The influence of meal composition on plasma serotonin and norepinephrine concentrations.

Reports concerning changes in plasma neurotransmitter values that result from dietary manipulations have not been published so far. The influence of various meal compositions on platelet-poor plasma (PPP) serotonin (5-HT) and norepinephrine (NE) levels was investigated. Healthy volunteers were subjected to three test meals: a carbohydrate-rich meal (86% carbohydrates), a protein-rich meal (70% protein), and a fat-rich meal (92% fat). After a carbohydrate-rich meal, PPP 5-HT values increased significantly (4.47-fold, P less than .02), whereas a smaller increase (1.66-fold, P = NS) was observed after a fat-rich meal. These effects on PPP 5-HT values could be correlated with insulin plasma levels. A protein-rich meal significantly reduced (P = 0.0011) PPP 5-HT to 28% of initial values, despite an increase in plasma insulin levels. This study has shown that (1) changes in meal compositions influence PPP 5-HT and, to a lesser extent, NE values; (2) the resulting changes in PPP 5-HT levels parallel those reported for brain neurotransmitters; and (3) these results seem to indicate that PPP 5-HT levels may be a model for brain synthesis and release of 5-HT.     

Fibrinolytic response to exercise in women using third-generation oral contraceptives.

The use of oral contraceptives (OC) is associated with an increased risk of thrombosis, suggesting OC exert procoagulant and/or antifibrinolytic effects. Given that physical exercise physiologically leads to an activation of blood coagulation and fibrinolysis, this study tested the hypothesis that OC might compromise the fibrinolytic response to exercise. Fibrinolytic variables were measured in 10 women (24 +/- 2 years) using OC (a formulation containing 30 micro g ethinylestradiol and 150 micro g desogestrel) and in 11 women without OC (mean +/- SD, 27 +/- 3 years) before, during and after a 1-h run on a treadmill at a velocity corresponding to an oxygen demand of 75-80% of maximum (anaerobic threshold). Exercise testing gave rise to considerable increases of tissue-type plasminogen activator antigen by seven-fold to eight-fold in women taking and not taking OC alike. In the presence of unchanged plasma levels of plasminogen activator inhibitor-1, exercise-induced release of tissue-type plasminogen activator led to enhanced plasmin formation with respect to plasmin-antiplasmin complexes, rising by (mean +/- standard error) 701 +/- 77 ng/ml (P < 0.001) in women using OC and by 695 +/- 117 ng/ml (P < 0.001 versus baseline; NS versus OC users) in controls. The fibrinolytic response to intensive physical exercise is preserved in women using OC and is similar to women not using OC.     

Hyperphosphataemia and hypocalcaemia induced by hypertonic phosphate enema--an experimental study and review of the literature.

1. The study objective was to determine the hyperphosphataemic and hypocalcaemic effect of hypertonic phosphate enema. The study was conducted in a department of Internal Medicine at a University Medical Center. 2. Fourteen patients were studied. Patients' mean age (+/- s.d.) was 78.5 +/- 9 years. The creatinine clearance was 48.2 +/- 17.4 ml min-1 (mean +/- s.d.). 3. 500 ml (approx. 7 ml kg-1) of Fleet enema (FE - Na2HPO4.7H2O 224 mmol l-1 and NaH2PO4.H2O 1160 mmol l-1) were administered to each patient. Blood was drawn before FE administration and 1/2, 1, 3, 5, 12 and 24 h thereafter. Serum was analysed for levels of inorganic phosphorus and for calcium. 4. The serum inorganic phosphorus level rose from 1.01 +/- 0.3 mmol l-1 to 1.4 +/- 0.5 mmol l-1 (P = 0.001) 1 h after FE was administered. Serum calcium decreased from 2.32 +/- 0.12 mmol l-1 to 2.12 +/- 0.1 mmol l-1 (P less than 0.001) 12 h after FE was administered. 5. We conclude that FE carries a potential risk for acutely ill elderly patients. To avoid untoward effects due to hyperphosphataemia and hypocalcaemia, the phosphate load must be adjusted to the patient's renal function, i.e. enema volume is to be lowered when phosphate concentration is high, so that if renal function is compromised the amount of phosphate absorbed does not exceed renal excretion capacity.     

Significant damage of the conduction system during cardioplegic arrest is due to necrosis not apoptosis.

OBJECTIVES: Ventricular conduction disturbances following cardioplegic arrest remains a serious, yet unsolved problem. In the present study we examined whether myocardial conduction cells (MCC, Purkinje fibers) are more vulnerable to ischemia/reperfusion injury than working myocardial cells and whether the damage is due to necrosis or apoptosis. METHODS: Mini-pigs were subjected to 60 min of crystalloid (St Thomas; n = 15 group I) or blood (Buckberg; n = 6 group II) cardioplegic arrest followed by 3 h of reperfusion. Animals not subjected to either procedures served as controls (n = 5). Ventricular myocardial specimens were investigated by hematoxylin and eosin (HE) and periodic acid Schiff (PAS) staining and immunohistochemical labeling of apoptosis-associated proteins (Bax, Bcl-2, Caspase-3). DNA-breaks were visualized by in situ end labeling (terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling, TUNEL). Electron microscopy confirmed apoptosis or necrosis. RESULTS: MCC of control hearts intrinsically expressed Bax, Bcl-2, and Caspase-3 without signs of either apoptotic or necrotic damage. Subendocardial Purkinje fibers of groups I and II hearts exhibited focal damage, with reduced labeling of apoptosis-associated proteins, glycogen loss, karyopycnosis and increased eosinophilia (15/21 hearts). The majority of damaged MCC displayed nuclear TUNEL-positivity (2.8+/-2.5% of MCC), whereas the average TUNEL-rate of the adjacent working myocardium was low (<0.1%). Electron microscopy demonstrated ischemic changes in MCC consistent with cellular necrosis. CONCLUSIONS: Ischemia/reperfusion injury due to cardioplegic arrest inflicts significant damage on subendocardial MCC, but not on working myocardium. Ultrastructural and light-microscopic findings are consistent with coagulation necrosis, rather than apoptosis.     

Mn-DPDP–enhanced MR imaging of malignant liver lesions: Efficacy and safety in 20 patients

Twenty patients with malignant liver lesions underwent magnetic resonance (MR) imaging with manganese (II) DPDP [N,N′-dipyridoxylethylenediamine-N,N′-diacetate 5,5′-bis(phosphate)] to evaluate the safety and efficacy of the contrast agent. In two groups of 10 patients each, 5 μmol/kg Mn-DPDP was administered intravenously (3 mL/min) at a concentration of either 50 or 10 μmol/mL. T1- and T2-weighted images were obtained with a 1.5-T imager. Six patients reported a total of eight instances of side effects (flush, feeling of warmth, metallic taste) of which seven occured at the 50 μmol/mL concentration. A significant decrease in alkaline phosphatase levels 2 hours after injection was recorded. On T1-weighted images, the 10 μmol/mL formulation yielded significantly greater increases in contrast-to-noise ratio (79.8%–137.5%) than the 50 μmol/mL formulation (46.2%–86.6%). In a blinded reader study of 10 patients with one to five lesions each, no lesion was missed on Mn-DPDP–enhanced T1-weighted images; however, four false-positive foci were identified. The authors conclude that slow administration of 5 μmol/kg Mn-DPDP at a concentration of 10 μmol/mL is safe and efficient enough to proceed to further clinical trials.     

Reducing susceptibility artifacts in fMRI using volume-selective z-shim compensation.

Susceptibility-induced magnetic field gradients (SFGs) can result in severe signal loss in the orbitofrontal cortex (OFC) in gradient-echo-based functional MRI (fMRI) studies. Although conventional z-shim techniques can effectively recover the MRI signal in this region, the substantial penalty in imaging time hampers their use in routine fMRI studies. A modified z-shim technique with high imaging efficiency is presented in this study. In this technique, z-shim compensations are applied only to a selective volume where the susceptibility artifact is severe. The results of an fMRI study (N=6) demonstrate the feasibility of detecting the OFC activation with z-shim in whole-brain fMRI studies at a temporal resolution of 2 s.