Reflex responsiveness

Cough is an essential protective reflex response to irritating stimuli in the respiratory tract. It involves the sudden, usually involuntary, expulsion of air from... 

Emesis is the forcefiil involuntary expulsion of the stomach contents through the mouth. It is a reflex response that may be initiated by a number of stimuli. 

Processes sensory input from the skin, joints, and muscles of the trunk and limbs and initiates reflex responses to this input... 

Reflexes may be classified in several ways. They may be named according to the effector tissues that carry out the reflex response ... 

A reflex response requires an intact neural pathway between the stimulated area and the responding muscle. This pathway is referred to as a reflex arc and includes the following components (see Figure 7.3) ... 

A reflex is initiated by stimulation of a sensory receptor located at the peripheral ending of an afferent or first-order sensory neuron. This afferent neuron transmits impulses to the spinal cord. Within the gray matter of the spinal cord, the afferent neuron synapses with other neurons. As such, the spinal cord serves as an integrating center for the sensory input. The afferent neuron must ultimately synapse with an efferent or motor neuron. When the afferent neuron synapses directly with the motor neuron, it forms a monosynaptic reflex. An example of this type of reflex is the stretch reflex. When the afferent neuron synapses with an intemeuron that then synapses with the motor neuron, it forms a polysynaptic reflex, e.g., the withdrawal reflex. Most reflexes are polysynaptic. The motor neuron then exits the spinal cord to innervate an effector tissue, which carries out the reflex response. 

Loss of plasma volume leads to a decrease in MAP. Baroreceptors located in the aortic and carotid sinuses detect this fall in MAP and elicit reflex responses that include an increase in the overall activity of the sympathetic nervous system. Sympathetic stimulation of the heart and blood vessels leads to an increase in cardiac output (CO) and increased total peripheral resistance (TPR). These adjustments, which increase MAP, are responsible for the short-term regulation of blood pressure. Although increases in CO and TPR are effective in temporary maintenance of MAP and blood flow to the vital organs, these activities cannot persist indefinitely. Ultimately, plasma volume must be returned to normal (see Table 19.1). 

Smatresk, N.J. 1986. Ventilatory and cardiac reflex responses to hypoxia and NaCN in Lepisosteus osseus, an air-breathing fish. Physiol. Zool. 59 385-397. 

Berge, O. G. (1982) Effects of 5-HT receptor agonists and antagonists on a reflex response to radiant heat in normal and spinally transected rats. Pain, 13 253-266. 

Many other changes make older adults more vulnerable regarding cardiovascular drugs. There is a decrease in baroreceptor reflex response. This may explain the increased sensitivity to nitrates (Marchionni et al. 1990). With age there is a loss of blood vessel distensibility and enhanced intimal thickness. This can partly explain the increase of systolic blood pressure. Aging is also associated with a reduction in baroreflex-mediated heart rate response to hypotensive stimuli (Verhaeverbeke and Mets 1997, Lakatta and Levy 2003). 

Upper respiratory tract irritation can occur from inhalation of a medicinal gas, vapor, or aerosol. For assessing the potential of an inhalant to cause URT irritation, the mouse body plethysmographic technique (Alarie, 1966, 1981a, b) has proven to be extremely usefid. This technique operates on the principle that respiratory irritants stimulate the sensory nerve endings located at the surface of the respiratory tract from the nose to the alveolar region. The nerve endings in turn stimulate a variety of reflex responses (Alarie, 1973 Widdicombe, 1974) that result in characteristic changes in inspiratory and expiratory patterns and, most prominently, depression of respiratory rate. Both the potency of irritation and the concentration of... 

While irritancy resulting from the above reflex reaction is one cause of altered respiratory parameters during exposure, there are many others. These include other types of reflex response, such as bronchoconstriction, the narcotic effects of many solvents, the development of toxic signs as exposure progresses, or simply a voluntary reduction in respiratory rate by the test animal due to the unpleasant nature of the inhaled atmosphere. The extent to which these affect breathing patterns and hence inhaled dose can only be assessed by actual measurement. 

General anesthesia is a state of drug-induced reversible inhibition of central nervous function, during which surgical procedures can be carried out in the absence of consciousness, responsiveness to pain, defensive or involuntary movements, and significant autonomic reflex responses (A). 

The ICH guideline lists assessment of the effects of the test compound on motor activity, behavioural changes, co-ordination and sensory/motor reflex responses. A so-called functional observation battery or Irwin s battery will cover these parameters. Effects on body temperature should also be measured. 

The acute effects of depressants can include euphoria, anxiety reduction, anticonvulsant activity, sedation, ataxia, motor incoordination, impaired judgment, anesthesia, coma, and respiratory depression resulting in death. The benzodiazepines are rarely involved in lethality, but all CNS depressants enhance the effects of other depressant drugs. The physiological effects of high-dose depressants include miosis, shallow respiration, and reduction in reflex responses. 

Figure 2.1 Fear responses involve the activation of many brain areas. The hypothalamus controls physical changes in the body, such as increased blood pressure and dilated pupils. The central gray area causes freezing behavior, the reticular net triggers a reflex response, and norepinephrine increases attention.

Recticular net—A brain stem region that accentuates the reflex response to a sudden loud noise that results in an increased startle reaction. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

The direct slowing of sinoatrial rate and atrioventricular conduction that is produced by muscarinic agonists is often opposed by reflex sympathetic discharge, elicited by the decrease in blood pressure (see Figure 6-7). The resultant sympathetic-parasympathetic interaction is complex because muscarinic modulation of sympathetic influences occurs by inhibition of norepinephrine release and by postjunctional cellular effects. Muscarinic receptors that are present on postganglionic parasympathetic nerve terminals allow neurally released acetylcholine to inhibit its own secretion. The neuronal muscarinic receptors need not be the same subtype as found on effector cells. Therefore, the net effect on heart rate depends on local concentrations of the agonist in the heart and in the vessels and on the level of reflex responsiveness. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Second, we can compare this hypothesis with the well-known fact that body temperature declines at sleep onset but then remains constant in REM despite a complete loss of central thermoregulatory reflex response in that state Because aminergic demodulation characterizes REM, it precludes a rise in body temperature (unless ambient temperature were suddenly to rise). The strong central cholinergic activation of REM may contribute to the loss of thermoregulatory reflex responsiveness in that state. 

However, activation of the central nervous system (CNS) does not equate with EEG arousals or awakenings. CNS activation implies that integrative neurons were activated and sent information to descending pathways, the nucleus tractus solitarius, and sympathetic controlling cells. An ANS modulation is always associated with an efferent response. CNS activation may lead to an arousal, an awakening, or an important ANS activity change, but activation may be limited to a polysynaptic reflex response with ANS change and no EEG arousal (6). 

Douse MA, White DP (1996) Serotonergic effects on hypoglossal neural activity and reflex responses. Brain Res 726 213-222... 

Administer 100 mg 10 mg/kg ketamine xylazine anesthetic solution i.p. (10 ml/kg). Wait until effective, i.e., no reflex response to a toe pinch. 

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