Post-prandial cardiovascular responses in man after ingestion of carbohydrate, protein or fat.

Changes in cardiac output and in superior mesenteric arterial flow were followed with Doppler ultrasound techniques in five young, healthy persons for 2 h after ingestion of medium-sized (4 MJ), fluid meals containing either carbohydrate, protein, fat or water only. Measurements were carried out before meals and at regular post-meal intervals, during which mean arterial blood pressure was also followed. All energy-containing meals caused marked and gradually developing post-prandial increases in cardiac output as well as in superior mesenteric arterial flow. The maximum flow levels were reached in the course of 30-60 min and maintained until the observations ended after 2 h. The intake of water caused no such flow increases. There were considerable interpersonal variations in the size and in the speed of development of the flow increases after the three types of energy-containing meals. The flow-increasing effects of the three meal types were not significantly different, even if the most marked increases (median values about 11 min-1 for both cardiac output and superior mesenteric arterial flow) occurred after carbohydrate meals. The marked effects on circulation of the three food components were also revealed in the calculated, integrated amounts of 'extra' cardiac output and superior mesenteric arterial flow observed in the course of the 2 h following the meal. Values of more than 100 1 for such 'extra' flows were seen after carbohydrate meals. The marked ingestion-released increase in blood flow to the splanchnic organs is apparently partly met by an increase in cardiac output, and partly by some redistribution of flow, which benefits the digestive system.     

The effect of meal size on postprandial increase in cardiac output

Heart rate, stroke volume, cardiac output and mean arterial blood pressure were followed from the resting primal situation and for 2 hours after intake of standardized meals in four healthy individuals. Continuous records of stroke volume and cardiac output were achieved with an improved method of Doppler ultrasonography. A smallish meal and one 2 1/2 times larger were both given twice and in random order to each of the four test persons. The consumption of a meal invariably resulted in a cardiac output increase, which developed gradually to reach a maximum level 30 to 60 min after end of the meal. The postprandial cardiac output increase resulted from significant increases in both heart rate and stroke volume. There were distinct and significant differences between the circulatory responses to small and large meals. The increase in cardiac output after a large meal was considerably larger and lasted for longer than the increase after a small meal. Two hours after a small meal cardiac output was nearly or fully back to pre-meal values, while cardiac output was still markedly elevated 2 hours after a large meal. Consequently, the total ‘extra’ amount of blood delivered by the heart over 2 post-meal hours was significantly — about 100%— larger after the large meal than after the small one. Mean arterial blood pressure either fell or remained almost unchanged in the hour after a meal, so that total peripheral resistance was consistently and significantly reduced in the postprandial period — and considerably more so after a large meal than after a small one.     

Priority of blood flow to splanchnic organs in humans during pre- and post-meal exercise

Cardiac output and superior mesenteric arterial flow in five healthy young men were followed using Doppler ultrasound techniques at rest and during 4 min bouts of bicycle exercise in both a pre- and a post-meal situation. The meal given was mixed and heavy, with an energy content (related to body size) of about 1400–1600 kcal (5.9-6.9 MJ). Two levels of exercise, 50–65 W and 150–200 W (about 75% of Vo_tmax), were tested, with the subjects cycling in a reclining position. Superior mesenteric arterial flow increased threefold, to about 1.11 min^-1, after the meal. During exercise in the fasting situation there were only modest changes in splanchnic vascular conductance, and moderate increases in superior mesenteric arterial flow were actually recorded. Exercise in the post-prandial state caused appreciable reductions in splanchnic vascular conductance, and a 38% reduction was observed during the most heavy exercise. However, not even such a decrease in conductance resulted in any definite reduction in superior mesenteric arterial blood flow, which was maintained at the pre-exercise level. Cardiac output increased by about 1.3 1 min^-1 after the meal. The exercise-induced increases in cardiac output were of the same order in the fasting and in the post-prandial state. Variance analyses showed the high cardiac output levels reached during postprandial exercise to be no different from levels that would be reached by pure summation of the changes caused by eating alone and by exercise alone. It is concluded that blood flow to the splanchnic organs in reclining man retains its high pre- and post-prandial priority during short exercise bouts of up to 75% of Vo_Smax.     

Circulatory responses to a meal in patients with a newly transplanted heart

It is well established that consumption of a meal releases a gradually developing and quite marked increase in blood flow to the gastrointestinal organs and a similar and simultaneous increase in cardiac output (CO). It is not known through which mechanism the pumping of the heart adjusts so accurately to the gastrointestinal flow increase. We have approached this problem by serving a standardized, mixed meal to five patients with recently transplanted and thus denervated hearts and to five sex- and age-matched controls. Pre- and postprandial levels of CO and blood flow in the superior mesenteric artery (SMA) were recorded with Doppler ultrasound technique. The patients with transplanted hearts had significantly higher preprandial levels of heart rate (HR) and CO than the controls. With a timing similar to that seen in the controls did all five patients develop considerable and synchronous postprandial increases in superior mesenteric arterial flow and in CO. Increases in superior mesenteric arterial flow were significantly greater than the controls. Also, COs, high even before meals were given, increased further and to the same relative extent as in the control persons. The marked postprandial increase in CO, probably secondary to the increase in intestinal blood flow, could hardly come about through any sort of nervous reflex to the recently transplanted and denervated hearts. It appears more likely that a humoral connection of some sort exists between the two circulatory events.     

Involvement of the human splanchnic circulation in pressor response induced by handgrip contraction

We have analysed the adjustment of blood flow and vascular conductance in the abundantly supplied splanchnic circulation to a generally released pressor reaction. Pressor responses were induced by 2-min periods of standardized, sustained handgrip in seven healthy students. The effects of handgrip tests were followed both in the fasting state and after the consumption of a substantial, mixed meal. In the first of the two sessions, changes in superior mesenteric artery blood flow were recorded and concomitant changes in local vascular conductance derived. In the other session, pressor released cardiac output changes were recorded and changes in total peripheral vascular conductance derived. Both types of flow changes were recorded using ultrasound Doppler technique. Typically, blood flow in the superior mesenteric artery increased two- to threefold after a meal. Handgrip contractions induced an initial rapid increase in heart rate, cardiac output and total peripheral conductance, followed by a gradual decline in total peripheral conductance and stroke volume and a gradual increase in heart rate and mean arterial pressure for the rest of the period. At the end of 2-min pressor periods, total peripheral conductance was only about 10% below the pre-handgrip level, whereas vascular conductance locally in the area of the superior mesenteric artery decreased by some 30%. Thus, it appears that the splanchnic vascular bed contributes markedly to the compound pressor response. Handgrips caused significantly less reduction in local vascular conductance in the post-prandial than in the pre-prandial state, indicating that blood flow to the digesting gastrointestinal tract retains a relatively high priority also in a pressor situation.     

The effect of a meal on cardiac output in man at rest and during moderate exercise

Cardiac output at rest increased by 11-63% in a group of healthy individuals after the consumption of a medium-sized, mixed meal. The maximum post-prandial levels of cardiac output were reached from 10 to 30 min after termination of the meal. Cardiac output values at rest fluctuate around a mean level, and this fluctuation was considerably more marked after a meal, when changes in cardiac output from one 15-s period to another could be of the order of 1-1.5 l min-1. Recording of flow in the superior mesenteric artery before and also after a meal was successful in two subjects in whom anatomical conditions were favourable. Flow in the artery was approximately doubled from the fasting to the post-prandial situation, an augmentation that accounted for about 50% of the concomitant increase in cardiac output. The increases in cardiac output caused by 2-min bouts of standardized, moderate and rhythmic exercise were consistently larger in the post-prandial than in the fasting situation. It thus appears that any tendency for redistribution of blood flow, for example from the gastrointestinal tract to the working muscles, during moderately intense exercise is less marked after a meal than before.     

Changes in cardiac output and peripheral flows on pentobarbital anesthesia in the rat

In rats chronically implanted with an electromagnetic flow probe around the ascending aorta, terminal aorta, or superior mesenteric artery as well as arterial and venous indwelling catheters, changes in cardiac output, hindquarter flow, splanchnic flow, and arterial pressure on pentobarbital anesthesia were observed. On intravenous injection of pentobarbital sodium at 30 mg/kg, arterial pressure dropped acutely from an average value of about 105 mmHg to a minimum of about 75 mmHg in about 5 min and then gradually recovered to an average level of about 90 mmHg in 30 min. Cardiac index gradually decreased about 30% on the average in 30 min. Hindquarter flow decreased about 25%. Superior mesenteric flow first increased about 40% within 5 min and then returned almost to the premedication level in 30 min. In adrenalectomized rats there was no decrease of hindquarter flow on pentobarbital anesthesia. The increase in superior mesenteric flow immediately after pentobarbital injection remained almost unchanged after adrenalectomy or splanchnicectomy. It is concluded that an appreciable portion of the decrease in cardiac output on pentobarbital anesthesia is induced by inhibition of tonic adrenomedullary secretion which has a dilating effect on muscle blood vessels through stimulation of beta-receptors. The marked increase in splanchnic flow immediately after pentobarbital injection, which is responsible for the concomitant drop in arterial pressure, is considered to be induced by a direct inhibitory effect of the anesthetic on splanchnic blood vessels.     

Involvement of the human splanchnic circulation in pressor response induced by handgrip contraction.

We have analysed the adjustment of blood flow and vascular conductance in the abundantly supplied splanchnic circulation to a generally released pressor reaction. Pressor responses were induced by 2-min periods of standardized, sustained handgrip in seven healthy students. The effects of handgrip tests were followed both in the fasting state and after the consumption of a substantial, mixed meal. In the first of the two sessions, changes in superior mesenteric artery blood flow were recorded and concomitant changes in local vascular conductance derived. In the other session, pressor released cardiac output changes were recorded and changes in total peripheral vascular conductance derived. Both types of flow changes were recorded using ultrasound Doppler technique. Typically, blood flow in the superior mesenteric artery increased two- to threefold after a meal. Handgrip contractions induced an initial rapid increase in heart rate, cardiac output and total peripheral conductance, followed by a gradual decline in total peripheral conductance and stroke volume and a gradual increase in heart rate and mean arterial pressure for the rest of the period. At the end of 2-min pressor periods, total peripheral conductance was only about 10% below the pre-handgrip level, whereas vascular conductance locally in the area of the superior mesenteric artery decreased by some 30%. Thus, it appears that the splanchnic vascular bed contributes markedly to the compound pressor response. Handgrips caused significantly less reduction in local vascular conductance in the post-prandial than in the pre-prandial state, indicating that blood flow to the digesting gastrointestinal tract retains a relatively high priority also in a pressor situation.     

A pressor response to vibration in conscious rats

Cardiovascular response in an alerted state induced by vibration was studied in conscious rats by giving a to-and-fro movement to their cages for 30 sec. Cardiac output, superior mesenteric flow, and hindquarter flow were observed with chronically implanted electromagnetic flow probes and arterial pressure with an indwelling catheter. Arterial pressure, heart rate, cardiac output and hindquarter flow increased and superior mesenteric flow decreased with vibration. The increase in heart rate was still present after adrenalectomy, but was abolished by beta-adrenoceptor blockade propranolol. The increase in hindquarter flow was greatly diminished by propranolol or after adrenalectomy, but was still present in adrenalectomized rats after alpha-adrenoceptor blockade phentolamine. The decrease in superior mesenteric flow in vibration was abolished by phentolamine. It was diminished by adrenalectomy. These findings indicate that the cardiovascular response to vibration includes excitation of the cardiac sympathetic nerves, adrenomedullary secretion, and excitation of sympathetic vasoconstrictor fibers and exercise hyperemia in skeletal muscles.     

Cardiovascular changes during spontaneous micturition in conscious cats.

The hemodynamic changes occurring during spontaneous micturition were recorded in conscious cats. Arterial blood pressure was continuously measured by chronically implanted arterial catheter, heart rate (HR) by a cardiotachometer, and cardiac output (CO), superior mesenteric (MF), renal (RF), and external iliac blood flows (IF) by chronically implanted electromagnetic flow probes. Spontaneous micturition was accompanied by little change in mean arterial pressure (-9.7 +/- 0.7%), but by a marked decrease in HR (-49.0 +/- 1.2%) and CO (-28.6 +/- 2.5%), and therefore by a marked decrease in total peripheral conductance (-21.0 +/- 3.5%). Visceral and hindlimb blood flows were markedly reduced during micturition (MF, -34.7 +/- 2.1%; RF, -22.6 +/- 1.5%; and IF, -48.7 +/- 1.5%, respectively) due to a marked reduction in regional conductances in both these areas. The vasomotor changes in the regional circulations were prevented by local sympathectomy. Thus spontaneous micturition is associated with marked changes in cardiac function and systemic circulation. Cardiac output is decreased, but diffuse nervous systemic vasoconstriction compensates for this and provides maintenance of arterial blood pressure level.     

Blood flow redistribution during spontaneous wheel walk of the rat

Changes in regional blood flow and arterial pressure in the rat during spontaneous walk in a wheel were observed. An electromagnetic flow probe was implanted around the carotid, superior mesenteric, or renal artery, or the terminal aorta and a catheter for pressure measurement was inserted into the terminal aorta or the common carotid artery. The wheel had a diameter of 35 cm and rotated passively as the rat walked. When hindquarter (terminal aortic) flow increased markedly during wheel walk, carotid flow decreased, superior mesenteric flow decreased or remained unchanged, and renal flow did not change. Arterial pressure remained almost unchanged and heart rate increased an average of about 10%. Semiquantitative considerations indicated that arterial pressure was maintained in the face of the profuse increase in hindquarter flow during wheel walk by an increase in cardiac output rather than shifts of blood flow from other regions.     

The effects of intraportl infusions of glucagon on the hepatic arterial and portal venous vascular beds of the dog: Inhibition of hepatic arterial vasoconstrictor responses to noradrenaline

The sympathetically-innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously in situ. Glucagon was infused into the hepatic portal vein (1–10 g/min); it caused increases in hepatic portal vascular resistance and tended to reduce the hepatic arterial vascular resistance. Extrahepatic effects of intraportal infusions of glucagon included increases in superior mesenteric blood flow and heart rate and falls in systemic arterial pressure.A test dose of noradrenaline (10 g) injected into either the hepatic artery or the portal vein caused both hepatic arterial and portal venous vasoconstriction. The hepatic arterial constrictor responses to noradrenaline were antagonized intraportal infusions of glucagon. In contrast, intraportal glucagon did not antagonize the portal constrictor responses to intraarterial or intraportal noradrenaline.Elevated portal blood glucagon concentrations may protect the hepatic arterial blood flow from vasoconstriction due to elevated systemic levels of vasoactive substances including catecholamines.     

Hemodynamic characteristics of conscious deoxycorticosterone acetate hypertensive rats

An electromagnetic flow probe was chronically implanted around the common carotid, superior mesenteric, or renal artery or the terminal aorta in deoxycorticosterone acetate (DOCA) hypertensive rats (prepared with DOCA and saline after uninephrectomy) and uninephrectomized control rats. A catheter for pressure measurement was inserted into the terminal aorta through a femoral artery. At rest the carotid and hindquarter (measured at the terminal aorta) blood flows in DOCA hypertensive rats were similar to the respective, corresponding values in normal rats with intact bilateral kidneys. The group mean of superior mesenteric flow was about 70% and that of renal flow about 40% larger than in normal rats. Cardiac output was estimated to be greater in DOCA hypertensive rats than in normal rats. In uninephrectomized control rats, superior mesenteric flow was larger than in normal rats to such an extent that an increase in cardiac output was assumed as in DOCA hypertensive rats, but renal flow was normal (about twice the unilateral renal flow in normal rats). Estimation of regional sympathetic vasoconstrictor tone from the decrease in peripheral resistance with hexamethonium and vasopressin antagonist revealed a substantial tone also in the superior mesenteric and hindquarter areas, where the tone was estimated to be almost absent in normal rats and uninephrectomized rats. It is suggested that hypertension in DOCA hypertensive rats is sustained by an increase in cardiac output and an elevation of vasoconstrictor tone in resistance vessels. Since increase in cardiac output appears to be similarly present in uninephrectomized control rats, the elevation of sympathetic tone due to administration of DOCA and salt seems to be indispensable for DOCA hypertension.     

Regional blood flow in conscious spontaneously hypertensive rats

In spontaneously hypertensive and normal control rats in the conscious state, blood flow was observed in the carotid artery, superior mesenteric artery, renal artery, and terminal aorta with a chronically implanted electromagnetic flow probe. At rest, flow per body weight was not different between the two groups except at the terminal aorta where it was significantly smaller in hypertensive rats (P less than 0.05). Regional peripheral resistance was higher in hypertensive rats than in normal rats in all the four arteries, but its elevation in the former was not uniform but most marked in the hindquarter area supplied by the terminal aorta. Quantitatively, this area was estimated to contribute about 40% of the total conductance decrease in hypertensive rats in comparison with the control. This suggests the importance of elevation of resistance in muscle blood vessels in hypertension. The contributions from the superior mesenteric area and the bilateral kidneys were estimated to be about 15% each. In the transposition response induced by transposing rats from their home cage to a new cage, the increase in hindquarter flow was significantly greater in hypertensive rats than in normal rats (P less than 0.01). The sum of the mean flows of the four arteries, a measure of cardiac output, was not different between hypertensive and normal rats at rest but greater in the former during transposition response. Elevation of arterial pressure in the response in hypertensive rats but not in the normal rats was ascribable largely to a greater increase in cardiac output in the former than the latter.     

Regional distribution of vasoconstrictor tone in acute spinal rats

Rats, chronically instrumented with an electromagnetic flow probe around the carotid, superior mesenteric, or renal artery, or the terminal aorta as well as having an arterial and venous catheter, were anesthetized with either and submitted to high spinal cord transection. One hour later, when the rats had recovered consciousness and the arterial pressure had recovered partially, hexamethonium was intravenously injected for ganglionic blockade. Peripheral resistance (arterial pressure/regional flow) was decreased significantly by ganglionic blockade in the carotid and renal areas but not in the superior mesenteric and hindquarter (terminal aortic) areas. This suggests the presence of sizable vasoconstrictor tone to resistance vessels in the carotid and renal areas but not in the superior mesenteric and hindquarter areas in the acute spinal rat. This distribution of vasoconstrictor tone is similar to that in intact conscious rats in the resting state and suggests the possibility that the vasoconstrictor tone for resistance vessels in intact rats is also for the most part generated in the spinal cord. Spinal transection decreased blood flow in all the four regions, suggesting a decrease in cardiac output due to dilation of capacitance vessels. It is possible that, in intact rats at rest, the so-called medullary vasomotor center is sending tonic impulses for the most part to capacitance vessels.     

Differential transit of liquids and solid residue through the human ileum

We determined transit of liquids and the solid residue of a mixed meal through the ileocecal region of six healthy men. A multilumen polyvinyl tube was passed from above into a 20-cm segment of terminal ileum, and flow of liquid was assessed by indicator dilution techniques. Three test meals were eaten in random order at 5-hourly intervals. Meal A contained baked beans and polyethylene glycol (PEG 4000). Recovery of PEG 4000 from the ileum served to mark transit of the liquid phase, whereas arrival of solid residue (beans) in the cecum was heralded by a signal of H2 in the breath. PEG 4000 appeared promptly in ileal aspirates, peaking at 1-1.75 h postprandially. Breath H2 excretion was first detected at 1.5-2.5 h after meal A and always peaked later than PEG 4000. When meals shown to be unassociated with generation of breath hydrogen (meals B and C) followed meal A, an augmentation of hydrogen excretion was noted in the early postprandial period. The total volume calculated to pass from ileum to cecum over 24 h was 1,790 +/- 234 ml (range, 1,180-2,515 ml). Ileal flow increased promptly and significantly after each meal (P less than 0.005) and remained high for 3 h or more. These results confirm that, in healthy humans, about 2 liters of chyme pass from ileum to colon each 24 h and ileal flow increases postprandially. They also suggest that the liquid and solid phases of a mixed meal are separate in the ileocecal region.     

Dynamics of canine pancreatic blood flow and of insulin secretion during an intravenous glucose load

Blood flow through the superior pancreaticoduodenal artery of anaesthetized dogs increases immediately after an i.v. glucose load and parallels to glycemia, but not to insulin output. Flow of superior mesenteric, and femoral arteries as well as of portal vein are also enhanced after rapid i.v. injections of glucose or mannitol. Extent and duration of all flow increases are dose-dependent and strongly related to the alterations of arterial plasma osmolality (maximum increase 24 mosmoles/kg). Heart rate, mean arterial blood pressure, and hematocrit remain unchanged after the first test minute. There is a considerable decrease of peripheral vascular resistance in the circulatory regions investigated. Flow through aorta ascendens is augmented for a short time. Possible mechanisms of vasodilatation are reflexes produced by osmoreceptors and/or local effects of osmolality on the tonus of vascular muscle. Within the physiological range pancreatic perfusion does not determine the amount of insulin released.     

Superior mesenteric sympathetic tone in conscious renovascular hypertensive rats

Blood flow in the superior mesenteric artery was observed with a chronically implanted electromagnetic flow probe in two-kidney, one-clip renovascular hypertensive rats (2K1C), one-kidney, one-clip renovascular hypertensive rats (1K1C), and normotensive control rats (NCR) in the conscious state. Arterial pressure was recorded with an indwelling catheter. Superior mesenteric resistance was calculated as arterial pressure divided by superior mesenteric flow. In all three groups of rats, superior mesenteric resistance remained almost unchanged when arterial pressure decreased markedly on ganglionic blockade with hexamethonium bromide. However, subsequent injection of a vasopressin antagonist (Manning compound) decreased superior mesenteric resistance significantly in 2K1C but not in 1K1C and NCR. Injection of vasopressin antagonist alone was without effect on arterial pressure and superior mesenteric flow in the three rat groups. Only 2K1C were judged to have appreciable sympathetic tone in resistance vessels of the superior mesenteric area, which was blocked by hexamethonium but compensated for by secondarily secreted vasopressin.     

Portable arteriovenous rewarming for hypothermia: cardiovascular considerations

In trauma patients, continuous arteriovenous (AV) rewarming can effectively reverse hypothermia even if associated with hypovolemia. In battlefield conditions, however, portable fluid warmers driven by battery power show limited capacities. We studied the efficacy and safety of a portable fluid warmer that utilizes controlled hydrocarbon combustion (nonflame) for heat generation during continuous AV rewarming in a large animal model of hypothermia and hemorrhagic shock. Six dogs (26.1 +/- 0.8 kg) were cooled to a core temperature of 30 degrees C (hypo 1). After rewarming to 37 degrees C, dogs were bled by 20% of their estimated blood volume and cooled again to 30 degrees C (hypo 2) followed by rewarming. We recorded temperature (blood, esophageal, rectal, and bladder), left ventricular performance, hemodynamic parameters including superior mesenteric artery (SMA) flow and blood flow through the fluid warmer. Especially, we measured the effect of the AV-shunt on cardiac output and regional blood flow (superior mesenteric artery). Rewarming after hypothermia took 45 +/- 6 minutes (hypothermia 1) and 55 +/- 6 minutes (hypothermia 2), respectively. The AV-shunt flow was correlated to the cardiac output and affected neither cardiac output nor regional blood flow at any time point during the experiment. Arteriovenous rewarming, using the tested portable fluid warmer, effectively reversed hypothermia without compromising hemodynamics or regional blood flow.     

Dopamine-induced cyclic AMP increase in canine myocardium, kidney and superior mesenteric artery

The effect of dopamine on cyclic AMP levels in tissue slices of canine myocardium and kidney, and in chopped superior mesenteric arterial wall was investigated to identify dopamine receptors. Tissues were incubated in modified Krebs-Henseleit Ringer bicarbonate solution at 37 degrees C for 20 min with test drugs, after 20-min preincubation. In the presence of 3-isobutyl-1-methylxanthine (IBMX), dopamine and apomorphine caused dose-dependent increases in cyclic AMP levels in the myocardium, kidney and superior mesenteric artery. Phentolamine significantly intensified the cyclic AMP-increasing effect of dopamine in the superior mesenteric artery, but it did not influence the cyclic AMP increase caused by dopamine or apomorphine in the myocardium and kidney. Propranolol markedly blocked the effect of dopamine on cyclic AMP levels in all tissues studied. Haloperidol slightly inhibited the effect of dopamine and completely blocked the effect of apomorphine in the myocardium and kidney. These data suggest that dopamine increases cyclic AMP levels by activating predominantly beta-adrenergic receptors and partly dopamine receptors in the canine myocardium, kidney and superior mesenteric artery. The present results also suggest that dopamine acts not only on beta-adrenergic and dopamine receptors but also on alpha-adrenergic receptors in the superior mesenteric artery. Contrary to the activation of beta-adrenergic and dopamine receptors, the activation of alpha-adrenergic receptors resulted in a decrease in cyclic AMP levels in this tissue.