Activity of pulmonary surfactant after blocking the associated proteins SP-A and SP-B

1991 ◽  
Vol 71 (2) ◽  
pp. 530-536 ◽  
Author(s):  
T. Kobayashi ◽  
K. Nitta ◽  
R. Takahashi ◽  
K. Kurashima ◽  
B. Robertson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Capillary Flow ◽  
Local Heating ◽  
Doppler Flowmetry ◽  
Cell Velocity ◽  
Associated Proteins ◽  
Flow Through ◽  
Unanesthetized Animals ◽  
Indirect Heating

This study investigated the role of sympathetic withdrawal on blood flow responses in cutaneous arteriovenous anastomoses (AVAs) and capillaries to direct and indirect heat stress. This was achieved by clamping sympathetic activity (SC) to the tail of anesthetized rats so that constrictor tone remained invariant during exposure of either the animal's tail (direct heating) or body (indirect heating) to a 35 degrees C environment. Flow through the AVAs in the tail was evaluated by laser-Doppler flowmetry (LDF), while capillary flow was investigated by videodensitometry measurements of blood cell velocity (CBV) in single capillaries within the subepidermal vascular plexus. Both direct and indirect heating significantly increased LDF and CBV. In comparison to blood flow responses in sham-operated control rats, the SC procedure resulted in significantly lower LDF responses to both direct and indirect heat stress. By contrast, the response of CBV was not significantly affected by SC during either mode of heating. These results indicate that the withdrawal of sympathetic constrictor tone plays a role in the response of cutaneous AVAs, but not precapillary arterioles, to direct as well as indirect heat stress. Additional studies on unanesthetized animals showed that superimposing body heating on a base of local heating elicited a further increase in LDF, suggesting that local heating does not deplete neural mediated dilatory reserve.

Effects of invariant sympathetic activity on cutaneous circulatory responses to heat stress

1991 ◽  
Vol 71 (2) ◽  
pp. 521-529 ◽  
Author(s):  
D. Richardson ◽  
Q. F. Hu ◽  
S. Shepherd
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Sympathetic Activity ◽  
Capillary Flow ◽  
Local Heating ◽  
Doppler Flowmetry ◽  
Cell Velocity ◽  
Flow Through ◽  
Unanesthetized Animals ◽  
Indirect Heating

This study investigated the role of sympathetic withdrawal on blood flow responses in cutaneous arteriovenous anastomoses (AVAs) and capillaries to direct and indirect heat stress. This was achieved by clamping sympathetic activity (SC) to the tail of anesthetized rats so that constrictor tone remained invariant during exposure of either the animal's tail (direct heating) or body (indirect heating) to a 35 degrees C environment. Flow through the AVAs in the tail was evaluated by laser-Doppler flowmetry (LDF), while capillary flow was investigated by videodensitometry measurements of blood cell velocity (CBV) in single capillaries within the subepidermal vascular plexus. Both direct and indirect heating significantly increased LDF and CBV. In comparison to blood flow responses in sham-operated control rats, the SC procedure resulted in significantly lower LDF responses to both direct and indirect heat stress. By contrast, the response of CBV was not significantly affected by SC during either mode of heating. These results indicate that the withdrawal of sympathetic constrictor tone plays a role in the response of cutaneous AVAs, but not precapillary arterioles, to direct as well as indirect heat stress. Additional studies on unanesthetized animals showed that superimposing body heating on a base of local heating elicited a further increase in LDF, suggesting that local heating does not deplete neural mediated dilatory reserve.

scholarly journals Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 111 (3) ◽  
pp. 818-824 ◽  
Author(s):  
Ilkka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Heat Stress ◽  
Local Heating ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow ◽  
Whole Body Heat Stress ◽  
Body Heat ◽  
Indirect Heating

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g−1·min−1 ( P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g−1·min−1 ( P < 0.01). While whole body heat stress increased intestinal temperature by ∼1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g−1·min−1; heat stress: 1.7 ± 0.3 ml·100 g−1·min−1; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g−1·min−1) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.

scholarly journals Minimal role for H1 and H2 histamine receptors in cutaneous thermal hyperemia to local heating in humans

2006 ◽  
Vol 100 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah J. Williams ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Histamine Receptor ◽  
Receptor Activation ◽  
Control Site ◽  
Doppler Flowmetry ◽  
Histamine Receptor Antagonist ◽  
And Control

The precise mechanism(s) underlying the thermal hyperemic response to local heating of human skin are not fully understood. The purpose of this study was to investigate a potential role for H1 and H2 histamine-receptor activation in this response. Two groups of six subjects participated in two separate protocols and were instrumented with three microdialysis fibers on the ventral forearm. In both protocols, sites were randomly assigned to receive one of three treatments. In protocol 1, sites received 1) 500 μM pyrilamine maleate (H1-receptor antagonist), 2) 10 mM l-NAME to inhibit nitric oxide synthase, and 3) 500 μM pyrilamine with 10 mM NG-nitro-l-arginine methyl ester (l-NAME). In protocol 2, sites received 1) 2 mM cimetidine (H2 antagonist), 2) 10 mM l-NAME, and 3) 2 mM cimetidine with 10 mM l-NAME. A fourth site served as a control site (no microdialysis fiber). Skin sites were locally heated from a baseline of 33 to 42°C at a rate of 0.5°C/5 s, and skin blood flow was monitored using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/mean arterial pressure. To normalize skin blood flow to maximal vasodilation, microdialysis sites were perfused with 28 mM sodium nitroprusside, and control sites were heated to 43°C. In both H1 and H2 antagonist studies, no differences in initial peak or secondary plateau phase were observed between control and histamine-receptor antagonist only sites or between l-NAME and l-NAME with histamine receptor antagonist. There were no differences in nadir response between l-NAME and l-NAME with histamine-receptor antagonist. However, the nadir response in H1 antagonist sites was significantly reduced compared with control sites, but there was no effect of H2 antagonist on the nadir response. These data suggest only a modest role for H1-receptor activation in the cutaneous response to local heating as evidenced by a diminished nadir response and no role for H2-receptor activation.

Vital microscopy of islet blood flow: catecholamine effects in normal and ob/ob mice

1987 ◽  
Vol 252 (1) ◽  
pp. E130-E135 ◽  
Author(s):  
P. Rooth ◽  
I. B. Taljedal
Keyword(s):  
Blood Flow ◽  
Capillary Flow ◽  
Inhibitory Influence ◽  
Video Recordings ◽  
Islet Blood Flow ◽  
Visible Effect ◽  
Flow Through ◽  
Vital Microscopy ◽  
Semiquantitative Method ◽  
Normal Controls

The pancreatic microcirculation in noninbred ob/ob mice and normal controls was visualized in a fluorescence microscope and examined for responses to intravenous infusions of epinephrine or norepinephrine. Evaluations of coded video recordings revealed a smooth dose-response relationship and validated a semiquantitative method of analysis. In ob/ob mice the islet microcirculation was markedly and reversibly inhibited by 0.14–4 micrograms of epinephrine X min-1 X kg body wt-1; the flow was almost totally stopped at the highest infusion rates. Capillary flow in the exocrine pancreas appeared unaffected, except for some inhibition at 4.0 micrograms X min-1 X kg-1. Norepinephrine was less potent an inhibitor of islet blood flow. Normal lean mice exhibited minor responses to 1–11.3 micrograms of epinephrine X min-1 X kg-1; in most cases there was no visible effect. It is concluded that there is a selective regulation of blood flow through the endocrine portion of the pancreas and that the islet microcirculation is hypersensitive to catecholamines in noninbred ob/ob mice. A defective inhibitory influence from the brain may play a role in the development of excessive hyperinsulinemia in ob/ob mice.

scholarly journals Endothelial nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo

2008 ◽  
Vol 295 (1) ◽  
pp. H123-H129 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Local Heating ◽  
Ringer Solution ◽  
Whole Body ◽  
Control Mechanisms ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in locally mediated vasodilation induced by increased local skin temperature (Tloc) and in sympathetically mediated vasodilation during whole body heat stress. We hypothesized that endothelial NOS (eNOS) participates in the former, but not the latter, response. We tested this hypothesis by examining the effects of the eNOS antagonist NG-amino-l-arginine (l-NAA) on skin blood flow (SkBF) responses to increased Tloc and whole body heat stress. Microdialysis probes were inserted into forearm skin for drug delivery. One microdialysis site was perfused with l-NAA in Ringer solution and a second site with Ringer solution alone. SkBF [laser-Doppler flowmetry (LDF)] and blood pressure [mean arterial pressure (MAP)] were monitored, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF ÷ MAP). In protocol 1, Tloc was controlled with LDF/local heating units. Tloc initially was held at 34°C and then increased to 41.5°C. In protocol 2, after a normothermic period, whole body heat stress was induced (water-perfused suits). At the end of both protocols, 58 mM sodium nitroprusside was perfused at both microdialysis sites to cause maximal vasodilation for data normalization. In protocol 1, CVC at 34°C Tloc did not differ between l-NAA-treated and untreated sites ( P > 0.05). Local skin warming to 41.5°C Tloc increased CVC at both sites. This response was attenuated at l-NAA-treated sites ( P < 0.05). In protocol 2, during normothermia, CVC did not differ between l-NAA-treated and untreated sites ( P > 0.05). During heat stress, CVC rose to similar levels at l-NAA-treated and untreated sites ( P > 0.05). We conclude that eNOS is predominantly responsible for NO generation in skin during responses to increased Tloc, but not during reflex responses to whole body heat stress.

Effect of functional electrostimulation on impaired skin vasodilator responses to local heating in spinal cord injury

2009 ◽  
Vol 106 (4) ◽  
pp. 1065-1071 ◽  
Author(s):  
Noortje T. L. Van Duijnhoven ◽  
Thomas W. J. Janssen ◽  
Daniel J. Green ◽  
Christopher T. Minson ◽  
Maria T. E. Hopman ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Axon Reflex ◽  
Doppler Flowmetry ◽  
Cord Injury ◽  
Cutaneous Vascular Conductance ◽  
Functional Electrostimulation

Spinal cord injury (SCI) induces vascular adaptations below the level of the lesion, such as impaired cutaneous vasodilation. However, the mechanisms underlying these differences are unclear. The aim of this study is to examine arm and leg cutaneous vascular conductance (CVC) responses to local heating in 17 able-bodied controls (39 ± 13 yr) and 18 SCI subjects (42 ± 8 yr). SCI subjects were counterbalanced for functional electrostimulation (FES) cycling exercise (SCI-EX, n = 9) or control (SCI-C, n = 9) and reanalyzed after 8 wk. Arm and leg skin blood flow were measured by laser-Doppler flowmetry during local heating (42°C), resulting in an axon-reflex mediated first peak, nadir, and a primarily nitric oxide-dependent plateau phase. Data were expressed as a percentage of maximal CVC (44°C). CVC responses to local heating in the paralyzed leg, but also in the forearm of SCI subjects, were lower than in able-bodied controls ( P < 0.05 and 0.01, respectively). The 8-wk intervention did not change forearm and leg CVC responses to local heating in SCI-C and SCI-EX, but increased femoral artery diameter in SCI-EX ( P < 0.05). Interestingly, findings in skin microvessels contrast with conduit arteries, where physical (in)activity contributes to adaptations in SCI. The lower CVC responses in the paralyzed legs might suggest a role for inactivity in SCI, but the presence of impaired CVC responses in the normally active forearm suggests other mechanisms. This is supported by a lack of adaptation in skin microcirculation after FES cycle training. This might relate to the less frequent and smaller magnitude of skin blood flow responses to heat stimuli, compared with controls, than physical inactivity per se.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

2002 ◽  
Vol 93 (4) ◽  
pp. 1215-1221 ◽  
Author(s):  
D. L. Kellogg ◽  
Y. Liu ◽  
K. McAllister ◽  
C. Friel ◽  
P. E. Pérgola
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Ringer Solution ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Hoe 140 ◽  
Control Body ◽  
Cutaneous Vascular Conductance

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites ( P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

Decreased active vasodilator sensitivity in aged skin

1997 ◽  
Vol 272 (4) ◽  
pp. H1609-H1614 ◽  
Author(s):  
W. L. Kenney ◽  
A. L. Morgan ◽  
W. B. Farquhar ◽  
E. M. Brooks ◽  
J. M. Pierzga ◽  
...  
Keyword(s):  
Heat Stress ◽  
Local Heating ◽  
Interactive Effect ◽  
Older Men ◽  
Whole Body ◽  
Age Difference ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Age Related ◽  
The Right

Older men and women respond to local and reflex-mediated heat stress with an attenuated increase in cutaneous vascular conductance (CVC). This study was performed to test the hypothesis that an augmented or sustained noradrenergic vasoconstriction (VC) may play a role in this age-related difference. Fifteen young (22 +/- 1 yr) and 15 older (66 +/- 1 yr) men exercised at 50% peak oxygen uptake in a 36 degrees C environment. Skin perfusion was monitored at two sites on the right forearm by laser-Doppler flowmetry: one site pretreated with bretylium tosylate (BT) to block the local release of norepinephrine and thus VC and an adjacent control site. Blockade of reflex VC was verified during whole body cooling using a water-perfused suit. CVC (perfusion divided by mean arterial pressure) at each site was reported as a percentage of the maximal CVC (%CVCmax) induced at the end of each experiment by prolonged local heating at 42 degrees C. Neither age nor BT affected the %CVCmax (75-86%) attained at high core temperatures. During the early rise phase of CVC, the %CVCmax-change in esophageal temperature (delta T(es)) curve was shifted to the right in the older men (effective delta T(es) associated with 50% CVC response for young, 0.22 +/- 0.04 and 0.39 +/- 0.04 degrees C and for older, 0.73 +/- 0.04 and 0.85 +/- 0.04 degrees C at control and BT sites, respectively). BT had no interactive effect on this age difference, suggesting a lack of involvement of the VC system in the attenuated CVC response of individuals over the age of 60 yr. Additionally, increases in skin vascular conductance were quantitatively compared by measuring increases in total forearm vascular conductance (FVC, restricted to the forearm skin under these conditions). After the initial approximately 0.2 degrees C increase in T(es), FVC was 40-50% lower in the older men (P < 0.01) for the remainder of the exercise. Decreased active vasodilator sensitivity to increasing core temperature, coupled with structural limitations to vasodilation, appears to limit the cutaneous vascular response to exertional heat stress in older subjects.

scholarly journals Skin blood flow measurements during heat stress: technical and analytical considerations

2020 ◽  
Vol 318 (1) ◽  
pp. R57-R69 ◽  
Author(s):  
Georgia K. Chaseling ◽  
Craig G. Crandall ◽  
Daniel Gagnon
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Research Question ◽  
The Body ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Subsequent Increase ◽  
Flow Measurements ◽  
Doppler Flowmetry

During heat stress, the skin vasculature can greatly increase conductance secondary to vasodilation. The subsequent increase in skin blood flow allows for convective heat transfer from the core to the skin and between the skin surface and the surrounding environment. Measurement of skin blood flow, therefore, provides valuable information regarding heat exchange between the body and the environment. In addition, assessment of skin blood flow can be used to study vascular control mechanisms. Most often, skin blood flow is measured by venous occlusion plethysmography, Doppler ultrasound, laser-Doppler flowmetry, and, more recently, optical coherence tomography. However, important delimitations to each of these methods, which may be dependent on the research question, must be considered when responses from these approaches are interpreted. In this brief review, we discuss these methods of skin blood flow measurement and highlight potential sources of error and limitations. We also provide recommendations to guide the interpretation of skin blood flow data.

Sign in / Sign up

Export Citation Format

Share Document