Stress and stressors

Characterize stress

• Stress is any event that provokes increased adrenocorticotropic hormone (ACTH), and threatens homeostasis in the animal.

• Stressors are environmental factors like climate, overcrowding, excitement, pain, etc.

• Stress is the situation arising when an animal relates to situations in certain ways.

• Animals are not disturbed by situations per se but by the ways they appraise and react to situations.

• Animals experience stress when a demand exceeds an animal´s coping abilities, resulting in reactions such as disturbances of behavior that can adversely affect well-being.

 

Positive and negative impacts of stress

Positive impacts of stress:

• Mobilizes activity, attention, determination, purposeful action

• During stress we give high performance, and we experience emotionally strong experiences (climbing and other risky sports)

             → Eustress = positive stress

             → Distress = negative stress

• Adaptation to stressors by both physical and mental training → by repeating a certain activity, the stimulus loses the character of a stressor and becomes a routine (actors, athletes, military exercises, autogenous training)

The negative impact of stress:

• Diseases of civilization or diseases of insufficient adaptation (diseases associated with lack of adaptation to the changes in the environment)

   → Primary arterial hypertension

   → Atherosclerosis

   → Myocardial infarction, stroke, ischemic heart disease

   → Erosions and ulcers of GIT

   → Neuroses

   → Sexual disorders

Characterize stress

• Stress is any event that provokes increased adrenocorticotropic hormone (ACTH), and threatens homeostasis in the animal.

• Stressors are environmental factors like climate, overcrowding, excitement, pain, etc.

• Stress is the situation arising when an animal relates to situations in certain ways.

• Animals are not disturbed by situations per se but by the ways they appraise and react to situations.

• Animals experience stress when a demand exceeds an animal´s coping abilities, resulting in reactions such as disturbances of behavior that can adversely affect well-being.

 

Positive and negative impacts of stress

Positive impacts of stress:

• Mobilizes activity, attention, determination, purposeful action

• During stress we give high performance, and we experience emotionally strong experiences (climbing and other risky sports)

             → Eustress = positive stress

             → Distress = negative stress

• Adaptation to stressors by both physical and mental training → by repeating a certain activity, the stimulus loses the character of a stressor and becomes a routine (actors, athletes, military exercises, autogenous training)

The negative impact of stress:

• Diseases of civilization or diseases of insufficient adaptation (diseases associated with lack of adaptation to the changes in the environment)

   → Primary arterial hypertension

   → Atherosclerosis

   → Myocardial infarction, stroke, ischemic heart disease

   → Erosions and ulcers of GIT

   → Neuroses

   → Sexual disorders

Functions/roles of catecholamines during stress/in GAS

• Stressors stimulate the release of catecholamines (epinephrine and norepinephrine) which force organs to perform high performance under very uneconomically conditions to mobilize resources of animals for prompt and rapid use

Catecholamines effects on cardiovascular system:

→ increased cardiac output

→ vasoconstriction of resistant arterioles and increased blood pressure

→ constriction of capacity veins and increased veinous return

→ Vasoconstriction of vessels on skin and mucus membranes → Increase blood flow to heart, brain, skeletal muscles

→ blood redistribution in skeletal muscles and vasodilation of coronary arteries and arterioles

Catecholamines effect on metabolism:

• Epinephrine:

  → reacts with beta-sympathetic receptors in the liver → activity of phosphorylase B → increased glycogenolysis in liver → hyperglycemia →  increased glucose → source of energy for CNS

• Epinephrine and norepinephrine:

  → increase lipoprotein lipase of fat tissue → increased lipolysis and FFA + glycerol from fat tissue → increased FFA → source of energy for myocardium and skeletal muscles

 

Hormonal mechanisms in regulation to stress, what type of hormones

Stressors activate these hormonal mechanisms:

• Hypothalamus activates the Sympathetic-adrenomedullary system (SAM)

  → release catecholamines (epinephrine and norepinephrine)

• Hypothalamic-pituitary-adrenal (HPA) axis:

  → hypothalamus release corticotropin releasing hormone (CRH) to anterior pituitary which then release adrenocorticotropic hormone (ACTH) to adrenal cortex which stimulate release of glucocorticoids (cortisol, corticosterone)

• The renin-angiotensin-aldosterone system (stimulate release of aldosterone)

• The system involving vasopressin (ADH)

• The system involving endogenous opioids (precursors of endorphins)

Explain porcine stress syndrome and explain three examples

Porcine stress syndrome:

• PSS includes various forms of exercise-related myopathies, which are induced by stressors.

• Susceptibility to the PSS: inherited as a single recessive gene with other genes determines the character of muscles and sensitivity to halotane (Hal-gen).

• Stressors impact stress-susceptible pigs

  → leading to intolerance of stress → which elevates catecholamine levels and causes loss of control of skeletal muscle metabolism.

  → increased muscle metabolism, causing anaerobic glycolysis, lactic acid production, and the release of K+ from the cells → leading to hyperkalemia

  → catecholamines induce peripheral vasoconstriction, resulting in hyperthermia

Examples:

• Acute stress-induced heart failure (stressors → stress susceptible pigs → catecholamines → dyspnoe, cyanosis, collapse within 4-6min, rapid tremor of the tail, tachycardia, arrhythmia, increased metabolism in muscles → stiffness, lactic acidosis, muscular rigidity, pale, soft and exudative muscles

• Back muscle necrosis (stressors → german landrace → increased catecholamines → increased metabolism in m.longissimus dorsi → hyperthermia, swelling, pain, increased lactic acid production, and atrophy of affected muscles)

• PSE – pale, soft, and exudative stress syndrome

• DFD – dark, firm, and dry pork syndrome

• Transport death (transport, overcrowding, and hot weather → stressors - stress-susceptible pigs → stress heart failure → sudden death)

• Malignant hyperthermia

General adaptation syndrome (GAS)

GAS is a nonspecific stereotype response induced by stressors. The stages are:

1.        Alarm stage

• Stressors stimulate the peripheral nervous system, which activates the hypothalamus.

• Further, the hypothalamus activates the corticotropin-releasing hormone (CRH) and the sympathetic-adrenomedullary system.

• CRH makes adenohypophysis to release ACTH, which stimulates the release of glucocorticoids (cortisol and corticosterone) from the adrenal cortex.

• The sympathetic-adrenomedullary system releases catecholamines (epinephrine + norepinephrine)

2.        Resistance stage/adaptation

• This is the stage when the body needs to start adapting to the stressors by maintaining a high level of glucocorticoids to keep the energy levels high enough to cope with the stressors.

• The glucocorticoids tell the body to start catabolism of proteins, that in the end increases glycogen storage in the liver.

• Catabolism of protein leads to hyperacidema → free AA → gluconeogenesis → more glycogen in the liver.

• They also have an anti-inflammatory effect that gives resistance to infection and delays healing of injuries.

3.        Exhaustion stage

• Prolonged action of stressors and very intensive stressors will in the end use all the resources in the organism and end with hormonal insufficiency.

 

What is PSE and DFD

DFD: dark firm and dry pork syndrome

• Dark firm and dry pork syndrome

• May occur because of prolonged transport, starvation before slaughter in pig

• DFD is the result of chronic long-term stress before slaughter. Unlike PSE it occurs when the animal´s muscle glycogen stores are depleted due to stress

Mechanism of development of DFD syndrome:

• Stress before slaughter → increase release of catecholamines → increases metabolism in muscle → increase glycogenolysis in muscle → increase lactic acid in muscle.

• Lactic acid is excreted into the circulation before slaughter.

• In the time of slaughter and after slaughter there is a decrease in glycogen concentration in the muscle → decreased lactic acid formation → dark red, sticky meat with firm consistency and with pH higher than 6.2.

PSE: pale, soft and exudative pork syndrome

• Stress-susceptible pigs show worse meat quality after slaughter.

• Occurrence of PSE is influenced by genetic susceptibility to stress, transport stress, and handling before and during slaughter.

• PSE is often caused by acute-term stress right before slaughter, typically due to handling, transport or environmental factors.

Mechanism of development of PSE syndrome:

• Stressors → increased release of catecholamines → increased metabolism in the muscle → increased heat production and glycogenolysis.

• Glycogenolysis in the muscle → increased lactic acid production (pH below 6) → increased osmotic pressure in the muscle → influx of water from EC space → increased intramyofiber water content → sour-smelling meat

• Excessive heat production → hyperthermia (41degrees)

• Low pH and high temperature → muscle protein denaturation → deterioration of the water-binding capacity of the muscle → pale, soft, exudative loose-textured meat.

Consequences of hyperkalemia

• Hyperkalemia are abnormal levels of K+ in the blood

• Potassium is released from damaged muscle cells in PSS, due to increased muscular metabolism leading to metabolic acidosis.

• Consequences are:

→ Muscle weakness or paralysis.

→ It can also lead to bradycardia, causing ventricular fibrillation or cardiac arrest

Explain the role of glucocorticoids in GAS/during stress

• Glucocorticoids (cortisol) aid the animals in adapting to the adverse situation and survive.

• They stimulate:

→ Protein catabolism

→ Liver uptake of AAs → conversion to glucose → gluconeogenesis

→ Inhibit glucose uptake by some cells, except the brain

Glucocorticoids during stress causes:

• decreased permeability of vessels and increased blood coagulation

• decreased migration and phagocytosis of leukocytes,

• decreased release of histamine and serotonin, kinins, prostaglandins

• decreased cell and humoral-mediated immunity

• lysis of lymphocytes in the blood

  → lymphopenia, Increased involution of lymphatic tissue, and depression of antibody-synthesis

Changes in blood during stress caused by glucocorticoids:

• are seen as changes in stress leucogram (lymphopenia, eosinopenia, neutrophilia, monocytosis)

Explain development of malignant hyperthermia

• A drug-induced, often fatal stress syndrome that occurs in susceptible pigs within 3 minutes following inhalation of a mixture of halothane and oxygen or by administration of succinylcholine.

• Susceptible pigs develop limb rigidity and hyperthermia which may be fatal.

Mechanism of development of malignant hyperthermia:

• Stressor (halothane) in stress-susceptible pigs → alfa-adrenergic stimulation → release of catecholamines

  → increased blood pressure, tachycardia, and tachypnoea

  → increased metabolism in muscle → hyperthermia (42-45 degrees)

  → increases glycogenolysis in the liver → hyperglycemia → umulation of lactic acid in muscle → metabolic acidosis, muscle rigidity and injury of cells

  → peripheral vasoconstriction → hyperthermia, decreased O2 delivery to muscle → hypoxia

  → hypoxia → increased lactic acid production → accumulation of lactic acid in muscle → metabolic acidosis, muscle rigidity and injury of cells

  → Injury of cells → releasing K+ from cells → hyperkaliemia → death

  → Injury of cells → releasing creatinine kinase and aldolase from damaged cells → increased enzyme activity in blood

Describe stress leukogram

Effect of glucocorticoids on leukogram:

• Endogenous releasing or exogenous administration of glucocorticoids → affects neutrophils, eosinophils, lymphocytes, and monocytes.

• Glucocorticoids affect neutrophils: increased bone marrow release of neutrophils, and increase blood transient time of neutrophils → neutrophilia

• Glucocorticoids effect on eosinophils: increase migration of eosinophils from circulation, and inhibition of release of eosinophils from bone marrow → eosinopenia

• Glucocorticoids affect on lymphocytes: increase lysis of thymic cortical lymphocytes, and increase migration of lymphocytes from circulation into the tissues → lymphopenia

• Glucocorticoids effect on monocytes: increase mobilization of marginated monocytes within the blood vasculature → monocytosis