INTRODUCTION

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ISCHEMIC STIMULATION OF ABDOMINAL sympathetic afferents reflexly excites the cardiovascular system (34). Many ischemic metabolites produced during abdominal ischemia, such as bradykinin, contribute to activation of ischemically sensitive afferent nerve endings (32). Previous studies have established that thinly myelinated A- and unmyelinated C-fiber afferents mediate these cardiovascular reflex responses (34). Furthermore, increased sympathetic nervous activity is ultimately responsible for the excitatory cardiovascular reflex responses to stimulation of visceral afferents because such reflexes are diminished in the presence of -adrenergic receptor antagonists (22). It remains uncertain how the sympathetic outflow induced by stimulation of visceral afferents is distributed and integrated to cause these hemodynamic alterations. Because stimulation of visceral sympathetic afferents often simultaneously increases the blood pressure, heart rate, and cardiac contractility, it has been proposed that sympathetic outflows are evenly distributed to the heart and various vascular beds during cardiovascular reflex responses (21, 23). However, the role of regional sympathetic and blood flow responses to stimulation of visceral afferents has not been fully defined.

There is some evidence suggesting that sympathetic nerves supplying the heart and different vascular beds are not equally involved in cardiovascular reflexes (35, 38). Differential responses of sympathetic nerves can result in nonuniform redistribution of blood flows to the visceral and somatic tissues (2, 14, 15). In this regard, the splanchnic bed has been considered as the primary blood volume reservoir for reflex control of cardiovascular homeostasis during exercise (29). But its role often is overlooked for cardiovascular reflexes originating from visceral organs. Further support for the importance of splanchnic circulation in cardiovascular reflexes comes from clinical observations that patients receiving celiac plexus blocks for pain relief frequently manifest orthostatic hypotension, indicating inadequate cardiovascular control (9). On the other hand, it has been reported that cardiac transplant patients have normal cardiovascular responses to squatting and cold pressor test (12, 27), suggesting that sympathetic innervation of the heart is not actively involved in the physiological regulation of circulation. The blood vessels are tonically controlled by the sympathetic nervous system, and the sympathetic outflow to various vascular beds is indirectly reflected in alterations in regional blood flows. Blood redistribution among different vascular beds likely plays an important role in the overall cardiovascular reflex responses to stimulation of visceral afferents. Because the splanchnic bed is tonically involved in the neural control of circulation, we tested a hypothesis that stimulation of abdominal visceral afferents induces predominantly constriction of the splanchnic vascular bed. Furthermore, because the blood flow response is a combination of autoregulation and neural influences, we also examined specifically the regional distribution of sympathetic outflows in response to stimulation of abdominal visceral afferents.

	MATERIALS AND METHODS

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Surgical Preparations

For direct measurement of blood flows, we used a dual-channel Transonic flow meter system (model T206; Transonic Systems, Ithaca, NY), which provides a measure of volume flow by calculating integrated transit times of ultrasonic beams to reflect the motion of liquid flowing through the vessel. The coronary blood flow was measured from the left anterior descending coronary artery, isolated under an operating microscope. A midline abdominal incision was made to access the major abdominal blood vessels. The vessels were isolated for a segment of 2-4 mm, and care was taken not to denervate the nerve plexus around the blood vessels. Transonic flow probes were placed around the celiac, superior, and inferior mesenteric, renal, left anterior descending coronary, or femoral arteries, or the portal vein to directly measure the blood flow.

The tissue blood flows were determined with the colored microsphere technique. A midline sternotomy was performed to expose the heart, and a PE-60 catheter was inserted into the left atrium for microsphere injection. Stock-colored polystyrene microspheres, suspended in saline with 0.05% Tween-80 and surface coated with dyes, were agitated and vigorously vortexed before injection. For each blood flow measurement, 10⁶ colored microspheres (15 µm diameter; Interactive Medical Technology, Los Angeles, CA) were injected followed by saline flush. In the preliminary study, we found that this number of microspheres was sufficient to deposit 400 spheres per piece of tissue studied. A reference blood sample was withdrawn from the femoral artery, beginning 15 s before the microsphere injection and continuing for 2 min with a rate of 1.75 ml/min using a syringe pump (PHD 2000; Harvard Apparatus, Holliston, MA). The technique using colored microspheres to measure regional blood flow has been validated in small animals (16, 40). The microspheres were injected two to three times in each animal. At the end of the experiment, the animal was euthanized with intravenous overdose of pentobarbital sodium. The hindlimb skin and skeletal muscles, heart, stomach, pancreas, duodenum, jejunum, liver, spleen, and two kidneys were rapidly removed. All tissue samples were carefully stripped from the connective tissue, weighed, and processed according to the manufacturer's instructions. With the use of a computer-assisted microscopic imaging system (TRACKER 1000; Interactive Medical Technologies, Los Angeles, CA), the aliquot of the final microsphere suspension was placed in a hemocytometer and ~200 frames were imaged and recorded. The total number of each color microsphere imaged was converted to the total number for each individual blood and tissue sample by spreadsheet calculation. Regional blood flow values (ml · g¹ · min¹) were determined by the following equation: Q_m = (C_m × Q_r)/C_r, where Q_m is regional blood flow, C_m is microsphere count per gram of tissue, Q_r is withdrawal rate of the reference blood sample, and C_r is microsphere count in the reference blood sample. Tissue blood flows from the right and left kidneys were compared to ensure even distribution of the microspheres in each animal. Two to three pieces of tissues from each organ were used for microsphere counting, and the values were averaged.

In separate cats, sympathetic efferent nerve activity was recorded from the central cut end of the left splanchnic, inferior cardiac, and tibial nerves in cats anesthetized as described above. Previous studies have demonstrated that these nerves innervate splanchnic viscera, heart, and the skin and skeletal muscle in the hindlimb (14, 17, 18, 26). Briefly, the target nerve was isolated from the surrounding tissues under a surgical microscope and immersed in warm mineral oil. Small nerve filaments containing a few active units were attached to a stainless steel electrode. The nerve-discharge activity was amplified and filtered (bandwidths of 100 and 1,000 Hz) with an alternating current amplifier and processed through an audioamplifier (P511 and AM8; Grass Instruments, W. Warwick, RI) and displayed on an oscilloscope. The neurogram and blood pressure were simultaneously monitored on a recorder (model K2G, Astro-Med). Nerve activity also was fed into a Pentium computer through an analog-to-digital interface card for subsequent offline quantitative analysis. Discharge frequency was quantified by a software window discriminator by setting an amplitude threshold for all the recorded action potentials of nerve fibers (Experimental Workbench, DataWave Technology, Longmont, CO).

Experimental Protocols

Reflex-induced blood flow redistribution in different vascular beds. Eleven animals were used for this protocol. The animals were allowed to stabilize for 60 min after surgical preparations, and the arterial blood gases were measured and corrected, if necessary. Abdominal visceral afferents were activated by application of 10 µg/ml of bradykinin on the gallbladder (20, 31). Bradykinin was applied by placing a 1-cm² Whatman filter paper soaked with the bradykinin solution on the surface of the gallbladder. After the maximum pressor reflex was attained (typically 1-2 min), the filter paper was removed and the gallbladder was washed twice with normal saline using cotton-tipped applicators. Our previous studies have shown that bradykinin is produced during mesenteric ischemia and contributes to activation of sympathetic visceral afferents during abdominal ischemia (32). The blood flows of different vascular beds were randomly measured in pairs because only blood flows from two vessels could be examined at the same time using the dual-channel flow meter. Thirty minutes were allowed after repositioning flow probes before repeat bradykinin application. During control and the pressor response to afferent activation, the blood flow and arterial blood pressure were continuously monitored and recorded into a Pentium computer using WinDaq data-acquisition and analysis software (Dataq Instruments, Akron, OH). In 4 of 11 animals, reproducibility of cardiovascular responses and the blood flow change in the celiac artery was examined by washing off the bradykinin, waiting 30 min for recovery, then reapplying the bradykinin solution. This interval is sufficient to prevent tachyphylaxis (20, 31). In the remaining seven animals, the pressor response and the celiac blood flow were measured again after ganglionic blockade produced by intravenous injection of 10 mg/kg of hexamethonium (Sigma Chemicals, St. Louis, MO).

Tissue blood flow changes caused by afferent stimulation. A total of 12 animals was used. The animals were first allowed to stabilize for 60 min. Cardiovascular reflexes were induced by electrical stimulation of the central cut end of the right splanchnic nerve, which contains a major portion of afferent fibers innervating the upper abdominal viscera (17). The nerve was electrically stimulated (0.5 ms and 30 V, S48 Stimulator; Grass Instruments), and the frequency of stimulation was adjusted so that the magnitude of the pressor response produced was similar to that obtained with bradykinin application, as we described previously (33). This approach was used because, unlike bradykinin-induced short-lasting hemodynamic responses, the pressor response can be maintained constant for at least 2-2.5 min during the entire period of microsphere injection and withdrawal of reference blood samples. The colored microspheres were injected during control and the peak pressor response elicited by electrical stimulation of the central cut end of the right splanchnic nerve. The pressor response was repeated again 30 min later to ensure reproducibility of changes in tissue blood flows in 8 of 12 animals. To minimize the effect of blood loss on the organ blood flow, an equal volume of blood was transfused from a donor cat after withdrawal of each blood reference sample.

Reflex-induced regional sympathetic outflow. A total of 11 animals was used for electrophysiological recording of sympathetic nerve activity. On the basis of the blood flow experiments, three representative nerves, the splanchnic, inferior cardiac, and tibial nerves, were selected to examine the sympathetic outflow to the splanchnic region, heart, and the skin and skeletal muscle of the hindlimb. After spontaneous discharge activity was recorded, we first tested the nerve response to increase in blood pressure (220-250 mmHg) by briefly constricting the descending thoracic aorta. The nerve was selected for further study only if its activity was attenuated at least 50% by activation of baroreceptors (6, 14, 26). The nerve response to topical application of 10 µg/ml of bradykinin on the gallbladder was tested after a stabilization period of 15-20 min. Each nerve response was tested two times to ensure the reproducibility. In each animal, two of the above three nerves were randomly recorded. In some animals, a ganglionic blocker, hexamethonium (10 mg/kg), was injected intravenously to ensure that the recorded nerve was postganglionic efferent nerve.

	RESULTS

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Hemodynamic profiles. The mean arterial blood pressure and heart rate in all animals studied during control were 86 ± 9 mmHg and 136 ± 8 beats/min, respectively. Topical application of 10 µg/ml of bradykinin to the gallbladder in 11 animals increased significantly the mean blood pressure from 84 ± 15 to 145 ± 22 mmHg and the heart rate from 135 ± 8 to147 ± 11 beats/min (P < 0.05). Electrical stimulation of the central cut end of the right splanchnic nerve also elicited a significant increase in the blood pressure from 82 ± 6 to 144 ± 18 mmHg and the heart rate from 138 ± 8 to 150 ± 11 beats/min (P < 0.05, n = 12), which were similar to those observed with bradykinin. The frequency of electrical stimulation applied to the right splanchnic nerve was 4.2 ± 0.8 Hz.

Changes in organ blood flows and vascular resistances evoked by afferent activation. Topical application of 10 µg/ml of bradykinin to the gallbladder decreased significantly the blood flows in the celiac, renal, and superior and inferior mesenteric arteries (Figs. 1 and 2). By contrast, the coronary arterial blood flow and the portal vein flow were increased significantly after bradykinin application (Figs. 2 and 3). The blood flow in the femoral artery was also increased during this reflex response (Figs. 2 and 3). The peak changes in the resistance for the above vascular beds are shown in Fig. 2B. By examining the timing of the peak responses of blood pressure and splanchnic flows after afferent activation, we observed that maximal reduction of blood flows in celiac and superior mesenteric arteries occurred 16-22 s before the peak increase in the blood pressure (Fig. 1). Maximal increase in the coronary blood flow, on the other hand, occurred 34-42 s after the peak increase in the blood pressure (Fig. 3). The reflex-induced pressor responses and flow changes in the celiac artery, caused by three-time repeated applications of bradykinin on the gallbladder, separated by 30 min, were reproducible (Fig. 4A). Ganglionic blockade with hexamethonium abolished the pressor response and the reflex-evoked changes in the blood flow of the celiac artery (Fig. 4B).

View larger version (44K): [in this window] [in a new window]   Fig. 1.   Original records showing the time course of changes in the arterial blood pressure and blood flows in the celiac artery and portal vein caused by topical application of bradykinin to the gallbladder in 1 animal.

View larger version (28K): [in this window] [in a new window]   Fig. 2.   A: alterations in the blood flow in the portal vein and celiac, renal, coronary, superior (S), and inferior (I) mesenteric arteries during the pressor response to topical application of bradykinin to the gallbladder. B: peak changes in the resistance in the above vascular beds during the pressor response compared with the baseline control (0). Data presented as means ± SE (n = 11). *P < 0.05 compared with control.

View larger version (47K): [in this window] [in a new window]   Fig. 3.   Representative tracing showing the time course of changes in the arterial blood pressure and blood flows in the femoral and left anterior descending coronary arteries caused by topical application of bradykinin to the gallbladder in 1 animal.

View larger version (30K): [in this window] [in a new window]   Fig. 4.   Changes in blood flow of the celiac artery induced by topical application of bradykinin on the gallbladder. A: celiac arterial blood flow during repeat application of bradykinin (n = 4). B: changes in celiac arterial blood flow before and after treatment with hexamethonium (n = 7). Data presented as means ± SE. *P < 0.05 compared with control.

Alterations of tissue blood flows induced by afferent stimulation. Electrical stimulation of the right splanchnic nerve decreased significantly tissue blood flows in the splanchnic organs. Blood flows in the splanchnic viscera were reduced from 68% (jejunum) to 96% (spleen) after stimulation of the central cut end of the right splanchnic nerve, compared with the respective controls (Fig. 5). The magnitude of reduction of blood flow in splanchnic viscera was identical in eight animals in which nerve stimulation was repeated (data not shown). Similar to the changes of the coronary blood flow, the myocardial tissue flow also was increased significantly by splanchnic nerve stimulation (Fig. 6). Compared with the baseline controls, the blood flows in the adrenal glands and skin were not altered significantly, whereas the blood flow in the skin and skeletal muscle was only increased slightly after stimulation of abdominal visceral afferents (Fig. 6).

View larger version (11K): [in this window] [in a new window]   Fig. 5.   Tissue blood flow changes in splanchnic viscera in response to electrical stimulation of the central cut end of the right splanchnic nerve. Data presented as means ± SE (n = 12). *P < 0.05 compared with control.

View larger version (12K): [in this window] [in a new window]   Fig. 6.   Tissue blood flow changes in the kidney, myocardium, adrenal gland, skin, and skeletal muscles in response to electrical stimulation of the central cut end of the right splanchnic nerve. Data presented as means ± SE (n = 12). *P < 0.05 compared with control.

Regional sympathetic outflows induced by afferent stimulation. Topical application of 10 µg/ml of bradykinin onto the gallbladder increased significantly the sympathetic outflow in the splanchnic nerve (182 ± 44%, n = 8, Figs. 7 and 8). Intravenous injection of 10 mg/kg of hexamethonium abolished the response of the splanchnic nerve to bradykinin application in six of eight animals tested. Unlike the response of the splanchnic sympathetic nerve, bradykinin application did not alter significantly the nerve activity recorded from the inferior cardiac (n = 6) and tibial (n = 8) nerves (Figs. 7 and 8).

View larger version (31K): [in this window] [in a new window]   Fig. 7.   Original recordings showing the discharge activity of the splanchnic (A), inferior cardiac (B), and tibial (C) nerves during control and responses to bradykinin (BK) application to the gallbladder.

View larger version (9K): [in this window] [in a new window]   Fig. 8.   Changes in efferent nerve activity recorded from the splanchnic (n = 8), inferior cardiac (n = 6), and tibial (n = 6) nerves in reflex responses to topical application of BK on the gallbladder. Data presented as means ± SE. *P < 0.05 compared with the respective control.

	DISCUSSION

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Activation of abdominal sympathetic visceral afferents induces profound cardiovascular responses, including increases in blood pressure, heart rate, and cardiac contractility (7, 17, 22, 33). These pathophysiological cardiovascular reflexes occur during mesenteric ischemia and manipulation of visceral organs during abdominal surgery (13, 34). Although the afferent mechanisms have been studied extensively, the integrative mechanisms involved in initiation and distribution of sympathetic output during this visceral-cardiovascular reflex remain to be established. The present study provides new information that stimulation of abdominal sympathetic visceral afferents evokes distinct patterns of blood flow redistribution among peripheral vascular beds. We found that stimulation of abdominal visceral afferents reduced predominantly the blood flow in the celiac artery, whereas the blood flow in the portal vein was increased substantially at the same time. Thus a greater reduction in the splanchnic blood reservoir likely is the major mechanism that initiates systemic cardiovascular responses to stimulation of abdominal visceral afferents. More importantly, we have provided new electrophysiological evidence that stimulation of abdominal visceral afferents induces differential responses of regional sympathetic nerve activity, indicating that a selective increase in sympathetic output to the splanchnic bed is essential for this visceral-cardiovascular reflex.

In the present study, we measured initially regional tissue and organ blood flows to examine the extent of blood flow redistribution evoked by stimulation of abdominal visceral afferents. Two methods were combined to quantify the changes in regional blood flows. The microsphere technique is most suitable for this experiment because it can simultaneously measure blood flow changes in many different tissues. However, one limitation of this method is that it is not possible to continuously monitor the time course of flow changes. Thus, as a complementary approach, the Transonic flow meter system was used to provide a continuous monitoring of arterial flows in several important regions. This study provides substantial evidence that vasoconstriction of the splanchnic bed and, to a lesser extent, the renal vascular bed is involved primarily in blood flow redistribution caused by stimulation of visceral afferents. Data obtained with the microsphere technique indicate that even within the splanchnic region, the magnitude of reflex-evoked flow reduction is not identical in different visceral organs. This new information suggests that blood flows to some splanchnic viscera (e.g., spleen, pancreas, and stomach) are more susceptible to increased sympathetic outflow evoked by stimulation of visceral afferents, although species differences of neural control of circulation should be recognized.

The vasculature in the skin and skeletal muscles is actively involved in thermal regulation and cardiovascular adjustments during exercise (8, 29). We found that the peak femoral blood flow was significantly increased during the pressor response, and the estimated femoral arterial resistance was not significantly altered during the stimulation of abdominal visceral afferents. This observation suggests that sympathetic innervation of these somatic vascular beds is not responsible for the cardiovascular reflex originated from abdominal viscera. A lack of significant increase in blood flow to the skin and skeletal muscle during this reflex could be due to the limitation of the microsphere technique. In this regard, the blood flow to these tissues is very low, and alteration of blood flows elicited by this reflex is transient, which might prevent accurate counting of microspheres deposited in the tissue after single injection of microspheres. As to the coronary blood flow, we found no evidence of reflex vasoconstriction of the coronary vessel after stimulation of visceral afferents. Unlike what was reported previously (23), we observed that the coronary flow increased consistently in all animals studied after stimulation of abdominal visceral afferents. Because a decrease in splanchnic blood flow preceded the increase in myocardial blood flow, we believe that an increase in the myocardial blood flow is secondary to increased myocardial oxygen demand due to a substantial increase in blood pressure caused by blood redistribution. In fact, the cardiac responses (increases in heart rate and cardiac contractility) after stimulation of visceral afferents are likely due to the blood redistribution initiated by constriction of the splanchnic bed and increased circulating catecholamines released from the adrenal gland. Consistent with this notion, it has been shown that the enhanced cardiac output caused by activation of ₁-adrenergic receptors with phenylephrine is due entirely to the decrease in splanchnic intravascular volume, because cardiac output does not increase after the splanchnic vasculature has been removed (37). Thus the decreased splanchnic volume leads to an increased cardiac output through an increase in preload (37). Additionally, surgical removal of the adrenal glands or treatment with -adrenergic receptor antagonists diminishes the increased cardiac contractility associated with the cardiovascular reflex elicited by stimulation of gastric afferents (22), which further supports the notion that an increase in the heart rate and cardiac contractility after stimulation of abdominal visceral afferents is a secondary effect of strong activation of the splanchnic sympathetic nerve. By simultaneously measuring the blood pressure and regional blood flows, we were able to determine the sequence of changes in the hemodynamics and regional vascular reactivity after stimulation of visceral afferents. We demonstrated that stimulation of abdominal visceral afferents predominantly reduced splanchnic blood flow, which induced a blood redistribution leading to an increase in the blood pressure. The sympathetic reflex nature of the blood flow changes evoked by afferent stimulation was documented in the present study that treatment with a ganglionic blocker, hexamethonium, abolished the changes in the blood pressure as well as regional blood flows induced by activation of visceral afferents. We also have shown previously that surgical removal of the celiac and mesenteric ganglia eliminates the reflex cardiovascular responses to mesenteric ischemia (34), further indicating the importance of the splanchnic sympathetic innervation in cardiovascular reflexes originated from abdominal viscera.

The capacitance function of the venous system is critical for the regulation of regional and circulatory blood volume (10). Splanchnic veins, which contain 25% of the total blood volume, are richly supplied with sympathetic nerves (36). The -adrenergic mediated decrease in splanchnic volume is due to active constriction of both splanchnic resistance and capacitance vasculatures (30). With the use of the radionuclide imaging technique, it has been demonstrated that stimulation of ₁-adrenergic receptors with phenylephrine causes a dramatic decrease in splanchnic volume, which acts to increase cardiac output (4). The splanchnic bed accounts for almost all of the reflex capacitance response that buffers systemic circulatory volume changes associated with activation of ₁-adrenergic receptors (11). We have shown previously that complete occlusion of the celiac and superior and inferior mesenteric arteries can only slightly elevate the blood pressure (34). Thus the profound hemodynamic response induced by visceral afferent activation cannot be explained fully by constriction of the splanchnic resistence vessels. In the current study, the importance of splanchnic capacitance vessels in this reflex was examined indirectly by measuring the blood flow in the portal vein draining the splanchnic bed. We observed a substantial and persistent increase in the portal vein blood flow after stimulation of abdominal visceral afferents, strongly indicating an intense constriction of the splanchnic veins. Therefore, the splanchnic capacitance vessels likely play a key role in initiation of blood redistribution and the cardiovascular reflex responses to activation of visceral afferents.

It should be acknowledged that the local blood flow response is a combination of autoregulation and neural influences, and measurement of blood flow does not reflect accurately changes in the regional sympathetic outflow. Thus direct recording of the regional sympathetic nerve activity was also performed in the present study. We found that stimulation of abdominal visceral afferents induced a differential increase in regional sympathetic nerve activity. Although stimulation of visceral afferents evoked a profound increase in the splanchnic sympathetic activity, the sympathetic outflow to the somatic structures was little influenced. These nerve recording data are consistent with the changes in estimated vascular resistance for the splanchnic and femoral arteries. Also, the lack of increase in sympathetic efferent outflow to the heart is consistent with the concept that the coronary blood flow is largely influenced by autoregulation, and no sympathetic constriction of coronary arteries was evident in this reflex response. Interestingly, we observed that although the coronary vascular resistance was reduced significantly during this reflex, the efferent nerve activity recorded from the inferior cardiac nerve did not change. Therefore, it is inadequate to predict the sympathetic outflow based on the measurement of regional blood flow or vascular resistance. Accumulating evidence on regionally diverse changes of sympathetic activity has considerably modified the classic concept that the sympathetic nervous system responds in a massive and generalized manner. It has been increasingly appreciated that the regional diversity or differentiation of the sympathetic outflow to the peripheral effectors plays an important role in various integrative physiological responses (35, 38, 39). By comparing spillover of norepinephrine to the portal vein and arterial and hepatic sites as an index of sympathetic outflow, Aneman et al. (1) found that a major proportion of sympathetic outflow is directed to mesenteric organs in patients undergoing abdominal surgery. The diverse responses of the sympathetic nervous system also have been revealed by the studies on the recording of whole nerve and single-unit activity of sympathetic efferent nerves in anesthetized animals (2, 14, 15). A differential response of sympathetic efferent nerves innervating the mesenteric organs and somatic structures to stimulation of baroreceptors has been demonstrated previously (26). Furthermore, stimulation of intestinal mechanoreceptors or chemoreceptors is found to excite mesenteric nerve activity more than renal nerve activity (39).

In summary, the present study demonstrates that stimulation of abdominal visceral afferents causes predominantly vasoconstriction of the splanchnic vascular bed, leading to a substantial decrease in the splanchnic blood flow and reservoir volume. Furthermore, differential increase in the sympathetic outflow to the splanchnic viscera, but not to the heart and somatic tissues, is largely responsible for the blood flow redistribution in responses to stimulation of abdominal visceral afferents. Thus the primary (splanchnic bed constriction) and secondary (effect of catecholamines on the myocardium) effects of strong adrenergic activation of splanchnic sympathetic activity are critical mechanisms of excitatory hemodynamic responses to stimulation of abdominal visceral afferents. On one hand, increased sympathetic outflow to the splanchnic bed causes profound vaso- and venoconstriction. The substantial increase in blood pressure is primarily due to an increase in the splanchnic vascular resistance and an increase in cardiac preload resulting from the decreased splanchnic volume. On the other hand, increased splanchnic sympathetic activity to the adrenal gland could elicit massive release of catecholamines into the general circulation, which, in turn, increase the cardiac contractility and heart rate.

Perspectives