Læknablaðið - 01.04.1978, Blaðsíða 44

66
LÆKNABLAÐIÐ
minnkaðrar virkni vissra hvata í lysosom-
unum og æðakölkun sé því ein tegund af
„lysosomal storage disease".73 Talið er þó
líklegra af flestum, að fituútfellingarnar
ákvarðist fremur af innstreymi kólesteróls
sem LDL frá blóðinu, eins og stutt er af
tilraunum Smith o.fl., sem fundu sterka
fylgni milli LDL magns í æðaskellunum og
í blóði viðkomandi sjúklinga.98
Hvaða þættir ákvarða innstreymið af
LDL inn í æðavegginn er hinsvegar lítið
vitað um, enda þótt líklegt sé talið, að
haemodynamiskir þættir, svo sem blóð-
þrýstingur o.fl. ráði þar miklu um m.a. með
Mynd 1:
Two Possible Different Cycles of Events in the Response-to-Injury Hypothesis.
The large cycle may represent what occurs in all persons at varying times. Endothelial
injury may lead to desquamation, platelet adherence, aggregation and release, followed
by smooth-muscle proliferation and connective-tissue formation. If the injury is a single
event, the lesions may go on to heal and regress, leaving a slightly thickened intima.
The smaller, inner cycle demonstrates the possible consequences of repeated or chronic
injury to endothelium in which lipid deposition may occur and smooth-muscle prolifera-
tion may continue after a sequence of proliferation, regression, proliferation and regres-
sion, leading to a complicated lesion containing newly formed connective tissiue, and
lipids, which may eventually calcify. This sequence of events could lead to a complicated
Iesion that goes on to produce clinical sequelae, such as thrombosis and infarction. —
(Ross and Glomset).85