Effects of gastric distension on the cardiovascular system in rainbow trout (Oncorhynchus mykiss)

2008 ◽  
Vol 294 (5) ◽  
pp. R1648-R1656 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Susanne Holmgren ◽  
Michael Axelsson

When animals feed, blood flow to the gastrointestinal tract increases to ensure an adequate oxygen supply to the gastrointestinal tissue and an effective absorption of nutrients. In mammals, this increase depends on the chemical properties of the food, as well as, to some extent, on the mechanical distension of the stomach wall. By using an inflatable nitrile balloon positioned in the stomach, we investigated the cardiovascular responses to mechanical stretch of the stomach wall in rainbow trout ( Oncorhynchus mykiss). Distension with a volume equivalent to a meal of 2% of the body mass increased dorsal aortic blood pressure by up to 29%, and central venous blood pressure increased transiently nearly fivefold. The increase in arterial pressure was mediated by an increased vascular resistance of both the systemic and the intestinal circulation. Cardiac output, heart rate, and stroke volume (SV) did not change, and only transient changes in gut blood flow were observed. The increase in arterial pressure was abolished by the α-adrenergic antagonist prazosin, indicating an active adrenergic vasoconstriction, whereas the venous pressor response could be the consequence of a passive increase in intraperitoneal pressure. Our results show that mechanical distension of the stomach causes an instantaneous increase in general vascular resistance, which may facilitate a redistribution of blood to the gastrointestinal tract when chemical stimuli from a meal induce vasodilation in the gut circulation. The normal postprandial increase in gut blood flow in teleosts is, therefore, most likely partly dependent on mechanical stimuli, as well as on chemical stimuli.

1999 ◽  
Vol 202 (16) ◽  
pp. 2177-2190 ◽  
Author(s):  
S.F. Perry ◽  
R. Fritsche ◽  
T.M. Hoagland ◽  
D.W. Duff ◽  
K.R. Olson

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13–39 %) and dorsal aortic (17–54 %) blood pressures that reflected marked increases in systemic vascular resistance (16–78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4–7 beats min(−)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(−)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (α)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (α)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (α)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65–151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.


1994 ◽  
Vol 191 (1) ◽  
pp. 155-166 ◽  
Author(s):  
J Kagstrom ◽  
M Axelsson ◽  
S Holmgren

Changes in cardiac output, heart rate, dorsal aortic blood pressure and coeliac artery blood flow were measured in unrestrained rainbow trout, Oncorhynchus mykiss, following injections of the elasmobranch tachykinins scyliorhinin I and II. The resistance in the coeliac vascular bed and the total systemic vasculature were calculated from blood pressure and flow. In addition, isolated tails were perfused to investigate the effect of the peptides on the somatic vasculature. Scyliorhinin I (SCY I) produced a biphasic change in the coeliac vascular resistance: an initial decrease was followed by an increase. The decrease in coeliac vascular resistance was accompanied by a decrease in the total systemic vascular resistance, leading to an increased cardiac output. The ensuing increase in coeliac vascular resistance caused a slight increase in blood pressure. In the perfused tail, SCY I produced a marked increase in the somatic vascular resistance. Scyliorhinin II (SCY II) decreased the systemic vascular resistance, causing an increase in cardiac output. SCY II also caused a late increase in the coeliac vascular resistance, which led to hypertension and bradycardia. In vitro, SCY II produced a biphasic response in which an initial decrease in the somatic resistance was followed by a larger increase. The results demonstrate that exogenous SCY I and II are vasoactive peptides that act by different mechanisms in the rainbow trout cardiovascular system. Their actions also differ from the actions of substance P previously observed in the cod, Gadus morhua, and possibly involve a neural reflex.


2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.


1967 ◽  
Vol 46 (2) ◽  
pp. 297-305 ◽  
Author(s):  
G. F. HOLETON ◽  
D. J. RANDALL

1. Methods for cannulating the ventral aorta of the trout, which permit the measurement of blood pressure in the unanaesthetized, unrestrained, intact fish are described. 2. Rate and amplitude of breathing and blood pressure in the dorsal and ventral aortae increase during hypoxia. These changes are associated with a marked bradycardia. 3. There are increases in vascular resistance to blood flow in both respiratory and systemic circulations during hypoxia. 4. Post hypoxia is associated with large increases in ventral aortic and dorsal aortic pressures.


2010 ◽  
Vol 298 (5) ◽  
pp. R1240-R1248 ◽  
Author(s):  
Henrik Seth ◽  
Albin Gräns ◽  
Michael Axelsson

We have studied the potential role of CCK as a regulator/modulator of the postprandial increase in gastrointestinal blood flow. Rainbow trout ( Oncorhynchus mykiss ) were instrumented with pulsed Doppler flow probes to measure the effects of CCK on cardiac output and gastrointestinal blood flow. Furthermore, vascular preparations were used to study the direct effects of CCK on the vessels. In addition, we used in situ perfused hearts to further study the effects of CCK on the cardiovascular system. When the sulfated form of CCK-8 was injected at a physiological concentration (0.19 pmol/kg) in vivo, there was a significant increase in the gastrointestinal blood flow (18 ± 4%). This increase in gastrointestinal blood flow was followed by a subsequent increase in cardiac output (30 ± 6%). When the dose was increased to 0.76 pmol/kg, there was only a 14 ± 6% increase in gastrointestinal blood flow; possibly due to a dose-dependent increase in the gill vascular resistance as previously reported or a direct effect on the heart. Nevertheless, CCK did not affect the isolated vessel preparations, and thus, it seems unlikely that CCK has a direct effect on the blood vessels of the second or third order. CCK did, however, have profound effects on the dynamics of the heart, and without a change in cardiac output, there was a significant increase in the amplitude (59 ± 4%) and rate (dQ/d t: 55 ± 4%; -dQ/d t: 208 ± 49%) of the phasic flow profile. If and how this might be coupled to a postprandial gastrointestinal hyperemia remains to be determined. We conclude that CCK has the potential as a regulator of the postprandial gastrointestinal blood flow in fish and most likely has its effect by inducing a gastrointestinal hyperemia. The mechanism by which CCK acts is at present unknown.


2009 ◽  
Vol 296 (2) ◽  
pp. R345-R352 ◽  
Author(s):  
Henrik Seth ◽  
Erik Sandblom ◽  
Michael Axelsson

Mechanical gastric distension induces a dorsal aortic pressor response in rainbow trout ( Oncorhynchus mykiss) with no change in gastrointestinal blood flow. To elucidate what role chemical stimuli from the digested food has on the postprandial cardiovascular response, a new method was developed to investigate the contribution of individual nutrient components. Three predigested experimental diets were injected directly into the proximal intestine of rainbow trout and cardiac output (CO), gut blood flow (Qcma), heart rate (HR), and stroke volume (SV) were recorded. Specific dynamic action (SDA) was estimated by measuring oxygen consumption. When a balanced diet (50% protein, 25% fat, 15% carbohydrate) was injected, Qcma and CO increased within 1 h by 45 and 27%, respectively. The response to a high-protein diet (70% protein, 5% fat, 15% carbohydrate) was quantitatively similar but delayed, with a maximal blood flow response after 2 h. With a high-lipid diet (60% fat, 15% protein, 15% carbohydrate), the peak increase in Qcma by 22% occurred after 30 min and thereafter declined rapidly. The SDA response (19%) to the balanced diet was temporally matched with the hyperemia. With a high-protein diet, the response is delayed and enlarged (34%) compared with the balanced diet. The high-lipid diet gave no significant SDA response. We conclude that the chemical composition of the food influences the postprandial hyperemia and the SDA, such that the components appear to work in a synergistic fashion. The present results also demonstrate that both redistribution of blood flow and an overall increase in CO contribute to the postprandial increase in gut blood flow in this species.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jeroen Brijs ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Nicolas Pichaud ◽  
Catharina Olsson ◽  
...  

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