Reflex responses, changes caused

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... 

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.

Baroreflexes involving the sympathetic nervous system are responsible for the rapid moment-to-moment regulation of blood pressure. A fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the aortic arch and carotid sinuses) to send fewer impulses to cardiovascular centers in the spinal cord. This prompts a reflex response of increased sympathetic and decreased parasympathetic output to the heart and vasculature, resulting in vasoconstriction and increased cardiac output. These changes result in a compensatory rise in blood pressure (Figure 19.3, and Figure 3.5, see p. 31). 

The most readily observable change in cardiac function is sinus tachycardia, which occurs to a greater or lesser extent in more patients and which correlates weakly or inconsistently with plasma concentrations (4,17,18). The mechanism may be related to both central and peripheral effects on cholinergic and adrenergic systems, but is not simply a reflex response to hypotension (4). The presence of tachycardia can serve as an indirect measure of compliance (4), but it is seldom a cause for concern, except in individuals who anxiously monitor their own physiological functions. 

The opioids are considered relahvely safe from a cardiovascular standpoint. Myocardial depression is minimal. Changes in heart rate are species dependent and usually manifest as a mild decrease in heart rate however, a significant increase in heart rate can be seen in horses, which is consistent with the central excitatory effect that often occurs. Opioids inhibit the baroreceptor reflex response to changes in blood pressure. Certain opioids may cause systemic vasodilatation, decreased peripheral vascular resistance and hypotension secondary to histamine release. Morphine and meperidine (pethidine) are the opioids most likely associated with this effect. This is typically seen after rapid i.v. administration, is dose dependent and does not result from mast cell... 

Figure 1.2 Negative feedback. These types of responses are employed throughout the body in order to maintain homeostasis. In this example, any change in blood pressure, which is monitored within the circulatory system and processed within the CNS, will cause reflex changes in heart rate. The change in heart rate will be in the opposite direction of the change in blood pressure if blood pressure increases, then heart rate decreases if blood pressure decreases, then heart rate increases. In this way, blood pressure is adjusted back to its normal value.

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

A decrease in plasma volume leads to decreased MAP, which is detected by baroreceptors in the carotid sinuses and the arch of the aorta. By way of the vasomotor center, the baroreceptor reflex results in an overall increase in sympathetic nervous activity. This includes stimulation of the heart and vascular smooth muscle, which causes an increase in cardiac output and total peripheral resistance. These changes are responsible for the short-term regulation of blood pressure, which temporarily increases MAP toward normal. 

There is an excessive drop in BP during phase 2 with no associated overshoot in phase 4. There is no bradycardia in phase 4. The response is thought to be caused by a diminished baroreceptor reflex and so the normal compensatory changes in heart rate do not occur. 

All calcium-channel blockers cause vasodilatation, but the cardiac response to the decrease in peripheral resistance is variable. An initial reflex increase in heart rate usually occurs with the dihydropyridines (nifedipine, nicardipine, isradipine, and felodipine) verapamil and diltiazem cause little or no change in heart rate. Verapamil and diltiazem can, however, slow atrioventricular (AV) conduction and should be used with caution in patients also taking a beta-blocker dihydropyridines generally do not affect AV conduction and can be used with a beta-blocker, which decreases reflex tachycardia. All calcium-channel blockers should be used with caution in patients with heart failure. 

As discussed previously (Sec. II.B), bronchial smooth muscle tone is under autonomic control. Cold air and stimulation of receptors by irritants such as cigarette smoke, dust particles, and sulfur dioxide can also cause increased tone and hence bronchoconstriction (229). Bronchomotor tone is also modulated by vagal stretch reflexes and varies inversely with lung volume. Paradoxically, the rise in bronchomotor tone and/or increase in FRC during an attack of asthma may partially reverse the reduction in airway caliber that occurs in this condition, making assessment of response to therapy complex. Similarly, bronchodilators have been shown to cause paradoxical reductions in airflow and desaturation in some infants with history of wheeze, a phenomenon that has been attributed at least partially to changes in airway wall compliance (230-232). 

---