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.
Figure 6.1 The effects of arterial partial pressure of O2 and CO2, and perfusion pressure on cerebral blood flow.
E Cerebral perfusion pressure (CPP)
Intracranial pressure (ICP) is maintained at approximately 2 mmHg in conscious healthy horses, even when the head is lowered below heart level.
Normal neonatal foals in the first 24 hours after birth have ICP between 2 and 15 mmHg and a CPP of in the range 50–109 mmHg.
Mean (SD) values for ICP in adult standing horses are 2 (4) mmHg and for CPP are 102 (26) mm Hg.
Cerebral perfusion pressure is the difference between systemic mean arterial blood pressure and ICP, and should be at least 60 mmHg.
When CPP is below this value or cardiac output decreases to less than half‐normal values, cerebral circulation becomes insufficient.
In isoflurane‐anesthetized horses maintained at 1.2 MAC, ICP increases and is higher in dorsal than in lateral and sternal recumbency (34 vs 24 vs 19 mmHg, respectively). Head down position for dorsal and sternal recumbency increases ICP further. Because MAP is higher (105 mmHg) in sternal recumbency, CPP is higher (71 mmHg for sternal with head up and 87 mmHg for sternal with head down); intermediate for dorsal recumbency (MAP of 85 mmHg for head level with the thorax and CPP of 51 mmHg; MAP of 76 mmHg for head down and CPP of 55 mmHg); and lower for lateral recumbency (MAP of 72 mmHg and CPP of 48 mmHg).
Increasing end‐tidal concentrations of the inhalational anesthetic causes significant dose‐dependent decreases in MAP and CPP, but no change in ICP.
Mechanical ventilation causes a significant decrease in MAP and ICP but no change in CPP.
F Cerebrospinal fluid (CSF)
CSF is continuously formed by the choroid plexuses in the lateral and third ventricles and has a specific gravity of 1.002–1.009. The fluid passes into the fourth ventricle, and then into the subarachnoid
