Inotropic responses of the left ventricle to changes in aortic arch pressure in anaesthetized dogs

1. Inotropic changes in the left ventricle in chloralose anaesthetized dogs were determined in response to changes in non-pulsatile pressure perfusing the vascularly isolated aortic arch.2. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) in preparations in which heart rate, mean ascending aortic pressure and brachiocephalic (i.e. carotid sinus and cerebral) perfusion pressure were held constant.3. dP/dt max increased (average +43%) when aortic pressure was reduced from a level above that which produced maximum depression of the myocardium to a level below which no further responses could be obtained; responses occurred as aortic arch pressure was changed between 250 and 90 mm Hg.5. In the same preparations changes in the brachiocephalic artery perfusion pressure with aortic arch pressure held constant resulted in similar inotropic responses.6. It is suggested that aortic arch baroreceptors may be of importance in the control of the inotropic state of the heart.     

Reflex inotropic responses of the heart from lung inflation in anaesthetized dogs

In anaesthetized dogs a tracheal divider was inserted to allow inflation of one lung with various pressures. Left ventricular inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) using a preparation in which aortic pressure, carotid sinus pressure and heart rate were held constant.Heart responses to lung inflation were variable. In five dogs there was a consistent tachycardia, in three bradycardia and in six there was no change. In the dogs in which heart rate increased, inflation of one lung with pressures between 0.5 and 2.0 kPa (5 and 20 cm H₂O) resulted in no significant change in dP/dt max. In the remaining dogs there was a decrease in dP/dt max which was more pronounced at the higher inflation pressures. The negative inotropic response was shown to be a reflex with afferent nerve endings in the lung and with the efferent pathway in the sympathetic nerves.     

The inotropic effect on the heart of stimulating the vagus in the dog, duck and toad

1. The chronotropic and inotropic effects of stimulating the vagus on the hearts of the dog, duck and toad were studied.2. The maximum rate of rise of pressure in the left ventricle (dP/dt max) measured at a constant heart rate and mean aortic pressure was used as an index of the inotropic changes.3. The sensitivity of dP/dt max as an index of inotropic changes brought about by stimulating the vagus was established in the toad where a 49% reduction in heart rate was associated with a 30% reduction in dP/dt max.4. In the dog stimulation of the vagus resulted in a reduction in heart rate of 38% and only a small reduction in dP/dt max of 6%.5. Results similar to those found in the dog were obtained in the duck where the reduction in heart rate of 44% was associated with reduction in dP/dt max of only 3%.6. It is concluded that the vagus has only a small and negligible negative inotropic effect on the ventricles of the dog and duck.     

Effects of graded pulsatile pressure on the reflex vasomotor responses elicited by changes of mean pressure in the perfused carotid sinus-aortic arch regions of the dog

1. In the anaesthetized dog, the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. We have confirmed our previous observations that under steadystate conditions the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in carotid sinus pulse pressure, whereas those evoked by changes of mean aortic arch pressure are only weakly affected by modifications of aortic pulse pressure.3. When the carotid sinus and aortic arch regions are perfused in combination at constant pulse frequency (110 c/min), the relationship between mean carotid sinus-aortic arch pressure and systemic arterial perfusion pressure is dependent on the size of the pulse pressure.4. Increasing the pulse pressure alters the curve relating the mean carotid sinus-aortic arch pressure to systemic arterial perfusion pressure in such a way that the perfusion pressure is lower at a given carotid sinus-aortic arch pressure within the range 80-150 mm Hg. The larger the pulse pressure, up to about 60 mm Hg, the greater the fall in systemic arterial perfusion pressure. Above a mean carotid sinus-aortic arch pressure of about 150 mm Hg, alterations of pulse pressure have little effect.5. There is a family of curves representing the relation between mean carotid sinus-aortic arch pressure and systemic vascular resistance, depending on the pulse pressure.     

The maximum derivatives of left ventricular pressure and transverse internal diameter as indices of the inotropic state of the left ventricle in conscious dogs

1. In normal, conscious dogs, I.V. infusion of isoprenaline caused inases in heart rate and the maximal derivatives of left ventricular pressure (dP/dt max) and left ventricular internal diameter (dD/dt max). The changes in both derivatives were linearly related to the increase in heart rate.2. Increments in heart rate produced by right atrial pacing caused only minimally significant increases in both dP/dt max and dD/dt max at heart rates of 180 beats/min. Increases in heart rate, with end diastolic diameter maintained constant, resulted in small but significant increases in dP/dt max and no significant increase in dD/dt max.3. Increasing preload by volume infusion had little effect on either derivative, while increasing afterload by phenylephrine administration produced a small but significant increase in dP/dt max and no change in dD/dt max.4. Both dP/dt max and dD/dt max are equally reliable as indices of the inotropic state of the myocardium and are minimally influenced by changes in preload, afterload or heart rate.     

The effect of changes in cardiac frequency on left and right ventricular dP/dt max at different contractile states of the myocardium

Summary In 17 canine heart-lung preparations the dependence of frequency potentiation of the right and left ventricular myocardium on the basic inotropic state of the heart was investigated. The effect of unipolar stimulation of the right atrium on dP/dt max in both ventricles was measured. The aortic pressure was maintained constant.Shortly after isolation of the heart, a stepwise increase of rate from 140 to 200 beats/min only had a very weak influence on left ventricular dP/dt max. With deterioration of the myocardium the frequency potentiation of dP/dt max increased considerably. End-diastolic pressure regularly decreased with rising cardiac frequency. Since the real positive inotropic effect is masked by the concomitant fall in diastolic loading, the end-diastolic pressure was maintained constant in a second group of 8 hearts during rate variation. The most pronounced inotropic effect was now found shortly after isolation of the heart. A rate increase of 30 beats/min resulted in a 20% rise of dP/dt max. The frequency potentiation decreased with deterioration of the heart resulting in a 12% dP/dt max increase at an estimated inotropic state of 50% of control. When the contractile state of the heart was improved above the control state by calcium application the frequency potentiation of the myocardium decreased.In the right ventricle similar results were obtained except for the fact that no significant correlation between the steepness of the frequency characteristics and the contractile state of the heart could be found when the end-diastolic pressure was kept constant.Portions of this study have been presented at the 45th Congress of the German Physiological Society     

Chronotropic and inotropic effects on the dog heart of stimulating the efferent cardiac sympathetic nerves

1. The chronotropic and inotropic responses of the dog heart to stimulation of the ansae subclaviae were studied.2. The maximum rate of rise of pressure in the left ventricle (dP/dt max) was used as an index of the inotropic changes.3. In experiments in which the secondary inotropic effects of changes in heart rate and blood pressure were prevented it was shown that, using stimuli which produced the same chronotropic response, stimulation of the left ansa subclavia resulted in an inotropic change which was about eight times greater than that which resulted from stimulation of the right ansa subclavia.4. In experiments in which heart rate and blood pressure were allowed to change freely it was shown that the secondary inotropic effects of changes in blood pressure and heart rate amounted to about 70% of the total inotropic change when the right ansa subclavia was stimulated and about 20% of the total change when the left ansa subclavia was stimulated.     

Adrenal contribution to coronary regulation in the newborn.

Evidence for adrenergic regulation of the coronary vessels was sought in 27 newborn lambs. Sympathetic activity was altered by temporarily lowering cephalic perfusion pressure (CPP) from 90 to 20 mmHg while aortic pressure was held constant. Heart rate (HR) and left ventricular dP/dt max increased markedly, while end-diastolic pressure and stroke volume fell. These changes were accompanied by an increase in coronary blood flow (CBF), myocardial O2 consumption (MVO2), and reduced coronary resistance (CF) (P less than 0.005). After beta blockade, which prevented an augmentation of metabolic demand, the same maneuver resulted in coronary vasoconstriction, reflected by reduced CBF and increased CR (P less than 0.02). This response was eliminated by alpha blockade with phentolamine (2 mg/kg). In 13 lambs subjected to bilateral adrenalectomy or sham operation, lowering CPP elicited similar positive chronotropic and inotropic changes, increases of MVO2 and CBF, and reduced CR. Following beta blockade, lowering CPP in the sham group caused coronary constriction. However, no changes in CBF or CR were elicited in the adrenalectomized lambs. These observations indicate that integrity of the adrenal glands is required for adrenergic control of the coronary vessels in the newborn. Chronotropic and inotropic regulation is mediated by direct neural action and is not dependent on adrenal function.     

Reflex effects on the heart of stimulating left atrial receptors

1. Stimulation of left atrial receptors, by distension of the pulmonary vein/left atrial junctions, is known to cause a reflex increase in heart rate; the efferent pathway is known to be solely in the sympathetic nerves.2. In expectation of a concomitant positive inotropic response the effect of stimulating the left atrial receptors on the inotropic state of the left ventricle was studied, using as a known sensitive index of inotropic changes the maximal rate of rise of pressure in the left ventricle (dP/dt max).3. Stimulation of left atrial receptors resulted in an increase in heart rate but there were no significant concomitant changes in dP/dt max.4. It is concluded that activity in this discrete efferent pathway does not include an inotropic effect on the left ventricle and therefore the reflex involves only those sympathetic nerves which innervate the sinu-atrial node.5. The possible function of atrial receptors in the regulation of heart volumes is discussed.     

Hypoxaemia and aortic chemoreceptor function in foetal lambs

1. In foetal lambs the effect of raising and lowering arterial P(O2) (by varying the O(2) content of the maternal inspired gas mixture) was studied in order to determine whether the systemic arterial chemoreceptors regulated the circulation.2. From 0.7 of term relative hypoxaemia (e.g. reducing carotid P(O2) from 40 to 20 mm Hg) caused a rise of arterial pressure and femoral vaso-constriction. These changes were unaffected or even increased by bilateral section of the nerves from the carotid sinus and body. They were abolished by section of the vagi or aortic nerves.3. It is concluded that in foetal lambs during the last third of gestation the circulation is under reflex control by the aortic chemoreceptors.     

Erythropoietin changes contractility, cAMP, and nitrite levels of isolated rat hearts

There is enough evidence that erythropoietin (EPO) may be involved in cardiovascular function. Therefore we have investigated the possible effects of EPO on left ventricular developed pressure, +dP/dt(max), heart rate, tissue cAMP, and nitrite levels. Isolated rat hearts were perfused under constant flow (10 ml/min) conditions with modified Krebs-Henseleit solution and recombinant human erythropoietin at doses of 100, 200, 500, and 1,000 IU/kg was administered as bolus injections. EPO at 100 IU/kg decreased, but higher doses (500 and 1,000 IU/kg) raised the developed pressure and +dP/dt(max). However, it did not affect heart rate or coronary perfusion pressure when all the respective doses were applied. EPO at 100 IU/kg increased nitrite, and at 1,000 IU/kg it raised cAMP. Our results suggest that EPO may produce dose-dependently negative and positive inotropic effects on myocardial contractility in isolated rat hearts. NO and cAMP may be involved in negative and positive inotropic effects of EPO, respectively.     

Baroreflex inhibition of the human sinus node: importance of stimulus intensity, duration, and rate of pressure change.

1. Carotid baroreceptors were stimulated with electronically controlled neck suction in five healthy young men and pulse interval prolongation was measured. Timing of the onset of stimuli in relation to cardiac activity was held constant, and stimulus intensity, duration, and dP/dt were varied independently. 2. In the subjects studied, sinus node responses to neck suction were proportional to dP/dt. However, variations of stimulus dP/dt within or above the normal range for arterial dP/dt did not influence the magnitude of integrated baroreflex responses, or the earliest portion of baroreflex sinus node inhibition. 3. Carotid baroreflex responses were linear over a wide range which extended beyond the normal range for human systolic arterial pressures. 4. Saturation of the carotid baroreceptor-cardiac reflex occurred at distending pressures of about 160 mmHg. 5. The average baroreflex responses of the group studied were highly reproducible over time. 6. Baroreflex gain correlated very strongly with base line pulse interval. 7. The magnitude of baroreflex responses increased linearly with the duration of carotid sinus distension and reached a maximum level with stimuli lasting 0-5 sec or more. 8. The results demonstrate that carotid sinus transfer characteristics can be measured in normal man, and that human response patterns are strikingly similar to those observed earlier in experimental animals.     

Influence of carotid baroreceptors on different components of the vascular system

1. Reflex changes in wall tension of the lateral saphenous vein of one hind limb, the splenic veins and capsule, and the resistance vessels of the other hind limb caused by changes in baroreceptor activity were measured in vagotomized dogs under thiopentone-chloralose anaesthesia.2. Three different methods were used to alter pressure in one or both carotid sinuses. (1) Both carotid sinuses were vascularly isolated and filled with fully oxygenated Krebs-Ringer bicarbonate solution (pH 7.4) from a reservoir in which the pressure could be altered at will. (2) One sinus was denervated, and the contralateral sinus was perfused with arterial blood at different flow rates. (3) One sinus was denervated, and the innervated sinus was perfused with arterial blood at constant flow, the pressure being altered by changing the outflow resistance.3. The left saphenous vein was perfused at constant flow with autologous blood; changes in perfusion pressure were used as a measure of changes in veno-motor activity. The right common iliac artery was perfused at constant flow to measure changes in resistance vessel activity. Blood flow through the spleen was temporarily arrested, trapping a fixed volume of blood in the organ. Under these conditions, changes in splenic vein pressure were a measure of changes in smooth-muscle tension in the splenic capsule and veins.4. In order to assess the responses to baroreceptor stimulation in terms of alterations in sympathetic nerve traffic to different components of the peripheral vascular system, ;frequency-response curves' were constructed for spleen, saphenous vein, and limb resistance vessels by electrical stimulation of the splenic nerves and lumbar sympathetic chains.5. The saphenous vein showed no consistent response to changes in baroreceptor activity. Reduction in carotid sinus pressure from 180 to 100 mm Hg caused an increase in venous pressure in the isovolumetric spleen and in the iliac artery perfusion pressure. These results were confirmed by electrical stimulation of the carotid sinus nerve. Whereas the peak responses of the limb resistance vessels corresponded to an increase in lumbar sympathetic nerve traffic of 6-10 c/s, the maximal splenic responses were equivalent to an increase in splenic nerve traffic of 1-4 c/s. These results are consistent with selective autonomic nervous control of different components of the peripheral vascular system.     

Norepinephrine and isoprenaline induced changes of peripheral blood flow acceleration caused by changes of cardiac inotropy

Summary In anesthetized dogs the norepinephrine (NE) and isoprenaline (ISO) (1–1024 ng/kg i.v.)-induced increase of maximum peripheral flow acceleration (celiac artery, cranial mesenteric artery, renal artery, and femoral artery) and the changes of the maximum first derivative of arterial pressure were compared with the increases of maximum ascending aortic flow acceleration and maximum first derivative of left ventricle pressure (LV dP/dt max).The maximum effect of each dose on maximum acceleration of flows (dF/dt max) and maximum first derivative of pressures (dP/dt max) occurred simultaneously for all variables. The effect was dose-dependent. Sensitivity was similar for NE (D₅₀:2256–512 ng/kg) and for ISO (D₅₀: 128–256 ng/kg).We demonstrated that other variables than inotropic action (heart rate, left ventricular end diastolic pressure and diastolic aortic pressure) played only a minor role in the increases of LV dP/dt max in our studies.In contrast with the uniform response of dF/dt max and dP/dt max, the reaction of peripheral vascular resistance varied. In particular in the gastrointestinal tract the resistance could either be increased (NE, D₅₀: 115 ng/kg) or decreased (ISO, D₅₀: 15 ng/kg). Gastrointestinal resistance was a more sensitive variable for catecholamine stimulation than dF/dt max and dP/dt max.The data show that under the present experimental conditions enhancement of peripheral flow acceleration induced by NE and ISO is due to increase of cardiac inotropy.Supported by the Foundation for Medical Research FUNGO     

Performance of the hypertrophied left ventricle in spontaneously hypertensive rats. Effects of adrenergic stimulation

The performance of isolated hearts from adult male spontaneously hypertensive rats (SHR) and matched normotensive controls (NCR) was investigated in an antegrade perfusion system, where preload and afterload could be varied independently. During electrical pacing of the heart to constant heart rate, increases in afterload, but not in preload, considerably raised cardiac contractility, measured as left ventricular max dP/dt. At afterloads equalling their respective in vivo ones, max dP/dt was similar in SHR and NCR. This indicates that the SHR hearts by myocardial hypertrophy are so well adapted to their raised afterload that an increased inotropic state of the heart is not required. Upon adrenaline addition, SHR and NCR did not differ concerning either "chronotropic sensitivity", i.e. per cent increase in heart rate of the spontaneously beating heart or in "inotropic sensitivity", measured as increase in max dP/dt. However, in this in vitro situation adrenaline increased stroke volume only when the hearts worked at reduced inotropism, induced by lowered temperature (30 degrees C). At maximal inotropic stimulation by adrenaline and occluded outflow, the SHR hearts produced higher systolic pressures than the NCR ones. This reveals an increased maximal contractile capacity of the hypertrophied SHR left ventricle, rather than a reduced one as sometimes suggested.     

Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non-pulsatile pressures in the dog

1. In the anaesthetized dog the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. When the vasosensory areas were perfused at non-pulsatile pressures within the normal physiological range of mean pressures, the reflex reduction in systemic vascular resistance produced by a given rise in mean carotid sinus pressure was significantly greater than that resulting from the same rise of aortic arch pressure.3. On the other hand, when the vasosensory areas were perfused at normal pulsatile pressures and within the normal physiological range of mean pressures, there was no difference in the size of the reflex vascular responses elicited by the same rise in mean pressure in the carotid sinuses and in the aortic arch.4. Whereas the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in pulse pressure, those evoked by the aortic arch baroreceptors through changes of mean pressure are only weakly affected by modifications in pulse pressure. Evidence for this was obtained from single stepwise changes of mean pressure in each vasosensory area during pulsatile and non-pulsatile perfusion, and from curves relating the mean pressure in the carotid sinuses or aortic arch and systemic arterial perfusion pressure.5. The vasomotor response elicited by combined stimulation of the carotid sinus and aortic arch baroreceptors was greater than either response resulting from their separate stimulation.6. When the mean perfusion pressures in the two vasosensory areas are changed together, the curve relating mean pressure to systemic arterial pressure during pulsatile perfusion of the areas is considerably flatter than that for non-pulsatile perfusion.7. Increasing the pulse pressure in the carotid sinuses or aortic arch caused a decrease in systemic vascular resistance, the response elicited from the carotid sinuses being the larger.8. Altering the phase angle between the pulse pressure waves in the carotid sinuses and aortic arch had no effect on systemic vascular resistance.9. In both vasosensory areas, increasing the pulse frequency caused a reduction in systemic vascular resistance.     

Contraction and relaxation indices in the study of neural inotropic and loositropic influences on the heart

The possibility of using contraction and relaxation indices for evaluation of inotropic and loositropic influences on the heart was studied in experiments on cats. Increased pre- and afterload were used as the stimuli, which are simultaneously loading and reflexogenic. Under conditions of preserved innervation both stimuli elevated the indices selected according to the highest sensitivity/specificity ratio. Ganglionic blocker arfonad potentiated the effects of these stimuli. This attests to a considerable contribution of the myogenic component to the changes in the studied indices in response to increased pre- and afterload and to the existence of negative inotropic and loositropic influences on the heart under conditions of preserved innervation. These conclusions were supported when more specific indices were used: in most cases they decreased during load tests. Thus, when the contraction and relaxation indices are used for evaluation inotropic and loositropic influences on the heart, it seems reasonable either to compare heart responses under conditions of preserved or blocked innervation, or to apply more specific indices. Analysis of changes in most widely used indices (dP/dt)max and t showed that t reliably reflects neural loositropic influences, while the use of (dP/dt)max without proper control can be erroneous.     

The effect of an increase in aortic pressure upon the inotropic state of eat and dog left ventricles

1. The effect of increased aortic pressure on the inotropic state of the left ventricle was studied in isolated cat hearts, perfused with bovine red cells in Tyrode solution, ejecting into a hydraulic model with the same input impedance as that of the cat aorta.2. Inotropic state was assessed at a controlled left ventricular end-diastolic pressure by interpolating single isovolumic beats by means of an occluder in the aortic cannula.3. When such isovolumic beats during periods of raised aortic pressure were compared with those during control periods, the difference in peak isovolumic pressure ranged from -0.3 to +0.5 kPa indicating differences in inotropic state which were small and inconsistent in direction.4. The maximum rate of rise of left ventricular pressure (dP/dt(max).) of ejecting beats was little affected by a rise of aortic pressure and the direction of changes was inconsistent.5. The effect of increased aortic pressure was studied in intact dogs after cardiac denervation; left ventricular end-diastolic pressure was uncontrolled and therefore rose to a higher steady level.6. No consistent change of dP/dt(max). was found during the period of increased aortic pressure.7. All flow and pressure variables remained steady during the period of increased aortic pressure after the higher level of left ventricular end-diastolic pressure had been established.8. These results demonstrate that neither the positive inotropic effect nor the negative inotropic effect of increased load dominates in these preparations. This may be the result of a balance between the two effects, or they may be of unimportant magnitude under physiological conditions.     

Cerebrovascular transmural pressure and autoregulation

The cerebral blood flow (CBF) response to changes in perfusion pressure mediated through decreases in arterial pressure, increases in cerebrospinal fluid (CSF) pressure and increases in jugular venous pressure was studied in anesthetized dogs. A preparation was developed in which each of the three relevant pressures could be controlled and manipulated independently of each other. In this preparation, the superior vena cava and femoral vein were cannulated and drained into a reservoir. Blood was pumped from the reservoir into the right atrium. With this system, mean arterial pressure and jugular venous pressure could be independently controlled. CSF pressure (measured in the lateral ventricle) could be manipulated via a cisternal puncture. Total and regional CBF responses to alterations in perfusion pressure were studied with the radiolabelled microsphere technique. Each hemisphere was sectioned into 13 regions: spinal cord, cerebellum, medulla, pons, midbrain, diencephalon, caudate, hippocampus, parahippocampal gyrus, and occipital, temporal, parietal and frontal lobes. Despite 30 mm Hg reductions in arterial pressure or increases in jugular venous pressure or CSF pressure, little change in CBF was observed provided the perfusion pressure (arterial pressure minus jugular venous pressure or CSF pressure depending on which pressure was of greater magnitude) was greater than the lower limit for cerebral autoregulation (approximately 60 mm Hg). However, when the perfusion pressure was reduced by any of the three different methods to levels less than 60 mm Hg (average of 48 mm Hg), a comparable reduction (25–35%) in both total and regional CBF was obtained. Thus comparable changes in the perfusion pressure gradient established by decreasing arterial pressure, increasing jugular venous pressure and increasing CSF pressure resulted in similar total and regional blood flow responses. Independent alterations of arterial and CSF pressures, and jugular venous pressure produce opposite changes in vascular transmural pressure yet result in similar CBF responses. These results show that cerebral autoregulation is a function of the perfusion pressure gradient and cannot be accounted for predominantly by myogenic mechanisms.     

Cardiovascular Effects of Blood Borne Material Released from the Gat Small Intestine during Simulated Shock Conditions

Cardiac performance was studied in the cat during and after a mimicked shock situation in the small intestine (regional hypotension at 35 mm Hg during nervous vasoconstrictor fibre activation). Aortic blood flow was measured with an electromagnetic flow probe around the ascending aorta and, in some experiments, maximal dP/dt of the left ventricle was also followed. Upon restoration of intestinal perfusion pressure after a 2 h “shock” period a rapid reduction of aortic flow occurred due to a decreased stroke volume. Concomitantly maximal dP/dt was reduced in the face of an unchanged central venous pressure and left end diastolic pressure. This decline of cardiac performance could be prevented by substituting, during the first posthypotensive min, the intestinal venous blood with fresh blood from a healthy donor animal. However, when the shed intestinal venous blood was retransfused, a rapid decline of cardiac performance was evident. The reduced cardiac function was accompanied by an unchanged or slightly elevated total peripheral resistance. It is proposed that substances released front the “shocked” intestine cause a rapid and pronounced depression of cardiac function.