Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature ...regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved.
We assessed the conservation priority of 18 freshwater ecoregions in southern South America on the basis of Aegla (genus of freshwater crabs) genetic diversity and distribution. Geographical ...distributions for 66 Aegla species were taken from the literature and plotted against ecoregions and main river basins of southern South America. Species richness and number of threatened and endemic species were calculated for each area. To assess taxonomic and phylogenetic diversity, we generated a molecular phylogeny based on DNA sequences for one nuclear (28S) and 4 mitochondrial (12S, 16S, COI, and COII) genes. All species richness and phylogenetic methods agreed, to a large extent, in their rankings of the importance of conservation areas, as indicated by the Spearman's rank correlation coefficient (p < 0.01); nonetheless, some of the lowest correlations were observed between taxonomic and phylogenetic diversity indices. The 5 ecoregions of the Laguna dos Patos Basin (Eastern Brazil), Central Chile, South Brazilian Coast, Chilean Lakes, and Subtropical Potamic Axis (northern Argentina and southern Uruguay and Paraguay) had the highest biodiversity scores. Conservation of these regions will preserve the largest number of species and the greatest amount of genetic diversity within the South American freshwater Aegla fauna. Biodiversity across rivers and within areas was heterogeneously distributed in the ecoregions of Upper Paraná, Ribeira do Iguape, Upper Uruguay, and South Brazilian Coast (i.e., one river showed significantly more biodiversity than any other river from the same ecoregion), but homogeneously distributed in the other ecoregions. Hence, conservation plans in the former regions will potentially require less effort than plans in the latter regions.
The Frank–Starling ‘law of the heart’ is implicated in certain types of orthostatic intolerance in humans. Environmental conditions have the capacity to modulate orthostatic tolerance, where heat ...stress decreases and cooling increases orthostatic tolerance. The objective of this project was to test the hypothesis that heat stress augments and cooling attenuates orthostatic‐induced decreases in stroke volume (SV) via altering the operating position on a Frank–Starling curve. Pulmonary artery catheters were placed in 11 subjects for measures of pulmonary capillary wedge pressure (PCWP) and SV (thermodilution derived cardiac output/heart rate). Subjects experienced lower‐body negative‐pressure (LBNP) of 0, 15 and 30 mmHg during normothermia, skin‐surface cooling (decrease in mean skin temperature of 4.3 ± 0.4°C (mean ±s.e.m.) via perfusing 16°C water through a tubed‐lined suit), and whole‐body heating (increase in blood temperature of 1.0 ± 0.1°C via perfusing 46°C water through the suit). SV was 123 ± 8, 121 ± 10, 131 ± 7 ml prior to LBNP, during normothermia, skin‐surface cooling, and whole‐body heating, respectfully (P= 0.20). LBNP of 30 mmHg induced greater decreases in SV during heating (−48.7 ± 6.7 ml) compared to normothermia (−33.2 ± 7.4 ml) and to cooling (−10.3 ± 2.9 ml; all P < 0.05). Relating PCWP to SV indicated that cooling values were located on the flatter portion of a Frank–Starling curve because of attenuated decreases in SV per decrease in PCWP. In contrast, heating values were located on the steeper portion of a Frank–Starling curve because of augmented decreases in SV per decrease in PCWP. These data suggest that a Frank–Starling mechanism may contribute to improvements in orthostatic tolerance during cold stress and orthostatic intolerance during heat stress.
Mixed findings regarding the effects of whole-body heat stress on central blood volume have been reported. This study evaluated
the hypothesis that heat stress reduces central blood volume and alters ...blood volume distribution. Ten healthy experimental
and seven healthy time control (i.e. non-heat stressed) subjects participated in this protocol. Changes in regional blood
volume during heat stress and time control were estimated using technetium-99m labelled autologous red blood cells and gamma
camera imaging. Whole-body heating increased internal temperature (> 1.0°C), cutaneous vascular conductance (approximately
fivefold), and heart rate (52 ± 2 to 93 ± 4 beats min â1 ), while reducing central venous pressure (5.5 ± 07 to 0.2 ± 0.6 mmHg) accompanied by minor decreases in mean arterial pressure
(all P < 0.05). The heat stress reduced the blood volume of the heart (18 ± 2%), heart plus central vasculature (17 ± 2%), thorax
(14 ± 2%), inferior vena cava (23 ± 2%) and liver (23 ± 2%) (all P ⤠0.005 relative to time control subjects). Radionuclide multiple-gated acquisition assessment revealed that heat stress
did not significantly change left ventricular end-diastolic volume, while ventricular end-systolic volume was reduced by 24
± 6% of pre-heat stress levels ( P < 0.001 relative to time control subjects). Thus, heat stress increased left ventricular ejection fraction from 60 ± 1% to
68 ± 2% ( P = 0.02). We conclude that heat stress shifts blood volume from thoracic and splanchnic regions presumably to aid in heat
dissipation, while simultaneously increasing heart rate and ejection fraction.
As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of ...blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure (N = 41) and head-up tilt (N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg (P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units (P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).
The relationship between muscle sympathetic nerve activity (MSNA) and diastolic blood pressure has been used to describe two
sites for arterial baroreflex control of MSNA. By determining both the ...likelihood of occurrence for sympathetic bursts and
the area of each burst for a given diastolic blood pressure, both a âgatingâ and an âareaâ control site has been described
in normothermic humans. Assessing the effect of heat stress on these mechanisms will improve the understanding of baroreflex
control of arterial blood pressure under this thermal condition. Therefore, the purpose of this study was to test the hypothesis
that heat stress enhances arterial baroreflex control of burst gating and area. In 10 normotensive subjects (age, 32 ± 2 years;
mean ±
s.e.m. ), MSNA (peroneal) was assessed using standard microneurographic techniques. Five minute periods of data were examined during
normothermic and whole-body heating conditions. The burst incidence (i.e. number of sympathetic bursts per 100 cardiac cycles)
and the area of each burst were determined for each cardiac cycle and were placed into 3 mmHg intervals of diastolic blood
pressure. During normotheric conditions, there was a moderate, negative relationship between burst incidence and diastolic
blood pressure (slope =
â2.49 ± 0.38; r 2
= 0.73 ± 0.06; mean ±
s.e.m. ), while area per burst relative to diastolic blood pressure exhibited a less strong relationship (slope =
â1.13 ± 0.46; r 2
= 0.45 ± 0.09). During whole-body heating there was an increase in the slope of the relationship between burst incidence
and diastolic blood pressure (slope =
â4.69 ± 0.44; r 2
= 0.84 ± 0.03) compared to normothermia ( P < 0.05), while the relationship between area per burst and diastolic blood pressure was unchanged (slope =
â0.92 ± 0.29; r 2
= 0.41 ± 0.08) ( P
= 0.50). The primary finding of this investigation is that, at rest, whole-body heating enhanced arterial baroreflex
control of MSNA through increased sensitivity of a âgatingâ mechanism, as indicated by an increase in the slope of the relationship
between burst incidence and diastolic blood pressure. This occurrence is likely to afford protection against potential decreases
in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress.
Central venous pressure (CVP) provides information regarding right ventricular filling pressure, but is often assumed to reflect
left ventricular filling pressure. It remains unknown whether this ...assumption is correct during thermal challenges when CVP
is elevated during skin-surface cooling or reduced during whole-body heating. The primary objective of this study was to test
the hypothesis that changes in CVP reflect those in left ventricular filling pressure, as expressed by pulmonary capillary
wedge pressure (PCWP), during lower-body negative pressure (LBNP) while subjects are normothermic, during skin-surface cooling,
and during whole-body heating. In 11 subjects, skin-surface cooling was imposed by perfusing 16°C water through a water-perfused
suit worn by each subject, while heat stress was imposed by perfusing 47°C water through the suit sufficient to increase internal
temperature 0.95 ± 0.07°C (mean ± s.e.m. ). While normothermic, CVP was 6.3 ± 0.2 mmHg and PCWP was 9.5 ± 0.3 mmHg. These pressures increased during skin-surface cooling
(7.8 ± 0.2 and 11.1 ± 0.3 mmHg, respectively; P < 0.05) and decreased during whole-body heating (3.6 ± 0.1 and 6.5 ± 0.2 mmHg, respectively; P < 0.05). The decrease in CVP with LBNP was correlated with the reduction in PCWP during normothermia ( r = 0.93), skin-surface cooling ( r = 0.91), and whole-body heating ( r = 0.81; all P < 0.001). When these three thermal conditions were combined, the overall r value between CVP and PCWP was 0.92. These data suggest that in the assessed thermal conditions, CVP appropriately tracks
left ventricular filling pressure as indexed by PCWP. The correlation between these values provides confidence for the use
of CVP in studies assessing ventricular preload during thermal and combined thermal and orthostatic perturbations.
Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) ...in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions, L-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38-38.5 degreesC, internal temperature rose from 36.66 +/- 0.10 to 37.34 +/- 0.06 degreesC (P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 +/- 2 to 44 +/- 5% of maximum, but only rose from 13 +/- 2 to 30 +/- 5% of maximum at L-NAME-treated sites (P < 0.05 between sites) during heat stress. L-NAME had no effect on sweat rate (P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.
Prior findings suggest that baroreflexes are capable of modulating skin blood flow, but the effects of baroreceptor loading/unloading
on sweating are less clear. Therefore, this project tested the ...hypothesis that pharmacologically induced alterations in arterial
blood pressure in heated humans would lead to baroreflex-mediated changes in both skin sympathetic nerve activity (SSNA) and
sweat rate.
In seven subjects mean arterial blood pressure was lowered (â8 mmHg) and then raised (â13 mmHg) by bolus injections of sodium
nitroprusside and phenylephrine, respectively. Moreover, in a separate protocol, arterial blood pressure was reduced via steady-state
administration of sodium nitroprusside. In both normothermia and heat-stress conditions the following responses were monitored:
sublingual and mean skin temperatures, heart rate, beat-by-beat blood pressure, skin blood flow (laser-Doppler flowmetry),
local sweat rate and SSNA (microneurography from peroneal nerve).
Whole-body heating increased skin and sublingual temperatures, heart rate, cutaneous blood flow, sweat rate and SSNA, but
did not change arterial blood pressure. Heart rate was significantly elevated (from 74 ± 3 to 92 ± 4 beats min â1 ; P < 0.001) during bolus sodium nitroprusside-induced reductions in blood pressure, and significantly reduced (from 92 ± 4 to
68 ± 4 beats min â1 ; P < 0.001) during bolus phenylephrine-induced elevations in blood pressure, thereby demonstrating normal baroreflex function
in these subjects.
Neither SSNA nor sweat rate was altered by rapid (bolus infusion) or sustained (steady-state infusion) changes in blood pressure
regardless of the thermal condition.
These data suggest that SSNA and sweat rate are not modulated by arterial baroreflexes in normothermic or moderately heated
individuals.
PDF
