C A Rouzer

Hypertriglyceridemia associated with Trypanosoma brucei brucei infection in rabbits: role of defective triglyceride removal.

Rabbits infected with Trypanosoma brucei brucei develop a hypertriglyceridemia characterized by an increase in very low density lipoprotein and, to a lesser extent, low density lipoprotein, with a decrease in high density lipoprotein. Triglyceride production studies showed that the triglyceride production rate was not significantly different in trypanosome-infected rabbits from controls. Studies of triglyceride degradation using very low density lipoprotein triglyceride endogenously labelled with [3H]palmitate demonstrated a marked slowing of triglyceride removal in the infected rabbits when compared to controls. Lipase activity in post-heparin plasma was found to be deficient in trypanosome-infected animals. Furthermore, the greater the decrease in lipolytic activity, the greater the increase in serum triglyceride level. We conclude that the hypertriglyceridemia associated with T. b. brucei infection in rabbits results predominantly from a defect in triglyceride degradation.

Leukotriene C4 Is Released from the Anaphylactic Heart: A Case for Its Direct Negative Inotropic Effect

Data from our laboratory indicate that the heart reacts as a target organ in systemic hypersensitivity reactions (Capurro and Levi, 1975; Graver et al., 1983). Cardiac dysfunction observed during anaphylaxis in the guinea pig (Capurro and Levi, 1975; Zavecz and Levi, 1977) resembles that reported in humans (Bernreiter, 1959; Both and Patterson, 1970; Criep and Woehler, 1971; Petsas and Kotier, 1973; Sullivan, 1982) and is caused by mediators released intracardially and reaching the heart from the lung (Zavecz and Levi, 1977). “Cardiac anaphylaxis” (Feigen and Prager, 1969) is characterized by tachycardia, arrhythmias, contractile failure, coronary constriction, and mediator release (Capurro and Levi, 1975; Levi and Allan, 1980; Levi et al., 1982). Tachycardia and arrhythmias are caused by the release of endogenous cardiac histamine, since they are reproduced by the intracardiac administration of histamine and abolished by antihistamines (Levi and Allan, 1980; Levi et al., 1982). On the other hand, anaphylactic coronary constriction is markedly reduced by cyclooxygenase inhibitors such as indomethacin or aspirin or by thromboxane syn-thetase inhibitors such as 1-(2-isopropylphenyl)imidazole (Allan and Levi, 1981). Furthermore, the intracardiac administration of U 46619, a stable thromboxane analogue, causes coronary constriction (Allan and Levi, 1980a). Thus, prostanoate compounds, particularly thromboxane, contribute to the fall in coronary flow rate that characterizes cardiac anaphylaxis (Levi et al., 1982). Other potent coronary-constricting agents, such as platelet-activating factor (PAF, AGEPC), are also likely to contribute to anaphylactic coronary constriction (Levi et al., 1984).