Differences in finger skin contact cooling response between an arterial occlusion and a vasodilated condition

2006 ◽  
Vol 100 (5) ◽  
pp. 1596-1601 ◽  
Author(s):  
Ollie Jay ◽  
George Havenith

To assess the presence and magnitude of the effect of skin blood flow on finger skin cooling on contact with cold objects against the background of circulatory disorder risks in occupational exposures, this study investigates the effect of zero vs. close-to-maximal hand blood flow on short-term (≤180 s) skin contact cooling response at a contact pressure that allows capillary perfusion of the distal pulp of the fingertip. Six male volunteers touched a block of aluminium with a finger contact force of 0.5 N at a temperature of −2°C under a vasodilated and an occluded condition. Before both conditions, participants were required to exercise in a hot room for ≥30 min for cutaneous vasodilation to occur (increase in rectal temperature of 1°C). Under the vasodilated condition, forearm blood flow rate rose as high as 16.8 ml·100 ml−1·min−1. Under the occluded condition, the arm was exsanguinated, after which a blood pressure cuff was secured on the wrist inducing arterial occlusion. Contact temperature of the finger pad during the subsequent cold contact exposure was measured. No significant difference was found between the starting skin temperatures for the two blood flow conditions, but a distinct difference in shape of the contact cooling curve was apparent between the two blood flow conditions, with Newtonian cooling observed under the occluded condition, whereas a rewarming of the finger skin toward the end of the exposure occurred for the vasodilated condition. Blood flow was found to significantly increase contact temperature from 40 s onward ( P < 0.01). It is concluded that, at a finger contact force compatible with capillary perfusion of the finger pad (∼0.5 N), circulating blood provides a heat input source that significantly affects finger skin contact cooling during a vasodilated state.

Blood ◽  
2008 ◽  
Vol 111 (3) ◽  
pp. 1295-1298 ◽  
Author(s):  
Yasuaki Shida ◽  
Kenji Nishio ◽  
Mitsuhiko Sugimoto ◽  
Tomohiro Mizuno ◽  
Masaaki Hamada ◽  
...  

Abstract The metalloprotease ADAMTS13 is assumed to regulate the functional levels of von Willebrand factor (VWF) appropriate for normal hemostasis in vivo by reducing VWF multimer size, which directly represents the thrombogenic activity of this factor. Using an in vitro perfusion chamber system, we studied the mechanisms of ADAMTS13 action during platelet thrombus formation on a collagen surface under whole blood flow conditions. Inhibition studies with a function-blocking anti-ADAMTS13 antibody, combined with immunostaining of thrombi with an anti-VWF monoclonal antibody that specifically reflects the VWF-cleaving activity of ADAMTS13, provided visual evidence for a shear rate–dependent action of ADAMTS13 that limits thrombus growth directly at the site of the ongoing thrombus generation process. Our results identify an exquisitely specific regulatory mechanism that prevents arterial occlusion under high shear rate conditions during mural thrombogenesis.


2003 ◽  
Vol 40 (4) ◽  
pp. 345-354 ◽  
Author(s):  
J. H. Boss ◽  
I. Misselevich

Animal models of osteonecrosis of the femoral head are indispensable to the understanding of successful treatment modalities for avascular necrosis of the femoral head in adults and in children with Legg-Calvé-Perthes disease. Many of these models adequately reflect the current “vascular deprivation” theory regarding the etiology of the disease. In addition to spontaneous occurrence, surgical- and corticosteroid-induced models are suitable, common experimental ones. Osteonecrosis of spontaneously hypertensive rats appears to be due to defective bone formation and compression of the arteries entering the femoral head at its lateral facets by daily weight-bearing loads. Successful modeling of surgical-induced femoral capital necrosis can be a challenge in animals with a dual epiphyseal blood supply. High doses of corticosteroids are a pivotal risk factor in the development of osteonecrosis. The pathogenesis of corticosteroid-induced osteonecrosis likely resides in reduced blood flow. Steroids may reduce blood flow by numerous mechanisms, including marrow adipocytic hypertrophy leading to sinusoidal compression, venous stasis and, eventually, obstruction of the arteries, and arterial occlusion by fat emboli and lipid-loaded fibrin-platelet thrombi. Other, less common varieties of osteonecrosis include those secondary to endotoxin-induced disseminated intravascular coagulation, immune reactions, immoderately low or high temperatures, and high-impact-related injuries. Common to these diverse forms of osteonecrosis are fibrin thrombi clogging arterioles and small arteries.


1995 ◽  
Vol 33 (1) ◽  
pp. 87-91 ◽  
Author(s):  
L. -G. Lindberg ◽  
M. Vegfors ◽  
C. Lennmarken ◽  
P. Å. Öberg

2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.


1996 ◽  
Vol 81 (3) ◽  
pp. 1418-1422 ◽  
Author(s):  
D. N. Proctor ◽  
J. R. Halliwill ◽  
P. H. Shen ◽  
N. E. Vlahakis ◽  
M. J. Joyner

Estimates of calf blood flow with venous occlusion plethysmography vary widely between studies, perhaps due to the use of different plethysmographs. Consequently, we compared calf blood flow estimates at rest and during reactive hyperemia in eight healthy subjects (four men and four women) with two commonly used plethysmographs: the mercury-in-silastic (Whitney) strain gauge and Dohn air-filled cuff. To minimize technical variability, flow estimates were compared with a Whitney gauge and a Dohn cuff on opposite calves before and after 10 min of bilateral femoral arterial occlusion. To account for any differences between limbs, a second trial was conducted in which the plethysmographs were switched. Resting flows did not differ between the plethysmographs (P = 0.096), but a trend toward lower values with the Whitney was apparent. Peak flows averaged 37% lower with the Whitney (27.8 +/- 2.8 ml.dl-1.min-1) than with the Dohn plethysmograph (44.4 +/- 2.8 ml.dl-1.min-1; P < 0.05). Peak flow expressed as a multiple above baseline was also lower with the Whitney (10-fold) than with the Dohn plethysmograph (14.5-fold; P = 0.02). Across all flows at rest and during reactive hyperemia, estimates were highly correlated between the plethysmographs in all subjects (r2 = 0.96-0.99). However, the mean slope for the Whitney-Dohn relationship was only 60 +/- 2%, indicating that over a wide range of flows the Whitney gauge estimate was 40% lower than that for the Dohn cuff. These results demonstrate that the same qualitative results can be obtained with either plethysmograph but that absolute flow values will generally be lower with Whitney gauges.


2008 ◽  
Vol 130 (3) ◽  
Author(s):  
O. Ley ◽  
C. Deshpande ◽  
B. Prapamcham ◽  
M. Naghavi

Vascular reactivity (VR) denotes changes in volumetric blood flow in response to arterial occlusion. Current techniques to study VR rely on monitoring blood flow parameters and serve to predict the risk of future cardiovascular complications. Because tissue temperature is directly impacted by blood flow, a simplified thermal model was developed to study the alterations in fingertip temperature during arterial occlusion and subsequent reperfusion (hyperemia). This work shows that fingertip temperature variation during VR test can be used as a cost-effective alternative to blood perfusion monitoring. The model developed introduces a function to approximate the temporal alterations in blood volume during VR tests. Parametric studies are performed to analyze the effects of blood perfusion alterations, as well as any environmental contribution to fingertip temperature. Experiments were performed on eight healthy volunteers to study the thermal effect of 3min of arterial occlusion and subsequent reperfusion (hyperemia). Fingertip temperature and heat flux were measured at the occluded and control fingers, and the finger blood perfusion was determined using venous occlusion plethysmography (VOP). The model was able to phenomenologically reproduce the experimental measurements. Significant variability was observed in the starting fingertip temperature and heat flux measurements among subjects. Difficulty in achieving thermal equilibration was observed, which indicates the important effect of initial temperature and thermal trend (i.e., vasoconstriction, vasodilatation, and oscillations).


2018 ◽  
Vol 373 (1759) ◽  
pp. 20170330 ◽  
Author(s):  
Katherine Courchaine ◽  
Sandra Rugonyi

Blood flow conditions (haemodynamics) are crucial for proper cardiovascular development. Indeed, blood flow induces biomechanical adaptations and mechanotransduction signalling that influence cardiovascular growth and development during embryonic stages and beyond. Altered blood flow conditions are a hallmark of congenital heart disease, and disrupted blood flow at early embryonic stages is known to lead to congenital heart malformations. In spite of this, many of the mechanisms by which blood flow mechanics affect cardiovascular development remain unknown. This is due in part to the challenges involved in quantifying blood flow dynamics and the forces exerted by blood flow on developing cardiovascular tissues. Recent technologies, however, have allowed precise measurement of blood flow parameters and cardiovascular geometry even at early embryonic stages. Combined with computational fluid dynamics techniques, it is possible to quantify haemodynamic parameters and their changes over development, which is a crucial step in the quest for understanding the role of mechanical cues on heart and vascular formation. This study summarizes some fundamental aspects of modelling blood flow dynamics, with a focus on three-dimensional modelling techniques, and discusses relevant studies that are revealing the details of blood flow and their influence on cardiovascular development. This article is part of the Theo Murphy meeting issue ‘Mechanics of development’.


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