Factors associated with the drug use of fifth through eighth grade students.
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Adolescent↗
Biomedical subjects
L C Weaver
Publications and source records attributed to L C Weaver.
Capsaicin treatment attenuates the reflex excitation of sympathetic activity caused by chemical stimulation of intestinal afferent nerves.
Sympathetic reflexes elicited by stimulation of visceral receptors have been well investigated, but the central neurotransmitters mediating these reflexes are largely unknown. Therefore, experiments were done to evaluate the role of substance P in the central transmission of a sympathoexcitatory reflex elicited by stimulation of intestinal receptors. Activity of mesenteric and renal nerves was recorded electrophysiologically in chloralose/urethane-anesthetized rats. Stimulation of intestinal receptors by serosal application of 0.5-1.0 microgram bradykinin increased mesenteric nerve activity by 100 +/- 21%, renal nerve discharge by 33 +/- 9%, and systemic arterial pressure by 10 mm Hg. Chronic capsaicin treatment (cumulative dose 950 mg/kg) caused a 52% depletion of substance P-like immunoreactivity from dorsal root ganglia and a significant attenuation of these reflexes. Mesenteric nerve activity increased by 48 +/- 6% in the capsaicin-treated rats. Bradykinin did not cause significant changes in renal nerve activity or systemic arterial pressure in these rats. The excitation of mesenteric nerve activity was significantly greater than the increase in renal nerve activity int he untreated and capsaicin-treated rats; capsaicin treatment affected responses of both nerves similarly. Capsaicin treatment did not have generalized effects on sympathetic reflexes, as mesenteric and renal nerve activities were decreased by baroreceptor activation similarly in the untreated and capsaicin-treated rats. These results suggest that the central transmission of the reflex response to intestinal receptor stimulation is mediated in part by substance P or other capsaicin-sensitive peptides.
Animals↗
Rho Chi lecture. Pharmacy in a smaller world.
Health care is a business. Pharmacy is in the health business. The health care delivery system in the U.S. is rapidly becoming a managed system by corporations. Further, these corporations are moving toward international markets where some already have considerable experience. There are many parts of the world not participating in these developments in health care. Some are just off our shores in the Caribbean Basin. A review of activities occurring in recent years by various groups suggests that more could be done. Two modest approaches are presented. Support of the American Association of Colleges of Pharmacy's "Pharmacy School Twinning Project" through which U.S. pharmacy schools would work with pharmacy schools in Central and South America is recommended. Also, national pharmacy associations jointly with pharmaceutical companies would work together using their expertise in continuing pharmacy education to develop new education models for the needy areas of the world.
Delivery of Health Care↗
The effect of earlier or later transition into middle school on students' psychosocial adjustment and drug use.
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Adaptation, Psychological↗
Splenic, renal, and cardiac nerves have unequal dependence upon tonic supraspinal inputs.
Stimulation of visceral receptors can lead to unequal reflex responses in splenic, renal and cardiac sympathetic nerves. Activity of splenic nerves is often more excited or less inhibited than that of cardiac or renal nerves. This study was undertaken to determine potential differences in resting discharge among these 3 nerves. Dependence upon supraspinal drive was evaluated by comparing the relative decrease in activity of these nerves in chloralose-anesthetized cats 30 min to 2 h following high cervical spinal cord transection. After this transection, discharge rates of cardiac and renal nerves were significantly depressed to less than 50% of initial values. In contrast, splenic nerve activity was not significantly affected. To determine if this sustained splenic nerve activity resulted from greater responsiveness to potential external sources of excitation, splenic, renal and cardiac neural responses to factors known to affect sympathetic discharge in spinal animals were compared. Neither increased arterial pressure, decreased arterial pressure, systemic hypercapnia and acidosis, nor thoracolumbar dorsal rhizotomy revealed specific inputs responsible for the preferential maintenance of splenic nerve activity in spinal cats. It was concluded that ongoing activity of splenic nerves is less dependent upon supraspinal sources of excitation than is activity of renal or cardiac nerves. The cause of this difference among these 3 components of sympathetic outflow remains to be determined.
Animals↗
Organization of sympathetic responses to distension of urinary bladder.
Distension of the urinary bladder can cause reflex pressor responses, which appear to be mediated by increased sympathetic activity. However, preganglionic upper thoracic sympathetic activity is excited inconsistently by bladder distension in intact and spinal animals. The objective of this investigation was to determine if any of the postganglionic nerves originating from thoracic and lumbar spinal segments are consistently excited by vesical afferent nerves. Responses of external carotid, renal, and splenic sympathetic nerves to distension of the urinary bladder were evaluated in chloralose-anesthetized cats. In addition, the potential preferential spinal segmental distribution of vesico-sympathetic reflexes was assessed by comparing the magnitudes of external carotid, renal, and splenic nerve responses. Distension of the urinary bladder with 5-35 ml saline initiated vesical contractions to pressures of 45-90 cmH2O and caused inconsistent changes in arterial pressure and activity of renal and splenic sympathetic nerves. External carotid nerves were excited by this stimulus. Vesical distension with 12-50 ml saline caused contractions to vesical pressures of 135-175 cmH2O and produced consistent increases in arterial pressure and activity of all three nerves. Thus activation of vesical afferent nerves by high pressure produced excitation of upper thoracic vasomotor neurons and of two major components of splanchnic and lumbar sympathetic outflow. The magnitudes of external carotid, renal, and splenic sympathetic responses were not different, illustrating that propriospinal circuits thought to mediate vesicosympathetic responses are not organized segmentally.
Afferent Pathways↗
Comparison of the distributions of renal and splenic neurons in sympathetic ganglia.
Postganglionic neurons in different sympathetic ganglia are innervated selectively by preganglionic neurons originating from different segments of the spinal cord. These selective connections between pre- and postganglionic neurons may determine the specificity with which postganglionic nerves participate in differential reflex reactions. Because specificity of renal and splenic nerve responses to stimulation of visceral afferent nerves may depend on the distribution of postganglionic neurons in sympathetic ganglia, retrograde axonal transport of horseradish peroxidase was employed in this study to identify the ganglionic distribution of cell bodies of postganglionic neurons supplying the kidney and spleen in cats. Superior mesenteric, left and right celiac ganglia usually are fused together into a complex ganglion (solar plexus) in the cat. Most labeled cell bodies of renal nerves were clustered in groups within the solar plexus, but some cell bodies of renal neurons were observed in upper lumbar (L1-L3) and lower thoracic (T12-T13) paravertebral sympathetic ganglia. In contrast, 90% of labeled splenic neurons were scattered randomly throughout the left and right celiac poles of the solar plexus. In conclusion, the disparate distribution of renal and splenic neurons in sympathetic ganglia provides an anatomical basis for differential reflex responses in the two populations of nerves.
Animals↗
Central actions of angiotensin II oppose baroreceptor-induced sympathoinhibition.
Angiotensin II causes increased arterial pressure which may be mediated, in part, by effects on central sympathetic neurons or by interference with central or peripheral components of the baroreceptor reflex. This investigation was undertaken to determine actions of angiotensin II on sympathetic splanchnic efferent and carotid sinus afferent activity in chloralose-anesthetized cats. Neural responses during increases in arterial pressure caused by intracarotid or intravenous administration of angiotensin II were compared with responses to equivalent increases in arterial pressure induced by intravenously injected dextran or phenylephrine. Intracarotid injections of angiotensin II caused variable splanchnic sympathetic responses consisting of increased, decreased, or unchanged activity. In contrast, intravenous infusions of dextran or phenylephrine consistently inhibited sympathetic activity. Carotid sinus afferent activity was increased similarly by intracarotid angiotensin II and intravenous dextran or phenylephrine. Sympathetic and baroreceptor afferent responses to intravenously injected angiotensin II were not significantly different from responses to dextran or phenylephrine. These data demonstrate that angiotensin II can act centrally to excite sympathetic outflow or to interfere with inhibitory influences of arterial baroreceptors.
Angiotensin II↗
Differential renal and splenic nerve responses to vagal and spinal afferent inputs.
Specific contributions of the kidney and spleen to cardiovascular homeostasis may be determined partially by differential sympathetic influences on each organ. This investigation was a comparison of renal and splenic sympathetic responses to stimulation of vagally innervated cardiac receptors and receptors of abdominal visceral and muscle spinal afferent nerves. Experiments were performed in anesthetized, sinoaortic-denervated cats in which upper thoracic sympathetic ganglia had been removed. Left atrial injections of veratridine depressed renal and splenic nerve discharges by 68 and 44%, respectively. In contrast, injections of bradykinin into the abdominal aorta caused 18 and 104% excitation of renal and splenic nerves, respectively. Visceral ischemia and mesenteric stretch by snare occlusion of the celiac artery caused 20 and 64% excitation of renal and splenic nerves, respectively. Left atrial injections of bradykinin caused biphasic renal nerve responses (range, 200% excitation to complete inhibition) and 246% excitation of splenic nerves; after vagotomy both renal and splenic nerves were excited (21 and 117%, respectively). In conclusion, sympathetic control of the kidney and spleen can be selective, illustrating significant potential discreteness of sympathetic outflow to the viscera.
Animals↗
Splenic and renal sympathetic responses to stimulation of splenic receptors in cats.
The effect of selective stimulation of splenic receptors on reflex responses of splenic and renal efferent nerves was studied in anesthetized, vagotomized, sinoaortic denervated cats. The following substances were injected into the artery or vein of vascularly isolated spleens: warm physiological saline (congestion), capsaicin (CAPS), bradykinin (BK), and norepinephrine (NE). Splenic congestion increased efferent activity of splenic and renal nerves, splenic venous pressure, systemic arterial pressure, and heart rate. CAPS and BK elicited responses similar to those produced by congestion but caused greater excitation of splenic than renal nerves. Reflex responses were eliminated by section of splenic nerves. Injection of NE increased splenic venous pressure but did not elicit reflex responses. Finally, in contrast to a previous report light- and electron-microscopic examination of splenic nerves revealed myelinated, as well as unmyelinated, fibers. These results have demonstrated that activation of splenic receptors elicits reflex cardiovascular responses and excitation of splenic and renal efferent nerves, contraction of the spleen does not produce reflex responses, the adequate stimulus for reflex responses is stretch of vessels and possibly capsule, and splenic receptors play a role in the reflex control of circulation.
Animals↗
Role of sympathetic nervous system in ischemia-induced reduction of digoxin tolerance in anesthetized cats.
Acute myocardial ischemia reduces tolerance of the heart to arrhythmogenic actions of digitalis glycosides. Because both ischemia and the glycoside produce profound changes in activity of the autonomic nervous system and because sympathetic discharge or catecholamines enhance toxic actions of the cardiac glycosides, the possibility that alterations in digitalis sensitivity of ischemic heart involve changes in sympathetic nerve activity was examined using alpha-chloralose-anesthetized cats. Left anterior descending coronary artery (LAD) was completely occluded by ligation and, 40 min later, a slow i.v. infusion of digoxin was started at a rate of 1 microgram/kg/min. LAD ligation alone did not produce arrhythmias in that condition, but shortened the time to onset of digoxin-induced arrhythmias and thereby reduced the amount of digoxin required to produce the toxic manifestation. Concomitantly, digoxin concentration in plasma and nonischemic areas of the heart were lower in LAD-ligated cats at the onset of arrhythmias than those in sham-operated cats. Myocardial digoxin content in the ischemic area of the LAD-occluded heart was lower than that in nonischemic areas of the same heart. At the onset of digoxin-induced arrhythmias, Na,K-adenosine triphosphatase activity of ischemic myocardium was significantly higher than that in the nonischemic area, reflecting a lower digoxin occupancy of the glycoside binding sites on the sodium pump. Spinal cord (C1) transection or propranolol treatment prolonged the time to arrhythmias in both control and LAD-ligated cats, but failed to abolish the effect of LAD ligation to augment digoxin toxicity. Bilateral vagotomy also did not alter the enhancement of digoxin toxicity caused by ligation of LAD.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Differential sympathetic responses initiated by angiotensin and sodium chloride.
Angiotensin II (ANG II) and NaCl act on central receptors to cause pressor responses that may be mediated in part by the sympathetic nervous system. The inhibitory or excitatory nature of effects on central sympathetic outflow are not well defined. This study was undertaken to evaluate further the potential contribution of the sympathetic nervous system to central actions of angiotensin or hypertonic NaCl. Experiments were performed using anesthetized, sinoaortic denervated, vagotomized cats. Intracarotid injection of NaCl produced increased splenic sympathetic nerve activity and decreased renal sympathetic nerve activity. Intracerebroventricular (icv) administration of NaCl caused slight excitatory responses in splenic nerves and no change in renal nerve activity. Intracarotid injection of ANG II caused significantly greater splenic than renal excitation. Administration of ANG II icv caused excitation of splenic nerve activity and no change in renal nerve activity. These findings illustrate that stimulation of sodium-sensitive and angiotensin-sensitive CNS receptors produces differential responses in sympathetic outflow. These differential sympathetic responses may contribute to the complex cardiovascular responses to increased plasma or brain concentrations of angiotensin or sodium.
Angiotensin II↗
Widespread neural excitation initiated from cardiac spinal afferent nerves.
Reflex effects of cardiac sympathetic afferent nerve excitation on cardiac and renal components of sympathetic outflow have been well investigated, but the extent of these cardiac afferent influences on other sympathetic nerves or on respiratory or cortical neural systems is unknown. Therefore such influences were investigated electrophysiologically in anesthetized, vagotomized, baroreceptor-denervated cats. Stimulation of cardiac sympathetic spinal afferent neurons by the noxious substance bradykinin caused excitation of cardiac, renal, splenic, gastrohepatic, adrenal, and deep peroneal (muscle) vasoconstrictor sympathetic nerves, as well as excitation of phrenic nerves and concomitant desynchronization of the electroencephalogram. Possible supraspinal pathways mediating these responses were investigated. Sympathetic reflexes caused by cardiac afferent stimulation were unchanged after decerebration, thereby demonstrating that supramedullary mediation was not essential to the sympathetic responses. Potential contributions of the medulla to the observed sympathetic or other responses were demonstrated by recording from medullary neurons responsive to electrical and chemical stimulation of the afferent nerves. In summary, noxious stimulation of cardiac sympathetic afferent neurons leads to widespread neural excitation which may contribute to sensory, visceral, and somatic responses caused by cardiac pain or which occur during activated states such as exercise or emotional stress.
Afferent Pathways↗
Multisegmental spinal sympathetic reflexes originating from the heart.
Activation of cardiac sympathetic afferent nerves can initiate excitatory cardiocardiac reflexes through pathways that are exclusively spinal. In addition, stimulation of the same nerves also causes lower thoracic and lumbar sympathetic excitation, but the contribution of spinal pathways to these reflexes is unknown. Therefore experiments were performed to compare cardiac, splenic, and renal sympathetic responses to cardiac sympathetic afferent stimulation before and after cervical spinal cord transection in anesthetized, vagotomized, sinoaortic-denervated cats. Electrical stimulation of afferent cardiac sympathetic nerves produced excitatory responses in cardiac and renal nerves before transection but only cardiac nerve responses after transection. In contrast, afferent stimulation by epicardially applied bradykinin excited cardiac, renal, and splenic nerves before and after cord transection. Splenic nerve responses were greater than renal nerve responses in intact and spinal cats. These results demonstrate that spinal reflexes initiated by activation of cardiac sympathetic afferent nerves are not limited to cardiocardiac pathways. The similarity of patterns of responses in intact and spinal cats suggests that spinal pathways contribute significantly to the reflex excitation observed in intact animals.
Afferent Pathways↗
Cardiac sympathetic afferent influences on renal nerve activity.
Afferent neurons contained within cardiac sympathetic nerves can have excitatory influences on central sympathetic outflow. The normal or pathological circumstances during which such excitatory reflexes occur are not well understood. The purpose of this research was to investigate the possibility that cardiac sympathetic afferent neurons make a significant contribution to cardiovascular control during myocardial ischemia. Afferent influences on renal nerve activity were characterized during occlusion of coronary arteries and in response to chemical stimulation of cardiac receptors by bradykinin. Reflexes were investigated in chloralose-anesthetized cats in which arterial baroreceptors had been denervated. In vagotomized cats afferent stimulation by coronary occlusion or by bradykinin caused significant increases in renal nerve activity. When vagi remained intact, coronary occlusion or epicardially applied bradykinin caused increases, decreases biphasic responses or no significant change in renal nerve activity. Thus, excitatory reflexes could be initiated by the sympathetic afferent neurons in some cats despite simultaneous vagal afferent stimulation. The responses to chemical stimulation followed the same pattern as those to coronary occlusion suggesting that a component of the afferent stimulus during ischemia may be chemical in nature. Finally, the central pathways mediating these excitatory reflexes were investigated by comparing responses to epicardially applied bradykinin in vagotomized cats prior to and following high cervical spinal cord transection or midcollicular decerebration. Excitation of renal nerve activity by this chemical afferent stimulation was reduced but still present in spinalized cats and unchanged in decerebrate cats. Thus spinal pathways may mediate at least a component of these excitatory reflexes but forebrain regions are not essential to their initiation. In summary, these findings are consistent with the contentions that: (1) cardiac sympathetic afferent neurons may initiate significant excitatory reflexes during myocardial ischemia; (2) such reflexes may be due, in part, to chemical stimulation of cardiac receptors; and (3) these reflexes can be mediated partially by spinal pathways.
Afferent Pathways↗
Contrasting reflex influences of cardiac afferent nerves during coronary occlusion.
Afferent neurons contained within cardiac sympathetic nerves may have important influences on the circulation when activated during myocardial ischemia. Although such activation is known to reflexly excite upper thoracic sympathetic efferent neurons, effects on other components of sympathetic outflow are unknown. Therefore, cardiac sympathetic afferent nerves were stimulated by occlusion of coronary arteries to investigate their reflex influences on renal sympathetic nerve activity and systemic arterial blood pressure. Responses were observed in anesthetized cats in which sympathetic and/or vagal cardiac afferent nerves remained intact and arterial baroreceptors remained intact or had been denervated. Stimulating sympathetic afferent neurons caused excitation of renal nerve activity, which was accompanied by variable changes in arterial pressure. Stimulation of vagal afferents by coronary occlusion consistently produced inhibition of renal nerve activity and marked depressor responses. When both components of cardiac innervation remained intact, increases or decreases in renal nerve activity and blood pressure were elicited by coronary artery occlusion in the presence or absence of arterial baroreceptors. These results illustrate that cardiac sympathetic afferent nerves can contribute significantly to cardiovascular control during myocardial ischemia.
Afferent Pathways↗
Excitation of cardiac sympathetic afferent nerves: effects on renal function.
Cardiac sympathetic afferent nerves can reflexly alter renal efferent nerve activity during myocardial ischemia and in response to mechanical or chemical stimulation of cardiac receptors. They also may influence renal excretion of water and electrolytes; however, this potential influence on renal function has not been determined. Therefore, receptors of cardiac sympathetic afferent nerves were chemically stimulated by epicardial application of bradykinin to determine effects on renal function. Experiments were performed in anesthetized dogs in which cervical vagosympathetic trunks were severed and common carotid arteries were tied to diminish influences of arterial baroreceptors and vagal afferent nerves. Chemical stimulation of cardiac afferent neurons excited renal nerve activity and produced decreases in urine flow rate, glomerular filtration rate, and excretion of sodium and potassium. In contrast, no consistent changes in renal function were observed in control dogs, which did not undergo cardiac afferent stimulation. These data provide evidence that activation of cardiac sympathetic afferent neurons can lead to alterations in excretion of water and electrolytes as well as changes in renal nerve activity.
Afferent Pathways↗
Undergraduate education: a look to the future.
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Education, Pharmacy↗