of sodium, leading to a decrease in water reabsorption in the collecting duct.This inhibits reabsorption of Na+, Cl−, K+, and water.
It blocks the ability of the kidney to develop a counter‐current mechanism, limiting the ability to concentrate or dilute urine.
Furosemide induces renal synthesis of prostaglandins, and this increases RBF and leads to a redistribution of renal cortical blood flow.
Furosemide reduces plasma and extracellular fluid volume resulting in decreased blood pressure and cardiac output.
Its use can lead to volume depletion, azotemia, metabolic alkalosis, and electrolyte abnormalities (hyponatremia, hypokalemia).
The loss of H+ and K+ can be attributed in part to activation of the RAAS secondary to a decrease in blood volume and pressure.Aldosterone causes sodium reabsorption and increases K+ and H+ excretion.
Can potentiate the toxicity of aminoglycosides.
D Thiazide diuretics (e.g. hydrochlorothiazide)
This group of diuretics is rarely used in horses.
Thiazides inhibit the Na+/Cl− cotransporter in the DCT, decreasing sodium reabsorption.
However, this transporter is only responsible for reabsorbing about 5% of the filtered sodium.Thus, thiazides are not as effective as loop diuretics in promoting diuresis and natriuresis.However, like loop diuretics, part of the loss of H+ and K+ is due to activation of the RAAS.This can result in K+ loss leading to hypokalemia.
E Potassium sparing diuretics
Do not promote secretion of K+ into urine.
Have a weak diuretic effect because the sites of action are very distal in the nephron.
Aldosterone inhibitors (e.g. spironolactone)
Block effects of aldosterone on aldosterone‐receptors leading to reduced Na+ reabsorption.
This results in more sodium and water passing into the collecting duct and being excreted.
The potassium sparing results from inhibiting sodium reabsorption which causes less K+ and H+ to be exchanged for Na+, and thus not lost in the urine.
Sodium channel blockers (e.g. amiloride)
Also called “Epithelial Sodium Channel Inhibitors”
They directly inhibit sodium channels in distal tubule, reducing Na+ reabsorption.
Have similar effects to spironolactone on H+ and K+.
VI Nonsteroidal anti‐inflammatory drugs
NSAIDs can affect renal function by a variety of mechanisms.
The effects of NSAIDs on the kidney are more profound during episodes of hypotension and hypovolemia.
The renal effects of NSAIDs are discussed in detail in Chapter 16.
Suggested Reading
1 Cook, V. and Blikslager, A. (2015). The use of nonsteroidal anti‐inflammatory drugs in critically ill horses. J. Vet. Crit. Care 25: 76–88.
2 Geor, R. (2007). Acute renal failure in horses. Vet. Clin. North Am. Equine Pract. 23: 577–591.
3 Toribio, R. (2007). Essentials of equine renal and urinary tract physiology. Vet. Clin. North Am. Equine Pract. 23: 533–561.
6 Neurophysiology and Neuroanesthesia
Tanya Duke‐Novakovski
Anesthesia for horses with intracranial pathology is not common, but anesthesia for horses with head trauma might be required.
An understanding of the effects of anesthetic drugs on intracranial pathophysiologic processes is useful in the event that general anesthesia may be required.
Horses with seizures may have to be anesthetized for diagnostic procedures or for control of seizures.
I Neurophysiology
Membrane potentials
Nerve cell membrane potentials are maintained through differential distribution of ions across the membrane.
Depolarization causes movement of sodium and potassium ions, which depolarizes the next segment of the nerve cell. This allows transmission of impulses along nerve axons.
B Synaptic transmission
Junctions between nerve cells allow nerve transmission to take multiple pathways.
Excitatory or inhibitory neurotransmitters are released into the synaptic cleft to activate receptor sites on the post‐synaptic cell.
Excitatory neurotransmitters in the CNS include acetylcholine, norepinephrine, dopamine, 5‐hydroxytrytamine, substance P, glutamate, and other amino acids.
Inhibitory neurotransmitters include glycine, gamma aminobutyric acid (GABA), enkephalins, and endorphins.
Other transmitters include neurotensin, thyroid‐releasing hormone (TRH), gonadotropin‐releasing hormone (GnRH), melanocyte stimulating releasing‐inhibitory factor, adrenocorticotropic hormone (ACTH), and somatostatin.
C Brain metabolism
The brain almost exclusively uses glucose as a source of energy. The brain can also use two ketones, 3‐hydroxybutyrate and acetoacetate.
The selectivity of the blood–brain barrier makes the brain dependent on glucose as an energy substrate, and low concentrations decrease the level of consciousness.
Twenty‐five percent of glucose is used for energy, and the remainder is used for protein synthesis (e.g. glutamic and aspartic acid) which are also used for energy in some cell pathways.
D Cerebral blood flow
Cerebral blood flow increases with cerebral oxygen demand (especially when PaO2 decreases below 50 mmHg) and increases linearly with PaCO2 over the range 20–80 mmHg (see Figure 6.1).
Hypothermia blunts the response to changing PaCO2.
The response to CO2 is maintained during volatile and intravenous anesthesia.
Normal cerebral blood flow in humans is 50 ml/100 g/minute and it has not been quantified in horses.
Flow is greatest in neonates and declines with age, and within gray matter (80 ml/100 g/minute).
Autoregulation maintains constant brain–blood flow over a range of mean systemic blood pressures (60–130 mmHg). Autoregulation is dependent on two processes:Vascular smooth muscle responses which occur over 30–40 seconds.Neural mediated vasodilation through cranial nerve VII.
Arterial hypercapnia or hypoxemia, atropine, and volatile anesthesia administration may attenuate or abolish autoregulation.