN-α/β response, as well as the immunoregulatory role of IFN-α/β produced by DC.