2 Microvascular Alterations in Hypertension

2015 ◽  
pp. 31-59 ◽  
Author(s):  
Russell L. Prewitt ◽  
Haruhisa Hashimoto ◽  
D. Lowell Stacy
Keyword(s):  
Microvascular Alterations

Mimicking Microvascular Alterations of Human Diabetic Retinopathy: A Challenge for the Mouse Models

2013 ◽  
Vol 20 (26) ◽  
pp. 3200-3217 ◽  
Author(s):  
D. Ramos ◽  
A. Carretero ◽  
M. Navarro ◽  
L. Mendes-Jorge ◽  
V. Nacher ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Mouse Models ◽  
Microvascular Alterations

scholarly journals Microvascular alterations and the role of complement in dermatomyositis

Brain ◽  
2016 ◽  
Vol 139 (7) ◽  
pp. 1891-1903 ◽  
Author(s):  
Rajat Lahoria ◽  
Duygu Selcen ◽  
Andrew G. Engel
Keyword(s):  
Microvascular Alterations

scholarly journals Microvascular alterations in patients with SARS-COV-2 severe pneumonia

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Elisa Damiani ◽  
Andrea Carsetti ◽  
Erika Casarotta ◽  
Claudia Scorcella ◽  
Roberta Domizi ◽  
...  
Keyword(s):  
Severe Pneumonia ◽  
Microvascular Alterations

scholarly journals Microvascular alterations in adult conscious spontaneously hypertensive rats.

Hypertension ◽  
1990 ◽  
Vol 15 (4) ◽  
pp. 415-419 ◽  
Author(s):  
J L le Noble ◽  
T L Smith ◽  
P M Hutchins ◽  
H A Struyker-Boudier
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Microvascular Alterations

scholarly journals Microvascular Alterations During Cardiac Surgery Using a Heparin or Phosphorylcholine-Coated Circuit

2020 ◽  
Vol 34 (4) ◽  
pp. 912-919 ◽  
Author(s):  
Nicole A.M. Dekker ◽  
Dennis Veerhoek ◽  
Anoek L.I. van Leeuwen ◽  
Alexander B.A. Vonk ◽  
Charissa E. van den Brom ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Microvascular Alterations

Attenuated microvascular alterations in coarctation hypertension

1989 ◽  
Vol 256 (1) ◽  
pp. H213-H221 ◽  
Author(s):  
D. L. Stacy ◽  
R. L. Prewitt
Keyword(s):  
Fourth Order ◽  
Vascular Tone ◽  
Structural Parameters ◽  
Renal Hypertension ◽  
Second Order ◽  
Hypertensive Rats ◽  
Third Order ◽  
Flow Dependence ◽  
Vascular Beds ◽  
Microvascular Alterations

Arteriolar vasoconstriction, structural reductions in dilated diameter, and rarefaction have been observed in vascular beds with chronic renal hypertension. To determine their pressure or flow dependence, these functional and structural parameters were studied in the developing and chronic stages of coarctation hypertension in the cremaster muscle, a normotensive skeletal muscle bed that is protected from the effects of elevated microvascular pressures. Hypertension was produced in rats by placing a silver clip around the abdominal aorta above the branches of the renal arteries. In hypertensive rats, resting diameters were reduced in second-order arterioles after 4 and 8 wk, in third-order arterioles after 2, 4, and 8 wk, and in fourth-order arterioles after 4 and 8 wk, vs. controls. Vascular tone was elevated in second-order arterioles after 2, 4, and 8 wk and in third- and fourth-order arterioles after 8 wk in hypertensive rats. No increases in medial-intimal area were found at any stage of hypertension in any arteriolar order. The density of small arterioles (3rd-5th orders) was reduced by 20% in hypertensive rats at 8 wk but was unchanged at the other time periods. These arteriolar alterations, especially the absence of structural reductions in diameter, are attenuated compared with those observed in one-kidney, one-clip hypertension and suggest that most of the arteriolar alterations that occur in renal hypertension are pressure or flow dependent.

Leukotriene B4 promotes reactive oxidant generation and leukocyte adherence during acute hypoxia

2001 ◽  
Vol 91 (3) ◽  
pp. 1160-1167 ◽  
Author(s):  
Dawn R. S. Steiner ◽  
Norberto C. Gonzalez ◽  
John G. Wood
Keyword(s):  
Acute Hypoxia ◽  
Leukotriene B4 ◽  
Ros Generation ◽  
Leukocyte Adherence ◽  
Systemic Hypoxia ◽  
Microvascular Alterations ◽  
Reactive Oxidant ◽  
Underlying Mechanisms ◽  
Mesenteric Microcirculation

Acute systemic hypoxia produces rapid leukocyte adherence in the rat mesenteric microcirculation, although the underlying mechanisms are not fully known. Hypoxia is known to increase reactive oxygen species (ROS) generation, which could result in formation of the lipid inflammatory mediator leukotriene B4 (LTB4). The goal of this study was to examine the role of LTB4 in hypoxia-induced microvascular alterations. Using intravital microscopy, we determined the effect of the LTB4 antagonist, LTB4-dimethyl amide (LTB4-DMA), on ROS generation and leukocyte adherence in mesenteric venules during hypoxia. Exogenous LTB4 increased ROS generation to 144 ± 8% compared with control values and also promoted leukocyte adherence. These responses to LTB4 were blocked by pretreating the mesentery with LTB4-DMA. Leukopenia did not significantly attenuate the LTB4-induced increase in ROS generation (142 ± 12.1%). LTB4-DMA substantially, though not completely, reduced hypoxia-induced ROS generation from 66 ± 18% to 11 ± 4% above control values. Hypoxia-induced leukocyte adherence was significantly attenuated by LTB4-DMA. Our results support a role for LTB4in the mechanism of hypoxia-induced ROS generation and leukocyte adherence in the rat mesenteric microcirculation.

Late-onset renal hypertension in old rats alters myocardial microvessels

1990 ◽  
Vol 259 (6) ◽  
pp. H1681-H1687 ◽  
Author(s):  
R. J. Tomanek ◽  
M. R. Aydelotte ◽  
C. A. Butters
Keyword(s):  
Late Onset ◽  
Renal Hypertension ◽  
Age Groups ◽  
Left Ventricular ◽  
Numerical Density ◽  
Middle Aged ◽  
Absolute Increase ◽  
The Mean ◽  
Microvascular Alterations ◽  
O2 Supply

We tested the hypothesis that late-onset hypertension in middle-aged (15 mo) and senescent (24 mo) rats would adversely affect the coronary microvasculature. Morphometric analyses were performed on coronary capillaries and arterioles from rats with one-kidney, figure-8 renal wrap hypertension of 3-mo duration. Compared with control rats, wall-to-lumen ratios of arterioles with lumen diameters less than 25 microns were higher in the two hypertensive groups by approximately 30%; larger arterioles did not show consistent intergroup differences. A comparison of the two control groups revealed that wall-to-lumen ratio of arterioles with lumen diameters less than 50 microns tended to be greater in the senescent rats. Capillary numerical density was markedly reduced in the hypertensive animals of both age groups and caused an increase in the mean Krough cylinder radius and in the mean capillary domain. The latter increased by 28-63%; the largest increment occurred in the endomyocardium of the senescent group. A trend toward increased heterogeneity of capillary spacing was also noted in the hypertensive rats. The observed microvascular alterations occurred in the absence of an absolute increase in left ventricular mass but in the presence of cardiocyte hypertrophy. Thus the decrements in capillary numerical density are not only due to inadequate growth but reflect an absolute reduction in the number of these vessels associated with cardiocyte loss. It is concluded that late-onset hypertension in middle-aged and senescent rats is characterized by left ventricular wall remodeling that includes microvascular alterations that would be expected to limit maximal myocardial flow and O2 supply to the cardiocyte.

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