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Biomedical subjects

J C Longhurst

Publications and source records attributed to J C Longhurst.

At least 109 records · Page 6Linked to original sources
PubMed1987

Association of decreased myocardial beta-receptors and chronotropic response to isoproterenol and exercise in pigs following chronic dynamic exercise.

The effects of chronic dynamic exercise on myocardial beta-adrenergic and muscarinic cholinergic receptors and chronotropic sensitivity to isoproterenol were studied in 5 Yucatan miniswine. Right atrial and left ventricular biopsies, heart rate responses to isoproterenol, and maximal exercise treadmill testing were obtained before and after 10-19 weeks of treadmill running. Radioligand studies using 125I-iodocyanopindolol (ICYP) and 3H-quinuclidinyl benzilate (QNB) were used to determine the number of beta-adrenergic and muscarinic cholinergic receptors. Maximal oxygen consumption increased from 52 +/- 5 to 65 +/- 7 ml/kg/min (mean +/- SD; p less than 0.02), maximal workload from 530 +/- 111 to 1,074 +/- 179 KPM/min (p less than 0.01), resting heart rate decreased from 91 +/- 13 to 62 +/- 4 beats/min (p less than 0.01), heart rate at 75% of pretraining maximal workload decreased from 253 +/- 15 to 196 +/- 12 beats/min (p less than 0.01), and maximal exercise heart rate decreased from 273 +/- 6 to 254 +/- 9 beats/min (p less than 0.01). Decreased heart rate responsiveness to adrenergic stimulation was observed following chronic exercise. Maximal isoproterenol-stimulated heart rate decreased from 225 +/- 13 to 185 +/- 28 beats/min (p less than 0.05) and the slope of the isoproterenol dose-response relation decreased from 63 +/- 16 to 40 +/- 16 (p less than 0.05). Radioligand studies revealed a decrease in beta-receptor number in the right atrium following chronic exercise (61 +/- 9 vs. 34 +/- 8 fmol/mg; p less than 0.02), but receptor number in membranes from the left ventricle did not change (60 +/- 9 vs. 62 +/- 4 fmol/mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1987

Evaluation of coronary native and coronary collateral pressure gradients in the conscious dog.

Sixteen dogs were instrumented chronically with a left circumflex (CIRC) Ameroid constrictor, and with CIRC, left anterior descending (LAD), aortic, left atrial and pulmonary artery (PA) catheters. Premature mortality was 12.5% prior to the last measurements of pressure at 50 +/- 3 days (mean +/- SE). Five animals developed closure of the Ameroid constrictor at 5 +/- 1 days with an LAD to CIRC pressure gradient of 57 +/- 8 mm Hg. Eleven animals developed closure of the Ameroid constrictor at 18 +/- 1 days with an LAD to CIRC pressure gradient of 29 +/- 3 mm Hg. Three animals in the former group had gross evidence of a myocardial infarction on postmortem examination. None of the animals in the latter group showed evidence of a myocardial infarction. Thus, closure of a CIRC Ameroid constrictor and subsequent collateral vessel development can be monitored chronically by the LAD to CIRC pressure gradient with a high survival, low infarction rate. This chronic model thus provides an accurate measure of coronary native and collateral pressures in unsedated dogs.

Animals↗
PubMed1986

O2 consumption during exercise in dogs--roles of splenic contraction and alpha-adrenergic vasoconstriction.

To examine the influence of alpha-adrenergic vasoconstriction on the aerobic capacity of dogs, we calculated O2 consumption (VO2) by the Fick method during submaximal and maximal exertion before and during alpha-adrenergic blockade with phentolamine. Regional blood flow was measured with radioactive microspheres. alpha-Adrenergic receptor blockade reduced VO2 by 12.9% during submaximal and 17.9% during maximal exercise. Arterial and venous lactic acid approximately doubled during both levels of stress in the presence of alpha-adrenergic receptor blockade. Calculated VO2 decreased because arteriovenous O2 (A-V)O2 extraction was reduced by 11.6% during submaximal exercise. During maximal exercise a 16.7% decrease in (A-V)O2 extraction and a 5.7% decrease in cardiac output contributed to the decrease in maximal VO2. During both levels of stress, (A-V)O2 extraction was reduced because arterial O2 content was decreased. Since circulating hematocrits during exercise were reduced by alpha-adrenergic receptor blockade (43-38%), we postulate that splenic contraction likely was inhibited. Additionally, distribution of blood flow to skeletal muscle and visceral organs was unaltered by alpha-blockade. To examine the importance of splenic contraction during maximal exercise, we examined hemodynamic and metabolic responses before and after splenectomy. Compared with the spleen-intact condition, splenectomized dogs demonstrated a 12.6% reduction in VO2 as a result of 7.7 and 5.5% reductions in (A-V)O2 extraction and cardiac output, respectively. (A-V)O2 extraction was reduced because arterial O2 content and circulating hematocrit during exercise were decreased. Therefore, in the exercising dog, alpha-adrenergic receptor blockade reduces O2 consumption and causes a shift to anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1986

Evidence against high pressure, arterial baroreceptors in the abdominal viscera of cats.

The abdominal viscera of cats have been postulated to contain a site of cardiovascular regulation. In particular, a baroreceptive function has been ascribed to splanchnic afferent nerves. We wished to determine whether afferents with a cardiac-rhythmic discharge functioned as arterial baroreceptors. Nineteen afferents with a cardiac rhythmic discharge were studied. All afferents were A fibers, whose endings were located in either the pancreas, mesentery, or porta hepatis region. We examined their characteristics of discharge with regard to changes in mean pressure, pulse pressure, and dP/dt of the arterial pulse. Hemodynamic alterations were achieved by intravenous administration of isoproterenol, norepinephrine, or phenylephrine and by occlusion of the descending thoracic aorta. After isoproterenol, increases in nerve activity occurred when pulse pressure and dP/dt were increased but while mean pressure was decreasing, indicating that mean pressure was not the stimulus for discharge of these afferents. Additionally, under similar hemodynamic conditions, afferents did not demonstrate reproducible patterns of activity. The afferents generally discharged with one impulse per cardiac cycle, rarely with two to three impulses per cycle. None demonstrated a bursting pattern even when arterial blood pressure was quite elevated. The spontaneous pattern of discharge changed frequently, often after the viscera were repositioned, and sometimes remained even after complete occlusion of the aorta. The data indicate that these visceral afferents do not respond as high pressure, arterial baroreceptors. All afferents adapted extremely rapidly and exhibited a low gain (0.02 +/- 0.00 impulses X s-1 X mmHg-1), indicating that these fibers would be ineffective in signaling physiologically significant changes in hemodynamic variables. The data from this study do not support the existence of baroreceptors in the abdominal viscera of cats.

Afferent Pathways↗
PubMed1986

Substance P, 5-hydroxytryptamine, and bradykinin stimulate abdominal visceral afferents.

To determine if chemicals produced endogenously within the gastrointestinal system stimulate abdominal visceral sensory endings, we recorded the response of 42 A- and 25 C-fibers in the splanchnic nerve of cats as substance P (10-20 micrograms), 5-hydroxytryptamine (5-HT, 100-200 micrograms), or bradykinin (10 micrograms) was injected into the descending thoracic aorta. Approximately half of the sensory endings responded to each chemical. However, significantly more C- than A-fiber endings responded to 5-HT (64 vs. 39%) and bradykinin (76 vs. 41%). Most C-fiber endings were insensitive to external mechanical stimuli, supporting the concept that these endings are primarily chemosensitive. In contrast, most A-fiber endings were quite sensitive to external mechanical stimuli. Additionally, more A-fiber endings located in contractile (gut or vasculature) than in noncontractile (pancreas, liver, or spleen) regions responded to 5-HT (58 vs. 19%), bradykinin (67 vs. 15%), and substance P (57 vs. 29%), a response that frequently occurred coincident with the development of chemically induced gut contractions. Thus many A-fiber endings are primarily sensitive to mechanical stimuli. However, 15-30% of the A-fiber endings located in noncontractile regions responded to chemicals, although the endings likely were removed from the mechanical effects of these chemicals. Since these A-fiber endings are also quite sensitive to external mechanical stimuli, they may be polymodal in their function. We conclude that abdominal visceral sensory endings are not homogeneous in function and are stimulated by several chemicals produced endogenously within the gastrointestinal system, including substance P, 5-HT, and bradykinin.

Abdomen↗
PubMed1986

Bradykinin in reflex cardiovascular responses to static muscular contraction.

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3-4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000-30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500-750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Animals↗
PubMed1986

Validation of a respiratory mask for measuring gas exchange in exercising swine.

A respiratory mask was developed for resting and exercising swine. The lightweight, low-dead-space design fits airtight against the animals' snouts to provide breath-by-breath measurements of respiration and metabolism. Validation of the mask was carried out using the Fick principle with dye-dilution cardiac outputs and arterial and mixed venous O2 content measurements. Linear regression analysis of O2 consumption (VO2) measurements by the two techniques revealed a slope of 1.07 and a Y-intercept of -1.06 ml X kg-1 X min-1. The standard error of the estimate of VO2 was 3.5 ml X kg-1 X min-1. The mask design permits rapid measurements of ventilation and metabolism in response to acute and chronic exercise.

Animals↗
PubMed1986

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

The purpose of this study was to determine the contribution of prostaglandins to the reflex cardiovascular responses induced by static contraction of the hind limb in cats, i.e., the exercise reflex. To accomplish this, the cardiovascular responses to hind limb contraction induced by electrical stimulation of spinal cord ventral roots L6-7 and S1 were compared before and after inhibition of prostaglandin synthesis (indomethacin, 2-6 mg/kg i.v., n = 5, or sodium meclofenamate, 2-6 mg/kg i.v., n = 5) or after injection of prostaglandin E2 into the hind limb arterial blood supply. Treatment with indomethacin attenuated the contraction-induced increase in mean arterial pressure and left ventricular dP/dt by 76% and 86%, respectively. Heart rate and average developed triceps surae muscle tension were unchanged. After administering sodium meclofenamate, the reflex response was attenuated to a similar degree. In the indomethacin-treated animals, injection of exogenous prostaglandin E2 (PGE2) partially restored the pressor and myocardial contractile responses. In 6 animals, treatment with exogenous PGE2 without prior inhibition of prostaglandin synthesis did not significantly augment the contraction-induced cardiovascular response. Using the radioactive microsphere technique, we measured skeletal muscle blood flow during contraction before and after treatment with indomethacin (n = 6) to determine if an indomethacin-induced alteration in blood flow could account for the attenuated contraction-induced cardiovascular response. Blood flow during static muscle contraction was not significantly altered by indomethacin. We conclude that prostaglandins contribute to the exercise reflex through an action on afferent nerve endings rather than through a regional vascular effect.

Animals↗
PubMed1985

Extracardiac and coronary vascular effects of digitalis.

The administration of digitalis glycosides causes a variety of extracardiac effects. In both normal human subjects and in other species, digitalis increases smooth muscle tone of resistance and capacitance vessels. The vasoconstriction is mediated, in part, by a direct action of these glycosides on smooth muscle and, in part, by an increase in alpha-adrenergic tone. Constriction of coronary and splanchnic vessels may lead to myocardial or mesenteric ischemia. In contrast to normal subjects, patients with congestive heart failure demonstrate arteriolar and venodilation in response to these glycosides, possibly because the myocardial effect, to increase cardiac output and peripheral blood flow, overcomes the vasoconstrictor properties of these drugs. Other important actions of digitalis glycosides occur in the central and peripheral nervous systems. Their effects on the area postrema of the medulla oblongata are largely responsible for the alpha-adrenergic-mediated peripheral vasoconstriction, as well as the nausea and vomiting that frequently accompany digitalis intoxication. Actions of glycosides on the cerebral cortex are responsible for the wide range of neurotoxic effects that range from visual disturbances and headaches to seizures and coma. Finally, peripheral neurologic effects of digitalis glycosides on baroreceptor and cardiac afferent fibers may: improve the depressed function of these receptors in the situation of heart failure, and reflexly lower peripheral vascular resistance, thereby partially preventing the vascular constrictor action of these glycosides.

Animals↗
PubMed1985

Effect of prostaglandins on bradykinin-induced visceral-cardiac reflexes.

We examined the effect of prostaglandins on the reflex cardiovascular response to bradykinin applied to the abdominal organs of anesthetized cats. Bradykinin (10 micrograms/ml) was applied to the serosal surface of the stomach, gallbladder, or jejunum before and after injection of indomethacin (2-10 micrograms/ml iv) and after application of 1 microgram/ml of prostaglandins E1, E2, or F2 alpha (PGE1, PGE2, PGF2 alpha) or prostacyclin (PGI2). In six cats, stimulation of the stomach with bradykinin significantly increased mean arterial pressure (MAP) by 37 +/- 5 (SE) mmHg and maximal dP/dt by 633 +/- 101 mmHg/s. Following indomethacin the bradykinin-induced increases in MAP and dP/dt were significantly reduced to 19 +/- 4 mmHg and 191 +/- 58 mmHg/s, respectively. Treatment with PGE1, PGE2, or PGI2, but not PGF2 alpha, restored the initial bradykinin response. The gallbladder and jejunum responded similarly. Also application of exogenous prostaglandins, PGE2 or PGI2, to the stomach, gallbladder, or jejunum significantly augmented the cardiovascular response to bradykinin. Finally, PGE2 restored a portion of the cardiovascular response to bradykinin following the development of tachyphylaxis. We conclude that prostaglandins are necessary for the full manifestation of the cardiovascular response to bradykinin.

Animals↗
PubMed1985

Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses.

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8-12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.

Animals↗
PubMed1985

Bradykinin-induced chemoreflexes from skeletal muscle: implications for the exercise reflex.

We examined the cardiovascular response to bradykinin stimulation of skeletal muscle afferents and the effect of prostaglandins on this response. Intra-arterial injection of 1 microgram bradykinin into the gracilis muscle of cats reflexly increased mean arterial pressure by 16 +/- 2 mmHg, left ventricular end-diastolic pressure by 1.6 +/- 0.6 mmHg, maximal dP/dt by 785 +/- 136 mmHg/s, heart rate by 11 +/- 2 beats/min, and mean aortic flow by 22 +/- 3 ml/min. The hemodynamic responses were abolished following denervation of the gracilis muscle. The increases in mean arterial pressure and maximal dP/dt were reduced by 68 and 45%, respectively, following inhibition of prostaglandin synthesis with indomethacin (2-8 mg/kg iv). Treatment with prostaglandin E2 (PGE2, 15-25 micrograms ia) restored the initial increase in mean arterial pressure, but not dP/dt, caused by bradykinin stimulation. Injection of PGE2 (15-30 micrograms ia) into the gracilis, without prior treatment with indomethacin, augmented the bradykinin-induced increases in mean arterial pressure and dP/dt. We conclude that small doses of bradykinin injected into skeletal muscle are capable of reflexly activating the cardiovascular system and that prostaglandins are necessary for the full manifestation of the corresponding hemodynamic response. The pattern of hemodynamic adjustment following bradykinin injection into skeletal muscle is very similar to that induced by static exercise. Therefore, it is possible that intense exercise provides a stimulus for this bradykinin-induced reflex in vivo.

Animals↗
PubMed1985

Function of mature coronary collateral vessels and cardiac performance in the exercising dog.

Formation of extensive collateral vessels after chronic constriction of a coronary artery in dogs can provide for similar increases in blood flow to native and collateralized regions of myocardium during exertion. Previous investigations have not compared myocardial blood flow and cardiac functional responses during exercise in constricted and nonconstricted (sham) animals. Thus we evaluated left ventricular performance and myocardial blood flow at rest and during mild, moderate, and severe exertion in sham-operated dogs and in dogs 2-3 mo after placement of an Ameroid occluder around the proximal left circumflex artery. Changes in double product, maximal left ventricular dP/dt, and pressure-work index were similar in both groups for each level of exertion. Despite similar increases in estimated myocardial O2 demand and similar diastolic perfusion pressures, average transmural myocardial blood flow increased less in the constrictor animals, particularly during severe exercise (2.74 +/- 0.22 vs. 1.45 +/- 0.29 ml X min-1 X g-1). The smaller increases in blood flow occurred equally in native and collateralized regions as well as in the papillary muscles and boundary areas between the native and collateralized regions. The differences in flow in the native and collateralized regions were uniform across the wall of the myocardium. We also observed smaller increases in stroke volume and cardiac output in the constrictor group, disparities which increased with increasing exertion (stroke volume, severe exercise = 0.92 +/- 0.13 vs. 0.53 +/- 0.09 ml/kg). We postulate that myocardial active hyperemia is limited either because the coronary vessels remaining after chronic circumflex occlusion cannot dilate sufficiently or that there is inappropriate active vasoconstriction during severe exertion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Cardiovascular effects of haemorrhagic shock in spleen intact and in splenectomized dogs.

Cardiac performance was evaluated during haemorrhagic shock in 27 dogs with spleens intact, 24 splenectomized, and 23 splenectomized transfused dogs that were given a volume of packed red blood cells simulating splenic contraction. Contractile changes were evaluated by calculating dP/dt at 20 mmHg developed pressure (dP/dt DP20), and by relating stroke work to left ventricular end-diastolic volume measured by biplane cinefluorography. Although heart rate increased comparably during early shock, cardiac output, stroke volume, maximal dP/dt, dP/dt DP20, and arterial blood pressure decreased more in splenectomized and splenectomized transfused dogs than in those with spleens intact. During shock dP/dt DP20 was more depressed in the splenectomized and splenectomized transfused dogs than in those with spleens intact. In addition, an increase in left ventricular end-diastolic volume was accompanied by an increase in left ventricular stroke work in dogs with spleens intact. In contrast, stroke work remained depressed in both splenectomized groups despite increased left ventricular volume. Progressive acidosis and decreased left ventricular blood flow were similar in all dogs during haemorrhage. The greater reduction in left ventricular performance during haemorrhagic shock in the splenectomized and splenectomized transfused dogs was not related to excess lactate, changes in plasma volume, or red blood cell mass. Decreased left ventricular performance, despite improved ventricular filling, indicates greater cardiac dysfunction during haemorrhagic shock. This study suggests that, in dogs, the spleen maintains left ventricular performance during haemorrhage by mechanisms other than autotransfusion.

Animals↗
PubMed1984

Chemically induced cardiovascular reflexes arising from the stomach of the cat.

We examined the potential for cardiovascular reflexes caused by the application of either bradykinin or capsaicin to the serosal or mucosal surface of the stomach. After application to the serosa, bradykinin (10 micrograms/ml) evoked increases in mean arterial pressure of 12 +/- 2 mmHg, heart rate of 5 +/- 1 beats/min, left ventricular dP/dt (at 40 mmHg developed pressure) of 305 +/- 54 mmHg/s and systemic vascular resistance of 0.04 +/- 0.01 PRU. Capsaicin (200 microgram/ml) caused similar cardiovascular responses. There were no cardiovascular responses when either substance was applied to the gastric mucosa. The responses to both chemicals were abolished by celiac ganglionectomy but not by bilateral vagotomy. To determine whether the cardiovascular responses evoked by bradykinin were caused by smooth muscle contraction, we compared the increases in gastric smooth muscle tension and blood pressure elicited by bradykinin, bethanechol, or acetylcholine. Bethanechol and acetylcholine caused greater increases in tension than bradykinin, whereas bradykinin evoked greater increases in blood pressure than either bethanechol or acetylcholine. We conclude that stimulation of gastric afferents by capsaicin or bradykinin causes cardiovascular reflexes, primarily through activation of chemosensitive receptors.

Acetylcholine↗
PubMed1984

Reflex regional vascular responses during passive gastric distension in cats.

The increase in systemic vascular resistance during gastric distension in cats may result from variable vasomotor responses in several parallel regional vascular beds. Accordingly, in 23 anesthetized cats the stomach was passively distended with a balloon while systemic hemo-dynamics were monitored. Regional vascular responses were determined during control periods and during gastric distension either by injection of radioactive microspheres (15 cats) or by constant perfusion of vascularly isolated organs (8 cats). During distension, mean arterial pressure and systemic vascular resistance increased by 32 and 28%, respectively. Regional flow measurements indicated no significant alterations in any of the organs examined. Calculated regional vascular resistances indicated vasoconstriction in the kidneys (53%), small intestine (31%), and large intestine (37%) that was reversed by alpha-adrenergic blockade with phentolamine. Constant-flow perfusion studies confirmed the regional vasoconstriction in the renal, superior mesenteric, and hindlimb circulations. These studies suggest a regional heterogeneity of vasomotor response during passive gastric distension in cats that includes no change in vascular resistance in some organs and alpha-adrenergic vasoconstriction in others.

Adrenergic alpha-Antagonists↗
PubMed1984

Effects of bradykinin and capsaicin on endings of afferent fibers from abdominal visceral organs.

Stimulation of sensory endings in abdominal visceral organs with capsaicin or bradykinin reflexly increases heart rate, blood pressure, and myocardial contractility through afferent pathways in splanchnic nerves. To determine the afferent fiber types stimulated, we recorded impulses in the right splanchnic nerve in 12 anesthetized cats after either injecting capsaicin (50-200 micrograms) or bradykinin (6.5-20 micrograms) into the descending thoracic aorta or applying pledgets soaked with these chemicals to a visceral organ. We studied 26 A- and 23 C-fibers, each with one receptive field in the mesentery, stomach, duodenum, jejunum, ileum, pancreas, liver, gallbladder, or porta hepatis. Endings of C-fibers generally were mechanically insensitive, whereas endings of A-fibers were mechanically sensitive. After a latency of 10.7 +/- 3.3 s, capsaicin increased the activity of 10 of 26 A-fibers from 2.0 +/- 0.9 to 9.9 +/- 2.6 impulses/s and 23 of 23 C-fibers from 0.2 +/- 0.1 to 13.0 +/- 1.6 impulses/s after a latency of 3.3 +/- 0.9 s. Bradykinin increased the activity of 15 of 26 A-fibers from 2.6 +/- 0.9 to 7.4 +/- 1.5 impulses/s after a latency of 17.0 +/- 1.7 s and 16 of 22 C-fibers from 0.4 +/- 0.2 to 4.7 +/- 1.2 impulses/s after a latency of 19.0 +/- 1.9 s. Capsaicin stimulated significantly more C- than A-fibers (P less than 0.001) and a significantly greater fraction of C-fibers than did bradykinin (P less than 0.007). We conclude that stimulation of splanchnic C-fiber afferents by capsaicin and both A- and C-fiber afferents by bradykinin is primarily responsible for the reflex cardiovascular responses caused by these chemicals.

Abdomen↗