Comprehensive Physiology Wiley Online Library

Cardiovascular Adjustments to Heat Stress

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Cutaneous Vascular Responses to Heat Stress
1.1 Microvascular Anatomy
1.2 Efferent Neural Control of Skin Blood Flow
1.3 Local Thermal Control of Cutaneous Blood Vessels
2 Hemodynamic Responses to Heat Stress
2.1 Cardiac Output during Heat Stress
2.2 Cardiovascular Pressures
3 Regional Circulatory Responses to Heat Stress
3.1 Splanchnic Circulation
3.2 Renal Circulation
3.3 Skeletal Muscle Circulation
3.4 Circulation to Brain and Spinal Cord
3.5 Coronary Circulation
4 Modifiers of Control by Internal Temperature
4.1 Thermoregulatory Modifications
4.2 Nonthermoregulatory Modifications
5 Conclusion
Figure 1. Figure 1.

Effect of cutaneous nerve anesthesia on forearm blood flow response to indirect heating. Responses in anesthetized arm are denoted by A, those in control arm by C. Nerve block caused elevation in forearm blood flow prior to body heating (vasoconstrictor abolition in skin and muscle) but significantly reduced reflex vasodilator response to heating, indicating that active vasodilator system was blocked. After Edholm et al. 48.

Figure 2. Figure 2.

Cutaneous vascular responses to cold stress (upper panel) and heat stress (lower panel) from one area of skin iontophoretically treated with bretylium, which blocks release of norepinephrine from sympathetic vasoconstrictor nerve terminals (filled symbols) and from an adjacent untreated site (open symbols). Skin blood flow was measured by laser‐Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/blood pressure. The antiadrenergic effects of bretylium pretreatment blocked vasoconstrictor responses to cold stress (upper panel) but did not block vasodilator responses to heat stress (lower panel), indicating the presence of a non‐adrenergic vasodilator system 125. From Johnson 107.

Figure 3. Figure 3.

Three models for the relationship of active cutaneous vasodilation to control of sweating. A: Cholinergic control of sweat glands liberates an enzyme, which causes formation of the vasodilator peptide bradykinin 64. B: Vasoactive intestinal polypeptide (VIP) is co‐released with acetylcholine (ACH) from sudomotor nerves with endings on both sweat glands and cutaneous arterioles 101. C: Separate sudomotor and vasodilator nerves share control by central thermoregulatory centers (TRC) but are acted on differentially by nonthermoregulatory reflexes 106,126.

Figure 4. Figure 4.

Overall hemodynamic and regional circulatory adjustments by humans to whole‐body direct heating. Skin temperature (Ts) was held at high temperatures with water‐perfused suits. Blood temperature rose to 39.1°C, while cardiac output rose by an average of 6.6 l/min. The increase in skin blood flow of about 7.8 l/min, indicated by the rise in forearm blood flow (FBF), is met by this increase in cardiac output plus redistribution from splanchnic, renal, and skeletal muscle vasculatures. Arterial blood pressure shows a small fall which tends to recover. Right atrial pressure shows a sustained reduction. Stroke volume and central blood volume are not consistently changed (see text). From Rowell 215, by permission.

Figure 5. Figure 5.

gChange in superior mesenteric (intestinal) vascular resistance with internal temperature (Tc) during whole‐body heating in a representative baboon in unblocked state and during α‐adrenergic receptor blockade. Blockade eliminated vasoconstrictor response to heat stress, indicating its adrenergic nature. Adapted from Proppe 194.

Figure 6. Figure 6.

Average fall in renal blood flow and increase in renal vascular resistance vs. internal temperature (Tc) during whole‐body heating of five baboons on normal‐to‐high salt intake (N‐HSI) and low salt intake (LSI). Arrows indicate preheating control levels. Salt diet played no apparent role in renal vasoconstriction with environmental heating. FU, flow units; RU, resistance units. Adapted from Proppe 198.

Figure 7. Figure 7.

Decrease in renal blood flow (RBF) and increase in renal vascular resistance (RVR) per °C increase in internal temperature (%/ °C) during whole‐body heating of a representative baboon in three states: control (C), angiotensin‐II receptor blockade produced by saralasin (S), and β‐adrenergic receptor blockade produced by propranolol (P). Height of bar graph is average response from individual experiments. Renal vasoconstrictor responses to heat stress were less following S or P, indicating a role for β‐adrenergic stimulation of the renin‐angiotensin system. Adapted from Eisman and Rowell 49.

Figure 8. Figure 8.

Interrelationship of control of skin blood flow (SKBF) by internal (Ti) and skin (Tsk) temperatures. Elevation of skin temperature at normal body temperatures (A to A') will have little effect, whereas elevation of skin temperature at elevated internal temperatures (B to B') will have a marked effect on SKBF. See Johnson and Park 113. From Johnson 108, by permission.

Figure 9. Figure 9.

Increase in forearm blood flow (B.F.) with increase in esophageal temperature in one subject during exercise in warm environment in three different states: euhydrated (control), dehydrated by fluid restriction and exercise in heat (thermal dehydration), and dehydrated plus saline infusion (infusion). Thermal dehydration shifts the B.F.–esophageal temperature relationship rightward, an effect not totally reversed by saline infusion following dehydration. From Fortney et al. 61, by permission.

Figure 10. Figure 10.

Mean iliac (leg) blood flow, arterial blood pressure, and iliac vascular conductance vs. Tc before (leftmost data point of each curve) and during whole‐body heating of six baboons in euhydrated, dehydrated (65–69 h of fluid deprivation), and diuretic [furosemide (Lasix)]‐treated states. *Indicates that values in dehydrated and Lasix‐treated states are not statistically different from each other. From Proppe 199, by permission.



Figure 1.

Effect of cutaneous nerve anesthesia on forearm blood flow response to indirect heating. Responses in anesthetized arm are denoted by A, those in control arm by C. Nerve block caused elevation in forearm blood flow prior to body heating (vasoconstrictor abolition in skin and muscle) but significantly reduced reflex vasodilator response to heating, indicating that active vasodilator system was blocked. After Edholm et al. 48.



Figure 2.

Cutaneous vascular responses to cold stress (upper panel) and heat stress (lower panel) from one area of skin iontophoretically treated with bretylium, which blocks release of norepinephrine from sympathetic vasoconstrictor nerve terminals (filled symbols) and from an adjacent untreated site (open symbols). Skin blood flow was measured by laser‐Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/blood pressure. The antiadrenergic effects of bretylium pretreatment blocked vasoconstrictor responses to cold stress (upper panel) but did not block vasodilator responses to heat stress (lower panel), indicating the presence of a non‐adrenergic vasodilator system 125. From Johnson 107.



Figure 3.

Three models for the relationship of active cutaneous vasodilation to control of sweating. A: Cholinergic control of sweat glands liberates an enzyme, which causes formation of the vasodilator peptide bradykinin 64. B: Vasoactive intestinal polypeptide (VIP) is co‐released with acetylcholine (ACH) from sudomotor nerves with endings on both sweat glands and cutaneous arterioles 101. C: Separate sudomotor and vasodilator nerves share control by central thermoregulatory centers (TRC) but are acted on differentially by nonthermoregulatory reflexes 106,126.



Figure 4.

Overall hemodynamic and regional circulatory adjustments by humans to whole‐body direct heating. Skin temperature (Ts) was held at high temperatures with water‐perfused suits. Blood temperature rose to 39.1°C, while cardiac output rose by an average of 6.6 l/min. The increase in skin blood flow of about 7.8 l/min, indicated by the rise in forearm blood flow (FBF), is met by this increase in cardiac output plus redistribution from splanchnic, renal, and skeletal muscle vasculatures. Arterial blood pressure shows a small fall which tends to recover. Right atrial pressure shows a sustained reduction. Stroke volume and central blood volume are not consistently changed (see text). From Rowell 215, by permission.



Figure 5.

gChange in superior mesenteric (intestinal) vascular resistance with internal temperature (Tc) during whole‐body heating in a representative baboon in unblocked state and during α‐adrenergic receptor blockade. Blockade eliminated vasoconstrictor response to heat stress, indicating its adrenergic nature. Adapted from Proppe 194.



Figure 6.

Average fall in renal blood flow and increase in renal vascular resistance vs. internal temperature (Tc) during whole‐body heating of five baboons on normal‐to‐high salt intake (N‐HSI) and low salt intake (LSI). Arrows indicate preheating control levels. Salt diet played no apparent role in renal vasoconstriction with environmental heating. FU, flow units; RU, resistance units. Adapted from Proppe 198.



Figure 7.

Decrease in renal blood flow (RBF) and increase in renal vascular resistance (RVR) per °C increase in internal temperature (%/ °C) during whole‐body heating of a representative baboon in three states: control (C), angiotensin‐II receptor blockade produced by saralasin (S), and β‐adrenergic receptor blockade produced by propranolol (P). Height of bar graph is average response from individual experiments. Renal vasoconstrictor responses to heat stress were less following S or P, indicating a role for β‐adrenergic stimulation of the renin‐angiotensin system. Adapted from Eisman and Rowell 49.



Figure 8.

Interrelationship of control of skin blood flow (SKBF) by internal (Ti) and skin (Tsk) temperatures. Elevation of skin temperature at normal body temperatures (A to A') will have little effect, whereas elevation of skin temperature at elevated internal temperatures (B to B') will have a marked effect on SKBF. See Johnson and Park 113. From Johnson 108, by permission.



Figure 9.

Increase in forearm blood flow (B.F.) with increase in esophageal temperature in one subject during exercise in warm environment in three different states: euhydrated (control), dehydrated by fluid restriction and exercise in heat (thermal dehydration), and dehydrated plus saline infusion (infusion). Thermal dehydration shifts the B.F.–esophageal temperature relationship rightward, an effect not totally reversed by saline infusion following dehydration. From Fortney et al. 61, by permission.



Figure 10.

Mean iliac (leg) blood flow, arterial blood pressure, and iliac vascular conductance vs. Tc before (leftmost data point of each curve) and during whole‐body heating of six baboons in euhydrated, dehydrated (65–69 h of fluid deprivation), and diuretic [furosemide (Lasix)]‐treated states. *Indicates that values in dehydrated and Lasix‐treated states are not statistically different from each other. From Proppe 199, by permission.

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John M. Johnson, Duane W. Proppe. Cardiovascular Adjustments to Heat Stress. Compr Physiol 2011, Supplement 14: Handbook of Physiology, Environmental Physiology: 215-243. First published in print 1996. doi: 10.1002/cphy.cp040111