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were not efï¬cient in stopping the bleeding due to their
localization far away from the arterial laceration. Fur-
thermore, these aggregates were penetrated by channels
through which bleeding could continue [53]. This in
vivo study emphasized the importance of vWf not only
in the interaction of platelets with the blood vessel and
in the localization of the hemostatic plug to the dam-
aged vessel but also in platelet-platelet interactions as
demonstrated in humans [22, 23]. The pig model was
also used to measure platelet adhesion to damaged
coronary arteries [54]. A similar platelet adhesion was
observed in both normal and vWd pigs, but the
platelets appeared less activated in the affected pigs,
keeping a round morphology and fewer pseudopodia.
The shear rate in coronary arteries is low, which could
explain the absence of defect in platelet adhesion in the
vWf-deï¬cient pigs. That study uncovered a new role for
vWf in platelet activation at low shear rate. The role of
von Willebrand disease models
vWf in mediating platelet-vessel wall interactions at
various shear rates was investigated using in vitro and
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intimal thickening. In contrast, only 3 vWd pigs out of
7 developed signiï¬cant raised fatty atherosclerotic
plaques, which were smaller than those in the control
pigs. Additional studies conï¬rmed this protection
against atherosclerosis in vWd pigs [67]. However it was
noted in all these studies that normal pigs have a
tendency to have higher levels of diet-induced hyper-
cholesterolemia than do vWd pigs, a ï¬nding that was
not systematically explored and that might have been of
great importance. Indeed in one study, the amount of
coronary atherosclerosis was shown to be related to the
degree of hypercholesterolemia that the pigs develop
and not to the presence of vWf [68]. The controversy
about the involvement of vWf in atherosclerosis was
further reinforced by a report by Nichols et al. [69]
showing that the presence of a particular polymorphism
at the apolipoprotein B100 locus can signiï¬cantly influ-
ence the development of diet-induced hypercholes-
terolemia and coronary and aortic atherosclerosis in the
pig, independent of the vWd status. From this study,
the authors conclude that this polymorphism could
have affected the results of the previous atherogenesis
experiments in vWd animals. These results are in agree-
ment with autopsy ï¬ndings in three patients with vWd
[70]. Atherosclerosis lesions, but no occlusive thrombo-
sis, were present in patients with type 3 vWd. The
patients’ repeated transfusions of blood products con-
taining vWf could account for these observations.
However, considering the vWf role in platelet adhesion
and activation, a mechanism linking vWf to atherogene-
sis may still exist. It was shown that both pseudopod
formation and spreading of platelets adhering to injured
arterial walls was impaired in vWd pigs [71]. In order to
investigate the role of vWf in occlusive arterial throm-
bosis, normal and vWd pigs were fed a high cholesterol
diet, and at the end of the diet period coronary and
carotid arteries were subjected to a stenosis/injury pro-
tocol to produce occlusive thrombosis [72]. Coronary
atherosclerosis was present in both groups of pigs, but
occlusive thrombosis failed to develop in vWd pigs
despite the presence of atherosclerosis, severe hyper-
Review Article 981
t/data/demos/11212329.utf8 view on Meta::CPAN
23 Ikeda Y., Handa M., Kawano K., Kamata T., Murata M., 45
Araki Y. et al. (1991) The role of von Willebrand factor and
ï¬brinogen in platelet aggregation under varying shear stress.
J. Clin. Invest. 87: 1234–1240
24 Weiss H. J., Sussman I. I. and Hoyer L. W. (1977) Stabiliza- 46
tion of factor VIII in plasma by the von Willebrand factor.
J. Clin. Invest. 60: 390–404
25 Brinkhous K. M., Robert L., Read M. S., Nichols T. C., 47
Bellinger D. A. and Griggs T. R. (1991) von Willebrand factor
and animal models: contributions to gene therapy, thrombotic
thrombocytopenic purpura and coronary thrombosis. Mayo
Clin. Proc. 66: 733–742
26 Weiss H. J. (1974) Relation of von Willebrand factor to 48
bleeding time. N. Engl. J. Med. 291: 420
27 Lind S. E. (1984) Prolonged bleeding time. Am. J. Med. 77:
305–312
28 Burns E. R. and Lawrence C. (1989) Bleeding time. A guide 49
to its diagnostic and clinical utility. Arch. Pathol. Lab. Med.
113: 1219–1224
29 Lamme S., Wallmark A., Holmberg L., Nilsson I. M. and
Sjogren H. O. (1985) The use of monoclonal antibodies in
t/data/demos/11212329.utf8 view on Meta::CPAN
Cramer E. M., Caen J. P., Drouet L. and Breton-Gorius J.
(1986) Absence of tubular structures and immunolabeling for
von Willebrand factor in the platelets -granules from porcine
von Willebrand disease. Blood 68: 774–778
Sawada Y., Fass D. N., Katzman J. A., Bahn R. C. and Bowie
E. J. W. (1986) Hemostatic plug formation in normal and von
Willebrand pigs: the effect of administration of cryoprecipitate
and a monoclonal antibody to von Willebrand factor. Blood
67: 1229–1239
Reddick R. L., Griggs T. R., Lamb M. A. and Brinkhous K.
M. (1982) Platelet adhesion to damaged coronary arteries:
comparison in normal and von Willebrand disease swine.
Proc. Natl. Acad. Sci. USA 79: 5076–5079
Badimon L., Badimon J. J., Turrito V. T. and Fuster V. (1989)
Role of von Willebrand factor in mediating platelet-vessel wall
interaction at low shear rate; the importance of perfusion
conditions. Blood 73: 961–967
Bowie E. J. W., Solberg L. A. Jr, Fass D. N., Johnson C. M.,
Knutson G. J., Stewart M. L. et al. (1986) Transplantation of
normal bone marrow into a pig with severe von Willebrand’s
disease. J. Clin. Invest. 78: 26–30
t/data/demos/11212329.utf8 view on Meta::CPAN
Andre P., Brouland J. P., Roussi J., Bonneau M., Pignaud G.,
Bal dit Sollier C. et al. (1998) Role of plasma and platelet von
Willebrand factor in arterial thrombogenesis and hemostasis
in the pig. Hematology 26: 1–7
Roussi J., Samama M., Vaiman M., Nichols T., Pignaud G.,
Bonneau M. et al. (1996) An experimental model for testing
von Willebrand factor function: successful SLA-matched
crossed bone marrow transplantations between normal and
von Willebrand pigs. Exp. Hematol. 24: 585–591
Duguid J. B. (1946) Thrombosis as a factor in the pathogenesis
of coronary atherosclerosis. J. Pathol. Bacteriol. 58: 207–212
Stemerman M. B. and Ross R. (1972) Experimental arte-
riosclerosis. I. Fibrous plaque formation in primates, and
electron microscope study. J. Exp. Med. 136: 769–789
Ross R., Glomset J., Kariya B. and Harker L. (1974) A
platelet-dependent serum factor that stimulates the prolifera-
tion of arterial smooth muscle cells. Proc. Natl. Acad. Sci.
USA 71: 1207–1210
CMLS, Cell. Mol. Life Sci. Vol. 56, 1999
t/data/demos/11212329.utf8 view on Meta::CPAN
66 Fuster V. and Bowie E. J. W. (1978) The von Willebrand pig 84
as a model for atherosclerosis research. Thromb. Haemost.
39: 322–327
67 Badimon L., Steele P., Badimon J. J., Bowie E. J. W. and
Fuster V. (1985) Aortic atherosclerosis in pigs with het-
erozygous von Willebrand disease. Comparison with ho- 85
mozygous von Willebrand and normal pigs. Arteriosclerosis
5: 366–370
68 Griggs T. R., Bauman R. W., Reddick R. L., Read M. S., 86
Koch G. G. and Lamb M. A. (1986) Development of
coronary atherosclerosis in swine with severe hypercholes-
87
terolemia. Lack of influence of von Willebrand factor or
acute intimal injury. Arteriosclerosis 6: 155–165
88
69 Nichols T. C., Bellinger D. A., Davis K. E., Koch G. G.,
Reddick R. L., Read M. S. et al. (1992) Porcine von
89
Willebrand disease and atherosclerosis. Influence of poly-
morphism in apolipoprotein B100 genotype. Am. J. Pathol.
90
t/data/demos/11842027.iso-8859-1 view on Meta::CPAN
Carotid and vertebral artery blood flow in left and right handed healthy subjects measures with MR velocity mapping.
J Magn Reson Imaging
4:
37-42,
1994 [Medline] .
Celermajer, DS,
Sorensen KE,
Bull C,
Robinson J,
and
Deanfield JE.
Endothelium-dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction.
J Am Coll Cardiol
24:
1468-1474,
1994 [ISI] [Medline] .
De Goede, J,
Van der Hoeven N,
Berkenbosch A,
Olievier CN,
and
Van Beek JHGM
Ventilatory responses to sudden isocapnic changes in end-tidal O 2 in cats.
In: Modelling and Control of Breathing New York: Elsevier Biomedical, 1983, p. 37-45.
t/data/demos/12495435.MacRoman view on Meta::CPAN
CCCT(1/4) was 6.36 ± 3.01 (n = 67), CCCT(1) was 10.36 ± 4.2 (n = 33), S1/S2 was1.89 ± 0.94 (n = 140), T1/M1 was 1.44 ± 0.99 (n = 144), and D/S was 1.68 ± 0.27 (n = 172).
Conclusions
Using indicators CCCT(1/4) and CCCT(1) may be beneficial for evaluating cardiac contractility and cardiac reserve mobilization level, S1/S2 for considering the factor for hypotension, T1/M1 for evaluating the right heart load, and D/S for evaluating ...
Keywords: Cardiac contractility, systolic diastolic duration, cardiac reserve, auscultation
Background
Total cardiac reserve involves heart rate reserve, diastole volume reserve, systole volume reserve, coronary reserve [1], metabolic reserve [2], plasma norepinephrine reserve [3], etc. The measurement and evaluation of cardiac reserve is an important...
Previous studies of cardiac reserve mainly involved chronotropic incompetence, fewer involved inotropic incompetence [3-5]. It is a generally accepted concept that exercise capacity is a more powerful predictor of mortality than other established ris...
However, the distance covered during a 6-min walk test does not just represent cardiac reserve. Previous studies on the relationship between the amplitude of the first heart sound (S1) and cardiac contractility offer a way to reconcile the measuremen...
Based on the close relationship between the amplitude of the first heart sound (S1) and the cardiac contractility, we also devised another two indicators to evaluate specific cardiovascular status. One was the ratio of the amplitude of the first hear...
Furthermore, the time in diastole, when myocardial blood perfusion occurs, is an indicator of cardiac reserve. Whether or not this time during diastole is sufficient relates to how much nutrition and oxygen will be available during systole. This avai...
The primary objective of this work was to devise some indicators based on relative values for evaluating cardiac function, since the absolute value of S1 can not be used for evaluating cardiac contractility. We used the indicators described above to ...
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