Asystole with Syncope Secondary to Hyperventilation in Three Young Athletes

We describe three athletes who had syncope after (case 1) or during (cases 2, 3) hyperventilation. During the episode, ECG showed prolonged sinus arrest. Clinical data and noninvasive investigations were normal and the phenomenon was not reproducible. Electrophysiological study after autonomic blockade allowed a prolonged intrinsic heart rate in case 1, and abnormal corrected sinus node recovery time in cases 1 and 2. During follow-up, symptomatic sinus arrest provoked by deep inspiration occurred in case 3. These cases document prolonged asystole of unknown etiology, secondary to hyperventilation, and probably caused by different vagally-mediated mechanisms.     

Membrane glycoprotein modifications of G6PD deficient red blood cells

Abstract. In this study, the composition and the role of membrane glycoproteins in phagocytosis were determined in G6PD deficient RBCs. G6PD deficient RBCs were recognized and significantly phagocytosed by murine macrophages, without pre-exposure to oxidants in vivo . Phagocytosis was partially (60%) inhibited by incubating macrophages with either galactose or mannose, or by incubating RBCs with β-galactosidase, indicating the involvement of lectin-like receptors in the recognition of G6PD deficient RBCs. Membrane glycoproteins on G6PD deficient cells were detected by binding of Con A to both intact RBCs and to purified membrane proteins. The results demonstrated modifications in the glycoprotein pattern of G6PD deficient RBCs compared to untreated controls. These included reduction in the amounts of several high molecular weight glycoproteins and appearance of lower molecular weight bands. These results suggest that G6PD deficient RBCs undergo glycoprotein modifications, which may lead to premature removal from circulation, even in non-acute hemolysis.     

Comparative effects of nitric oxide synthesis inhibition and catecholamine treatment in a rat model of endotoxin shock

Catecholamines and volume repletion are currently used for the treatment of septic shock. However, the prognosis of patients suffering from this condition is very poor. An overproduction of nitric oxide (NO) seems to be related to the hypotension and tissue damage of endotoxin shock. Thus, treatment with NO synthase inhibitors has been proposed. Using a rat model of septic shock we have studied the effects of noradrenaline or the NO synthase inhibitor, N^G-nitro-l -arginine methylester (l -NMMA) on arterial pressure, tissue damage and NO production. Anaesthetized rats treated with Salmonella typhosa showed a decrease in blood pressure accompanied by an increase in the plasma concentration of cytosolic enzymes (transaminases and lactate dehydrogenase, markers of cell disruption) and nitrite plus nitrate (NO^?₂/NO^?₃, markers of NO production). A large proportion of these animals (40%) died before the end of the experiment. Co-treatment with noradrenaline resulted in temporary maintenance of arterial pressure followed by a decline, despite the dose being increased progressively. No differences were observed in plasma cytosolic enzymes, NO^?₂/NO^?₃ or mortality compared with animals treated with lipopolysaccharide (LPS) alone. In contrast, administration of l -NMMA (10 mg kg^?1) to septic animals prevented the fall in blood pressure and death caused by endotoxin. This treatment markedly diminished cell disruption, as measured by the plasma levels of necrosis enzymes, and partially, but significantly, reduced the production of NO as assessed by plasma NO^?₂/NO^?₃. We conclude that tissue damage in septic shock is related to the overproduction of NO and not exclusively to the hypotension that follows this increased production. Thus, maintenance of blood pressure with catecholamines fails to improve cellular damage. Instead, partial inhibition of NO generation is sufficient to ameliorate the haemodynamic and tissue-damaging effects of septic shock and improves survival in this model of endotoxaemia.     

Incidence of Atrial Fibrillation in Patients with Different Mode of Pacing. Long-term Follow-up

We evaluated the incidence of atrial fibrillation in 189 patients (92males, 97females, mean age 75 ± 12yrs, range 41–100yrs) with pacemaker, during a mean follow-up of 5.5yrs (range 1–24yrs). The indications for implant were: complete AV block (115pts), second degree Möbilz 2 AV block (51pts). bifascicular block (5pts). sick sinus syndrome (14pts), symptomatic bradycardia (4pts). The mode of stimulation considered were VVI (105pt), VVI rate responsive (21pts), single lead VDD (43pts), DDD (20pts). The occurrence of retrograde VA conduction in patients with VVI or VVI rate responsive pacing was also evaluated. Atrial fibrillation occurred in 40 pts (21%). The highest incidence was evidenced in patients with sick sinus syndrome (9pts, 64%), and in patients with VVI stimulation (28pts, 27%). On the contrary, the lowest incidence was found in single lead VDD stimulation (4pts, 9%). The patients with dual chamber pacing showed a relatively high incidence of the arrhythmia (5pts, 25%). Atrial fibrillation occurred in 9 out of 32 patients with retrograde VA conduction, and in 22 out of 94 patients without retrograde conduction (28% versus 23%, p=NS). In conclusion, it is confirmed that patients with sick sinus syndrome are at high risk for atrial fibrillation. Single lead VDD stimulation seems to be the better mode of pacing in preventing atrial fibrillation, while dual chamber pacing showed minor efficacy. The presence of retrograde VA conduction could not predict the occurrence of the arrhythmia.