Carotid Arterial Impedance During Oscillated Blood Flow

1994 ◽  
Vol 18 (9) ◽  
pp. 627-632 ◽  
Author(s):  
Shin-ichi Kobayashi ◽  
Shin-ichi Nitta ◽  
Tomoyuki Yambe ◽  
Shigeru Naganuma ◽  
Motonao Tanaka ◽  
...  
1971 ◽  
Vol 35 (3) ◽  
pp. 286-300 ◽  
Author(s):  
Gudru n ◽  
H. J. Ladegaard-Pedersen ◽  
H. Henriksen ◽  
L. Olesen ◽  
O. B. Paulson ◽  
...  

2000 ◽  
Vol 33 (8) ◽  
pp. 975-984 ◽  
Author(s):  
S.Z Zhao ◽  
X.Y Xu ◽  
A.D Hughes ◽  
S.A Thom ◽  
A.V Stanton ◽  
...  

1985 ◽  
Vol 72 (5) ◽  
pp. 348-351 ◽  
Author(s):  
R. Bullock ◽  
A. D. Mendelow ◽  
I. Bone ◽  
J. Patterson ◽  
W. N. Macleod ◽  
...  

Cephalalgia ◽  
1989 ◽  
Vol 9 (9_suppl) ◽  
pp. 41-46
Author(s):  
Marion J Perren ◽  
Wasyl Feniuk ◽  
Patrick Pa Humphrey

The haemodynamic effects of the selective 5-HT1-like agonist GR43175 have been compared with that of ergotamine in anaesthetized cats. Both GR43175 (30–1000 μg/kg intravenously) and ergotamine (0.3–30 μg/kg intravenously) caused a dose-dependent reduction in the proportion of cardiac output passing through arteriovenous anastomoses (AVAs). However, unlike GR43175, the effect of ergotamine (30 μg/kg intravenously) was associated with marked increases in diastolic blood pressure and total peripheral resistance. In further studies, the effect of GR43175 on the distribution of blood flow within the carotid bed has been examined. GR43175 caused a reduction in total carotid arterial blood flow which was entirely due to a reduction in flow through carotid AVAs. These results demonstrate that GR43175, unlike ergotamine, has a highly selective vasoconstrictor action on AVAs within the cranial circulation of anaesthetized cats. Such a mechanism may be important in its antimigraine activity.


1994 ◽  
Vol 267 (6) ◽  
pp. H2268-H2279 ◽  
Author(s):  
M. P. Bendeck ◽  
F. W. Keeley ◽  
B. L. Langille

We compared arterial growth to hemodynamic changes in the perinatal period in lambs. Blood pressure did not change significantly from 120 days gestation to 3 days postpartum, when it was 45.4 +/- 1.9 mmHg; however, pressure rose to 64.8 +/- 2.5 mmHg at 21 days postpartum. Thoracic and abdominal aortic and iliac and carotid arterial blood flows fell > 50% after birth but returned to fetal levels except in the abdominal aorta by 21 days postpartum. Blood flows in mesenteric (BFm) and renal (BFr) arteries increased between 120 days gestation (BFr = 13.4 +/- 1.4; BFm = 41.8 +/- 3.5 ml/min) and 140 days gestation (BFr = 25.9 +/- 1.8; BFm = 189 +/- 18 ml/min) and between 3 and 21 days postpartum (to BFr = 71.1 +/- 14.3; BFm = 334 +/- 59 ml/min). Elastin accumulation accelerated at 140 days gestation in all arteries except the thoracic aorta, in which elastin accumulation was always rapid. Collagen but not DNA accumulation also accelerated in most arteries. Postpartum dexamethasone (0.1 mg/kg twice a day) did not affect abdominal aortic elastin by 10 days of age (23.9 +/- 2.7 vs. 26.4 +/- 4.1 mg for controls); however, dexamethasone upregulated tropoelastin mRNA in fetuses. We hypothesize that cortisol stimulates elastin accumulation in late gestation. Postnatal elastin but neither collagen nor DNA correlated with blood flow changes at birth (r = 0.855, P < 0.05). We infer that accumulation of elastin is sensitive to blood flow rates during perinatal development.


1984 ◽  
Vol 247 (4) ◽  
pp. R626-R633 ◽  
Author(s):  
B. J. Buckley ◽  
N. Gootman ◽  
J. S. Nagelberg ◽  
P. G. Griswold ◽  
P. M. Gootman

The cardiovascular effects of graded arterial or venous hemorrhage were evaluated in developing swine (less than or equal to 1 day, 2–5 days, 1 wk, and 2 wk of age) anesthetized with halothane in 50% N2O–50% O2. Serial 5-ml/kg aliquots of arterial or venous blood were removed at 3- to 4-min intervals to a cumulative total of 20 ml/kg. Tachycardia occurred in most animals. Decreases in aortic pressure to arterial, but not to venous, hemorrhage were age dependent. Renal, femoral, and carotid arterial flows decreased with hemorrhage in all animals; the decreases in blood flow did not differ among the three circulations and were not age dependent. Increases in femoral resistance were obtained to both arterial and venous hemorrhage only in the 2-wk-old group. As the degree of hemorrhage was increased, aortic pressure, regional blood flow, and femoral resistance (2 wk olds) responses were larger in magnitude. Aortic pressure in piglets 1-5 days of age could not be restored to within 20% of the prehemorrhage level at a smaller bleeding volume with arterial than with venous hemorrhage. Pressor responses to norepinephrine (0.5 micrograms/kg) and to bilateral common carotid occlusion were still present after 20-ml/kg hemorrhage. These responses indicate the presence of a progressive maturation-related compensation to the stress of arterial but not venous hemorrhage.


1983 ◽  
Vol 102 (2) ◽  
pp. 294-298 ◽  
Author(s):  
W. Dean Wilcox ◽  
Timothy A. Carrigan ◽  
Kenneth J. Dooley ◽  
Don P. Giddens ◽  
Francine D. Dykes ◽  
...  

1992 ◽  
Vol 8 (3) ◽  
pp. 200-204 ◽  
Author(s):  
Yasuyuki Futagi ◽  
Kazumasa Otani ◽  
Tetsuzo Tagawa ◽  
Hyakuji Yabuuchi

Author(s):  
Giulia Fabbri ◽  
Quan Long ◽  
Hao Gao ◽  
Carola Koenig ◽  
Michael W. Collins ◽  
...  

Atherosclerotic plaques may rupture without warning and cause subsequential acute syndromes such as myocardial infarction and cerebral stroke. Plaque disruption tends to occur at points where the plaque surface is weakest i.e. at points where biomechanical stresses caused by the pulsatile blood flow are concentrated. Therefore, both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption [1]. The former predisposes the plaque to rupture while the latter may precipitate it.


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