Lipolysis of emulsion models of triglyceride-rich lipoproteins is altered in male patients with abdominal aorta aneurysm

Disorders of the lipid metabolism may play a role in the genesis of abdominal aorta aneurysm. The present study examined the intravascular catabolism of chylomicrons, the lipoproteins that carry the dietary lipids absorbed by the intestine in the circulation in patients with abdominal aorta aneurysm. Thirteen male patients (72 ± 5 years) with abdominal aorta aneurysm with normal plasma lipid profile and 13 healthy male control subjects (73 ± 5 years) participated in the study. The method of chylomicron-like emulsions was used to evaluate this metabolism. The emulsion labeled with 14C-cholesteryl oleate and ³H-triolein was injected intravenously in both groups. Blood samples were taken at regular intervals over 60 min to determine the decay curves. The fractional clearance rate (FCR) of the radioactive labels was calculated by compartmental analysis. The FCR of the emulsion with ³H-triolein was smaller in the aortic aneurysm patients than in controls (0.025 ± 0.017 vs 0.039 ± 0.019 min-1; P < 0.05), but the FCR of14C-cholesteryl oleate of both groups did not differ. In conclusion, as indicated by the triglyceride FCR, chylomicron lipolysis is diminished in male patients with aortic aneurysm, whereas the remnant removal which is traced by the cholesteryl oleate FCR is not altered. The results suggest that defects in the chylomicron metabolism may represent a risk factor for development of abdominal aortic aneurysm.

The intestinal tract as the major source of interleukin 6 production during abdominal aortic clamping and hind limb ischaemia-reperfusion injury

PURPOSE: The aim of this study was to investigate whether the hind limbs or intestinal tract is the most important initiator of the inflammatory response secondary aortic clamping and hind limb ischemia/reperfusion injury. METHODS: Blood samples of Wistar rats obtained from posterior cava vein, portal vein, and heart cavity during either laparotomy (control group, n=8) or laparotomy + 2 h of aortic clamping and bilateral hind limb ischemia (ischemia group, n=8), or 2 h after ischemia and 2 h of reperfusion (ischemia-reperfusion group, n=8) were assayed for interleukin 6 (IL-6) and C-reactive protein (CRP). RESULTS: Serum IL-6 at the heart (223.6±197.9 [10-832] pg/mL) was higher (p<0.001) than at both portal (133.08±108.52 [4-372] pg/mL) and posterior cava veins (127.58±109.15 [8-388] pg/mL). CRP was not significant different among groups. CONCLUSION: The splanchnic region is also a source of inflammatory response secondary to ischemia and reperfusion of the hind limbs.

OBJETIVO: Investigar qual o principal mediador da resposta inflamatória na lesao de isquemia/reperfusão após clampeamento da aorta abdominal e isquemia dos membros inferiores: o intestine ou as extremidades inferiores. MÉTODOS: amostra de sangue de ratos Wistar coletados da cava posterior, porta e cavidade cardíaca during tanto laparotomia (grupo controle n=8) ou laparotomia + 2 horas de clampeamento aórtico e isquemia bilateral de membros posteriores (grupo isquemia n=8), ou 2 h de isquemia seguido por 2 horas de reperfusão (grupo isquemia/reperfusão n=8), onde foram dosados interleucina 6 e proteína C-reativa. RESULTADOS: Il-6 no coração (223.6±197.9 [10-832] pg/mL) foi maior (p<0.001) tanto na veia porta (133.08±108.52 [4-372] pg/mL) quanto na veia cava posterior (127.58±109.15 [8-388] pg/mL). PCR não foi significativamente diferente entre os grupos. CONCLUSÃO: o trato intestinal foi responsável pela resposta inflamatória secundária a lesão de isquemia/reperfusão.