YR1 Lecture 1H - Balancing Heat Gain and Volume Loss 2019 PDF

Balancing heat gain and volume loss: Dr David A Mahns Director of Research Engagement School of Medicine Western Sydney University [email protected] Balancing heat gain & volume loss: Appreciate that control systems operate in dynamic environments in which there is transfer of substances...

Balancing heat gain and volume loss: Dr David A Mahns Director of Research Engagement School of Medicine Western Sydney University [email protected] Balancing heat gain & volume loss: Appreciate that control systems operate in dynamic environments in which there is transfer of substances (e.g. water) or energy (e.g. temperature) between the body and the outside world or between defined zones or compartments within the body Describe the maintenance of body temperature and the control of body fluid balances in the face of high temperatures and lack of fluid intake. Describe how the body detects and responds to changes in core or environmental temperature (assume set-point remains normal) Thermo regulatory feedback systems 1. A hypothalamic control centre 2. Thermal sensors i) ii) nerve endings that are distributed over the entire skin surface PERIPHERAL high concentration in the preoptic anterior hypothalamus; CENTRAL 3. Efferent nerve fibres that are principally part of the autonomic nervous system 4. Thermal effectors that control 1. heat transfer between the body and environment (Blood vessels, sweat glands) 2. the body's rate of heat production i) Endocrine:T3/T4; Adrenaline. ii) Functional / Behavioural Shivering Thermo regulatory feedback systems 1. A hypothalamic control centre 2. Thermal sensors – Peripheral detection of Heat Loss i) nerve endings that are distributed over the entire skin surface ii) high concentration in the preoptic anterior hypothalamus; Skin thermo receptors provide hypothalamic thermoregulatory centre with information about ambient temperature early-warning system in rapidly changing ambient temperature.  cooling Your Help Required [email protected] Central detection of Heat Gain 1. A hypothalamic control centre 2. Thermal sensors i) nerve endings that are distributed over the entire skin surface ii) high concentration in the preoptic anterior hypothalamus; Central Detection of Heat Gain 1. A hypothalamic control centre Information about ambient (Skin) temperature  Anticipatory reflexes that attempt to stabilise heat loss / gain prior to changes in core temperature Responses to changes in core (i.e., hypothalamic) temperature  –ve negative feedback  attempting to restore the core temperature to its regulated level. Set-point temperature: Where??? Infections ↑ prostaglandin E2  ↑central set point  FEVER Thermo regulatory feedback systems 1. A hypothalamic control centre 2. Thermal sensors 3. Efferent nerve fibres that are principally part of the autonomic nervous system 4. Thermal effectors that control 1. heat transfer between the body and environment (Blood vessels, sweat glands) 2. the body's rate of heat production i) Endocrine:T3/T4; Adrenaline. Functional: shivering ii) Functional / Behavioural Shivering Central detection of Heat Gain 1. 2. A hypothalamic control centre Thermal sensors i) nerve endings that are distributed over the entire skin surface i) high concentration in the preoptic anterior hypothalamus; ~ 10% of hypothalamic neurons co-vary their response level 2°C to 4°C about the mean. Hypothalamic Warmth receptors >> cold receptors especially important during exercise heat production >> dissipation rates  Marked & rapid changes in core temperature. Output: Autonomic NS Sympathetic Nervous system Thermo regulatory feedback systems 1. A hypothalamic control centre 2. Thermal sensors 3. Efferent nerve fibres that are principally part of the autonomic nervous system 4. Thermal effectors that control 1. 2. heat transfer between the body and environment (Blood vessels , sweat glands) the body's rate of heat production i) Endocrine:T3/T4; Adrenaline. Functional: shivering ii) Functional / Behavioural Shivering AVA Arterio-venous anastomoses prominent in apical regions of skin eg nose, lips, ears hands, and feet - Low ambient temperature  vasoconstriction of dermal blood flow  pallor  Flow via AVA Rising core temperature  Flow via dermal blood flow flow via AVA  Blood in capacitance (blood volume) in veins (venous distension) of skin sweating d Sweat Glands are innervated by Sympathetic (Cholinergic) nerves that release Ach. Ach release   Sweat formation  Blood Flow Blood Flow mediated by  i. Ach mediated vasodilatation (endothelial cell dependent) ii. secretion (within sweat) of enzymes that lead to the local formation of vasoactive molecules. Eg bradykinin  know vasodilator Balancing Heat Gain and Volume Loss Consequences NET ↓ Circulating volume At 40% VO2 max  ↓500ml plasma  Exercise  heat production   Increased skin/ muscle blood flow Increased sweat production  total-body water by evaporation of perspiration. ~ 2 L/hour in a hot environment or 5% H2O / hour Losing > 3% of body weight  clinical dehydration associated signs: lightheadedness and disorientation Detecting and Responding to Volume loss Osmoreceptors: sense ∆ plasma osmolality respond to the cell shrinkage ↑ secretion of AVP ↑ trigger thirst Mechanism: Cell Shrinkage  Activation of mechanosensitive cation (Na+ Ca2+) channels  membrane depolarization  ↑ frequency of action potentials.  Propagate (along axons) to Post. Pit.  Vesicular release of AVP Arginine Vasopressin Output  Endocrine Response Vasopressing (anti diuretic Hormone) organum vasculosum of the lamina Terminalis (OVLT) subfornical organ (SFO) Detecting and responding to Volume loss Hyperosmolality: ↑ AVP  instructs kidney to retain H20 Renal Response ↑ Vol Cut Post. Pit Preserved Peripheral Response Abolished central Response Mimicked by AVP Injection Threshold AVP release ~ 280 mOsm  Basal AVP release Hyperosmolality: ↑ AVP  instructs kidney to retain H20 Hypo –osmolar Hyper – osmolar Large Changes in circulating volume are required to directly change AVP release -↓ circulating volume will potentiate the response to Hyperosmolality by -↓ threshold & ↑ sensitivity (slope) AVP Release – left shift - e.g. hypovolemic / hemorrhagic shock ↑ circulating volume will attenuate the response to Hyperosmolality by - ↑ threshold & ↓ sensitivity (slope) AVP Release – right shift ADH – ↑ permeability of Collecting Ducts - by inserting water channels (aquaporins) - Always H2O impermeable Always highly H2O permeable Only H2O permeable if ADH present Renin-Angiotensin system · AVP ↓ Renal (Granular cells of JGA) ↓ Renin ↓ Angiotensinogen  Angiotensin II Stimulates OVLT & SFO to release AVP. ↑ vasoconstriction ↓ H2O excretion Renin-Angiotenin e A Linev & - This occure the a pre-rele ↓ ANGIOTENSINOGEN / action of ↑ through " RENIN" ↑ ↓ - converted through - the moning they When rephrons KIDNEY ↳ ↓ produces = Aldosterous system petough Released due to volume ↓ fluid enzyme te released - ~ This Due to called happens ↓. 9 i ~ converting angiotensiengme n Angiotenin I Angiotenin (ANGI) ~ ↑ Act Blood cells meet - "ALDOSTERONE ACE enzyme cause the to on repre the rac alomerula STEROID HORMONE , - ·. ACE enryme an artul(e) a · E (RAAS) Rendin aquaponie Adrena - tubule grand nimpatieenana - ter Retention ↓ Ifme - wate the bodyretain a Other simulants of AVP release ↓ circulating volume ↓ low arterial pressure AVP secretion varies inversely with left-atrial pressure ~ measure / indicator of circulating volume. Nausea , Pain (muscle fatigue, accumulation of metabolites) Summary What Is Sensed? REGULATION OF ECF VOLUME REGULATION OF OSMOLALITY Effective Circulating Volume Plasma Osmolality Sensors Carotid sinus, aortic arch, renal afferent arteriole, atria Hypothalamic osmoreceptors Efferent Pathways Hypothamic – pituitary –Adrenal axis Renin-angiotensin-aldosterone axis, sympathetic nervous system, AVP, ANP AVP Thirst Effector Short term: Heart, blood vessels Long term: Kidney Kidney Brain: drinking behavior What Is Affected? Short term: Blood pressure Long term: Na+ excretion Renal water excretion Water intake ANP, atrial natriuretic peptide; AVP, arginine vasopressin; ECF, extracellular fluid. Fluid Replacement When salt is given with H20 plasma [Na+] remains elevated. In such conditions, the salt-dependent thirst drive is maintained and the stimulation of urine production is delayed, leading to a more complete restoration of body water content. A better recovery of body fluid status provides a better ability to regulate body temperature, particularly in conditions of thermal stress.