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Biomedical subjects

G Vacca

Publications and source records attributed to G Vacca.

At least 55 records · Page 3Linked to original sources

Development of short-lasting alcohol deprivation effect in sardinian alcohol-preferring rats.

Alcohol deprivation effect (ADE), defined as a temporary increase in voluntary alcohol intake following a period of alcohol abstinence, was evaluated in selectively bred Sardinian alcohol-preferring (sP) rats. Alcohol was initially offered in free choice with water for 35 consecutive days (predeprivation phase). Subsequently, one group of rats was deprived of alcohol for 1, 3, 7, 15, 30, 90 or 180 consecutive days, while the second group had continuous access to alcohol (deprivation phase). Once alcohol was re-presented, alcohol intake in alcohol-deprived rats was recorded 1 and 24 h after alcohol re-presentation and compared to that monitored in alcohol-nondeprived rats over the same time periods (postdeprivation phase). Alcohol deprivation for 3 to 30 days resulted in a significant increase in voluntary alcohol intake only in the first hour of re-access. These results demonstrate the development of ADE in sP rats. However, the rapid return of alcohol intake to control levels is discussed as evidence in favor of a set-point mechanism capable of regulating alcohol-drinking behavior in sP rats.

Alcohol Drinking↗

The role of nitric oxide in the coronary vasoconstriction caused by growth hormone in anaesthetized pigs.

Intravenous injection of growth hormone in anaesthetized pigs has been shown to cause coronary vasoconstriction by antagonizing the vasodilatory effects of 2-adrenergic receptors. Because nitric oxide is believed to modulate or mediate 2-adrenergic effects, the present study was undertaken in the same experimental model to determine the role of nitric oxide in the above response to growth hormone. In fourteen pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous injection of 0.05 i.u. kg-1 of growth hormone at constant heart rate and arterial blood pressure were assessed using electromagnetic flowmeters. In a first control group of six pigs, growth hormone caused a decrease in coronary blood flow which averaged 13.1 % of the baseline values. In a second group of eight pigs, intravenous administration of N-nitro-L-arginine methyl ester (L-NAME) was used to block the endothelial release of nitric oxide. In these pigs, the subsequent injection of growth hormone did not cause any significant changes in coronary blood flow, even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. These results indicated that the coronary vasoconstricting effect of growth hormone, known to involve antagonism of 2-adrenergic vasodilatory effect, was mediated by inhibition of nitric oxide release.

Animals↗

Different sensitivity to ethanol in alcohol-preferring sP and -nonpreferring sNP rats.

BACKGROUND AND OBJECTIVES: Clinical research has proposed that initial sensitivity to ethanol may be negatively correlated with levels of subsequent ethanol intake; consistently, alcohol-preferring P rats were found to be less sensitive to the ataxic and sedative/hypnotic effects of ethanol than -nonpreferring NP rats. The present study investigated the initial sensitivity to the ataxic and sedative/hypnotic effects of ethanol and to the sedative/hypnotic effects of pentobarbital and diazepam in selectively bred Sardinian alcohol-preferring sP and -nonpreferring sNP rats. METHODS: In experiment 1, time to lose (onset) and regain (sleep time) the righting reflex after the acute intraperitoneal (ip) administration of 3.0 and 3.5 g/kg ethanol were measured in sP and sNP rats. In experiment 2, sP and sNP rats were required to perform a motor coordination task on a Rota-Rod after the acute intragastric administration of 2.0, 2.5, and 3.0 g/kg ethanol. Experiment 3 assessed onset and sleep time in sP and sNP rats after the acute injection of pentobarbital (40 mg/kg; ip) and diazepam (15 and 20 mg/kg; ip). RESULTS: In experiment 1, sP rats took shorter times to lose the righting reflex and regained this reflex over longer periods of time and at lower blood ethanol levels than sNP rats. In experiment 2, ethanol affected motor coordination to a greater extent in sP than sNP rats. In contrast, results from experiment 3 showed that sP and sNP rats were not differentially sensitive to the sedative/hypnotic effects of pentobarbital and diazepam. CONCLUSIONS: The results of experiments 1 and 2 suggest that sP rats possess a genetically determined, greater sensitivity to the motor impairing and sedative/hypnotic effects of ethanol than sNP rats. Although caution should be adopted before hypothesizing any comparison to humans, these results may feature sP rats as an experimental model of those subsets of human alcoholics with initial high sensitivity to ethanol challenges. Finally, the results of experiment 3 suggest a minimal involvement of the benzodiazepine and barbiturate recognition sites in the differential sensitivity to ethanol of sP and sNP rats.

Alcohol Drinking↗

The effect of 17beta-oestradiol on regional blood flow in anaesthetized pigs.

1. The present study was designed to investigate the effects of 17beta-oestradiol on the mesenteric, renal, iliac and coronary circulations and to determine the mechanisms involved. 2. In pigs anaesthetized with sodium pentobarbitone, changes in blood flow in the superior mesenteric, left renal, left external iliac and left circumflex coronary arteries caused by intravenous infusion of 17beta-oestradiol at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. 3. In eight pigs, infusion of 2 microg h-1 of the hormone caused an increase in renal, iliac and coronary blood flow without affecting mesenteric blood flow, left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In four pigs, these vasodilator effects were enhanced by graded increases in the dose of the hormone between 1, 2 and 3 microg h-1; the highest dose also caused an increase in mesenteric blood flow. 4. In five pigs, blockade of muscarinic cholinoceptors and adrenoceptors with the intravenous administration of atropine, propranolol and phentolamine did not affect the vasodilator responses caused by infusion of 2 microg h-1 of 17beta-oestradiol. 5. The increases in renal, iliac and coronary blood flow caused by infusion of 2 microg h-1 of 17beta-oestradiol were prevented, respectively, by the injection of Nomega-nitro-L-arginine methyl ester (L-NAME) into the renal artery (five pigs), the iliac artery (five pigs) or the coronary artery (five pigs). In five pigs, all responses were prevented by injection of L-NAME into all three arteries. In two pigs, injection of L-NAME into the mesenteric, renal, iliac and coronary arteries abolished the vasodilator responses to the infusion of 3 microg h-1 of 17beta-oestradiol. 6. The present study shows that intravenous infusion of 2 microg h-1 of 17beta-oestradiol primarily dilated renal, iliac and coronary circulations and that a higher dose of the hormone also caused vasodilatation in the mesenteric vascular bed. The mechanism of these responses was shown to be nitric oxide dependent.

Animals↗

Coronary effects of cyclovirobuxine D in anesthetized pigs and in isolated porcine coronary arteries.

The present study was undertaken in anesthetized pigs and in isolated porcine coronary arteries to determine the primary coronary effects of cyclovirobuxine D. In six pigs, the intravenous administration of 1.5 mg/kg of cyclovirobuxine D whilst preventing changes in heart rate and aortic blood pressure caused increases in left ventricular dP/dtmax and coronary blood flow which respectively averaged 10% and 23.9%. These responses were progressively augmented by graded increases in the dose of the drug (four pigs) and were not affected by blockade of cholinergic and adrenergic receptors (five pigs). Intravenous blockade of nitric oxide synthase (L-NAME, five pigs) abolished both responses, while intracoronary injection of L-NAME (five pigs) abolished only the coronary vasodilatation. In ten isolated coronary segments, cyclovirobuxine D significantly reduced the degree of potassium chloride-induced contraction. This reduction was not affected by inhibition of cyclooxygenase with indomethacin (five segments) or potassium channels blockade with glibenclamide (five segments), but it was abolished by L-NAME (five segments) or removal of endothelium (five segments). The present study showed that cyclovirobuxine D caused a primary effect of coronary vasodilatation, which involved mechanisms related to the endothelial release of nitric oxide.

Animals↗

The role of beta 2-adrenergic vascular receptors in the peripheral vasodilation caused by 17 beta-estradiol in anesthetized pigs.

It has been previously shown in anesthetized pigs that intravenous infusion of 2 microg/h of 17beta-estradiol primarily dilated renal, iliac and coronary circulations, while higher doses of the hormone were required to cause vasodilation also in the mesenteric vascular bed. In the same experimental model, a tonic beta2-adrenoceptor mediated vasodilation, which could be argued to attenuate the vasodilator effect of 17beta-estradiol, has been described. The present study was planned to investigate the role of beta2-adrenergic receptors in the hemodynamic responses of renal and mesenteric vascular beds to 17beta-estradiol. Changes in flow caused by intravenous infusion of 2 microg/h of the hormone at constant heart rate and aortic blood pressure in the left renal and superior mesenteric arteries were assessed using electromagnetic flowmeters. In six pigs, infusion of 17beta-estradiol caused an increase in renal blood flow, which averaged 12.1% of the control values, without affecting mesenteric blood flow. In the same pigs, after hemodynamic variables had returned to the baseline values, blockade of beta2-adrenergic receptors with butoxamine caused an increase in aortic blood pressure and an increase in renal and mesenteric resistance. The subsequent infusion of 17beta-estradiol elicited increases in renal and mesenteric blood flow which respectively averaged 19.6% and 12.8%. Therefore, the present study in anesthetized pigs have shown that the vasodilator responses of the renal and mesenteric circulations to 17beta-estradiol were attenuated and even masked by a tonic beta2-adrenoceptor mediated vasodilation. This indicates that some vasodilator effects elicited by normally used replacement doses of the hormone may not be apparent.

Adrenergic beta-Antagonists↗

Differential light scattering: probing the sonoluminescence collapse.

We have developed a light scattering technique based on differential measurement and polarization (differential light scattering, DLS) capable in principle of retrieving timing information with picosecond resolution without the need for fast electronics. DLS was applied to sonoluminescence, duplicating known results (sharp turnaround, self-similar collapse); the resolution was limited by intensity noise to about 0.5 ns. Preliminary evidence indicates a smooth turnaround on a less than approximately 0.5-ns time scale, and suggests the existence of subnanosecond features within a few nanoseconds of the turnaround.

Journal Article↗

The effect of distension of the uterus on plasma renin activity (PRA) in anaesthetized pigs.

It has recently been shown that distension of the uterus in anaesthetized pigs causes reflex haemodynamic responses through efferent sympathetic mechanisms. The present study was undertaken to determine whether these mechanisms include activation of the renin-angiotensin system. The same methods were used in 14 pigs which were anaesthetized with alpha-chloralose and artificially ventilated. Balloons positioned within the uterus were distended for periods of 30 min by injecting 20 ml of warm Ringer solution. The responses of arterial blood pressure and heart rate were respectively prevented by blockade of alpha-adrenergic receptors with phentolamine and atrial pacing. Changes in plasma renin activity (PRA) were assessed during the last minute of distension by radioimmunoassay of angiotensin I. In each of 10 pigs, distension of the uterus (mean uterine transmural pressure of 17 mmHg) caused an increase in PRA in the absence of changes of interfering haemodynamic variables. In the remaining four pigs, this response was graded by step increments of the distension. The increase in PRA caused by uterine distension was abolished by bilateral section of the renal nerves (five pigs) or by blockade of beta-adrenergic receptors with propranolol. The present study showed that distension of the uterus in anaesthetized pigs primarily caused a reflex increase in PRA. This reflex response was mediated by renal nerves and involved beta-adrenergic receptors.

Adrenergic alpha-Antagonists↗

Stimulation of locomotor activity by voluntarily consumed ethanol in Sardinian alcohol-preferring rats.

Stimulation of motor activity induced by ethanol has been proposed to reflect the positive reinforcing properties of the drug. The present study was designed to assess whether voluntary ethanol intake would stimulate locomotor activity in Sardinian alcohol-preferring (sP) rats, selectively bred for high ethanol preference and consumption. Rats were habituated to a) consume either water alone (water-consuming rats) or ethanol (10%, v/v) as free choice together with water (ethanol-consuming rats) according to a 15-min limited access protocol for 10 consecutive days prior to the test, and b) explore an open field for 10 min immediately after the drinking session in a trial on 3 consecutive days before the test. On the test day, voluntary ethanol consumption in ethanol-consuming rats averaged 1.2 g/kg. Values for activity measures (time spent moving, number of square crossings and number of rearings) were significantly higher in ethanol- than in water-consuming rats at both 5- and 10-min intervals. These results suggest that the euphorigenic effects of ethanol, supposedly represented by the stimulation of locomotor activity, are part of the reinforcing properties of ethanol in sP rats.

Animals↗

Haemodynamic effects of the intravenous administration of growth hormone in anaesthetized pigs.

Administration of growth hormone in humans has been reported variably to affect arterial blood pressure and ventricular contractility. The present study was undertaken in anaesthetized pigs to establish whether increases in the blood levels of growth hormone primarily affect haemodynamic variables and to determine the mechanisms involved. In pigs anaesthetized with pentobarbitone sodium, left circumflex or anterior descending coronary blood flow was measured with an electromagnetic flowmeter. In a first group of 23 pigs, growth hormone administration (0.05 IU kg-1 i.v.) increased aortic blood pressure and reduced coronary blood flow when heart rate and aortic blood pressure were held constant. These responses were augmented by graded increases in plasma levels of growth hormone. The mechanisms of the above responses were studied in a second group of 29 pigs and involved beta2-adrenergic receptors since they were abolished by propranolol or butoxamine but not by atropine, phentolamine or atenolol. The present study showed that administration of growth hormone in anaesthetized pigs primarily increased aortic blood pressure and vasoconstricted the coronary circulation. The mechanisms of these responses involved beta2-adrenoceptor effects.

Adjuvants, Anesthesia↗

The effects of combined distension of the stomach and the descending colon on coronary blood flow in anaesthetized pigs.

The effects of the combined distension of the stomach and the descending colon on coronary blood flow were examined in seven alpha-chloralose anaesthetized pigs whilst preventing changes in heart rate and aortic blood pressure. Changes in coronary blood flow in the left circumflex or anterior descending coronary artery were assessed using electromagnetic flowmeters during distension with Ringer solution of balloons positioned in the viscera. In a first set of studies, graded distension of the stomach with distending volumes of 0.8, 1.1 and 1.4 l always caused graded decreases in coronary blood flow. The additional distension of the descending colon at a distending volume of 0.25 l augmented the response of decrease in coronary blood flow caused by the first two levels of gastric distension, but it did not have any further effect when added to the higher level of gastric distension. Similar results were obtained in a second set of studies in which distension of the stomach at a volume of 0.8 l was additionally performed during graded distension of the descending colon with distending volumes of 0.25, 0.35 and 0.45 l. These effects elicited by combined distension of the two viscera were not affected by the administration of propranolol, but they were abolished by subsequent administration of phentolamine. The results showed that combined distension of the stomach and the descending colon in anaesthetized pigs augmented the reflex response of coronary vasoconstriction and that the response to distension of one viscus was attenuated during increased levels of distension of the other viscus. These combined responses to distension of the two viscera involved efferent sympathetic mechanisms related to alpha-adrenoceptors.

Adrenergic alpha-Antagonists↗

Changes in regional blood flow in response to distension of the uterus in anaesthetised pigs.

The present study was undertaken in anaesthetised pigs to determine the primary reflex effects of distension of the uterus on the peripheral circulation. Experiments were performed in seven pigs anaesthetised with alpha-chloralose and artificially ventilated. Blood flow in the superior mesenteric, left renal and left external iliac arteries was assessed using electromagnetic flowmeters. Distension of the uterus was performed whilst preventing changes in heart rate and aortic blood pressure by injecting 20 ml of warm Ringer solution in a balloon positioned within the viscus (mean transmural pressure of about 18 mmHg). In each pig, distension of the uterus caused decreases in all measured blood flows. In four pigs, these decreases were graded by step increments of distension. In the seven pigs, the responses of decrease in mesenteric, renal and iliac blood flows were not affected by blockade of beta-adrenergic receptors with propranolol, but were abolished by the subsequent blockade of alpha-adrenergic receptors with phentolamine. The present study showed that distension of the uterus in anaesthetised pigs primarily caused reflex vasoconstriction in the mesenteric, renal and iliac vascular beds. This reflex response was mediated by sympathetic mechanisms which involved alpha vascular adrenergic receptors.

Adrenergic beta-Antagonists↗

Reflex haemodynamic responses caused by distension of the uterus in anaesthetized pigs.

The present study was undertaken in anaesthetized pigs to determine whether distension of the uterus reflexly affects the aortic blood pressure, heart rate, left ventricular inotropic state and the coronary circulation. Experiments were performed in 17 pigs anaesthetized with alpha-chloralose and artificially ventilated. Coronary blood flow was measured with an electromagnetic flowmeter positioned around the origin of the left circumflex coronary artery. The uterus was distended by injecting 20 ml warm Ringer solution into a balloon positioned within the uterus (mean transmural pressure of about 17 mmHg). Distension of the uterus without controlling any haemodynamic variable caused an increase in aortic blood pressure. When this response was prevented, an increase in heart rate was obtained in each animal. When the heart rate and blood pressure responses were prevented, the distension did not cause significant changes in the maximum rate of change of left ventricular pressure, but always caused a decrease in mean coronary blood flow. In five pigs, the increase in heart rate and the decrease in mean coronary blood flow were graded by step increments of distension. In six pigs, the haemodynamic responses to distension of the uterus were not affected by the administration of atropine. In 12 pigs, which included the six given atropine, the increase in heart rate was abolished by the administration of propranolol and the increase in aortic blood pressure and the decrease in mean coronary blood flow were abolished by the subsequent administration of phentolamine. In the remaining five pigs, the haemodynamic responses caused by uterine distension were abolished by the administration of bretylium tosylate. The present study showed that distension of the uterus in anaesthetized pigs primarily caused reflex increases in heart rate and aortic blood pressure and coronary vasoconstriction. These reflex responses were mediated by efferent sympathetic mechanisms.

Afferent Pathways↗

Hemodynamic effects of the intravenous administration of cyclovirobuxine D [correction of cyclorirobuxine D] in anesthetized pigs.

The present study was undertaken in anesthetized pigs to determine the primary effects of cyclovirobuxine D [corrected] given intravenously on hemodynamic variables. In eight pigs, the administration of 1.5 mg/kg of cyclovirobuxine D [corrected] caused a small increase in aortic blood pressure. When this response was prevented, a decrease in heart rate was obtained in each of the eight pigs. When this response was also prevented, an increase in the maximum rate of change of left ventricular systolic pressure (left ventricular dP/dtmax) was observed. In four pigs, the decrease in heart rate and the increase in left ventricular dP/dtmax were progressively augmented by graded increases in the dose of cyclovirobuxine D [corrected]. In six pigs, the responses of hemodynamic variables to cyclovirobuxine D [corrected] were not affected by blockade of cholinergic and adrenergic receptors. In a further six pigs, blockade of nitric oxide synthase with N omega-nitro-L-arginine methyl ester did not affect the decrease in heart rate caused by the drug, but abolished the increases in left ventricular dP/dtmax and aortic blood pressure. The present study showed that intravenous administration of cyclovirobuxine D [corrected] primarily caused a decrease in heart rate and an increase in left ventricular inotropic state, which secondarily determined an increase in aortic blood pressure, and suggested that the response of heart rate involved a direct effect of the drug on the heart, while the response of left ventricular contractility was related to mechanisms dependent on the release of nitric oxide.

Anesthesia↗

Reflex coronary vasoconstriction caused by gallbladder distension in anesthetized pigs.

BACKGROUND: Gallbladder distension in anesthetized pigs reflexly increases heart rate and arterial pressure by means of afferent vagal pathways and efferent sympathetic mechanisms. The effect of such distension on the coronary circulation is unknown. The present study was undertaken to determine whether gallbladder distension primarily causes reflex changes in left circumflex blood flow. METHODS AND RESULTS: In 21 pigs anesthetized with sodium pentobarbitone (16) or alpha-chloralose (5), left circumflex blood flow was measured with an electromagnetic flowmeter. A balloon positioned within the gallbladder was distended with volumes of Ringer's solution equal to the volumes of bile previously withdrawn (mean vol: 62 mL; mean gallbladder pressure: 12 mm Hg). Heart rate and arterial pressure were kept constant by atrial pacing and by a pressurized reservoir connected to the left femoral artery. Gallbladder distension always caused a decrease in circumflex blood flow. In 6 of the 16 sodium pentobarbitone-anesthetized pigs, this decrease was graded by step increments of distension. In 5 of these 16 pigs, the decrease in circumflex blood flow was not affected by atropine. In 10 of these 16 pigs, including those given atropine, the response was not affected by propranolol but was abolished by subsequently giving phentolamine. Cervical vagotomy abolished the coronary vasoconstriction in the remaining 6 pigs. In the 5 alpha-chloralose-anesthetized pigs, the response was not significantly affected by cutting the splanchnic nerves but was abolished by subsequent cervical vagotomy. CONCLUSIONS: The present study showed that innocuous distension of the gallbladder in anesthetized pigs caused a reflex coronary vasoconstriction that involved efferent sympathetic mechanisms related to alpha-adrenoceptors and afferent vagal pathways.

Adjuvants, Anesthesia↗

The effects of hypertonic saline solution on coronary blood flow in anaesthetized pigs.

1. The effects of intracoronary bolus infusion of hypertonic saline solution on left circumflex coronary blood flow were examined in sixteen anaesthetized and artificially ventilated pigs whilst preventing changes in heart rate and arterial blood pressure. 2. In fourteen pigs, bolus infusion of 7.5% hypertonic saline solution (2 ml within 30 s) caused a steady-state increase in coronary blood flow without significantly affecting right atrial or left ventricular pressure and its rate of rise (dP/dtmax). Infusing normal saline solution (0.9%) at the same rate and volume in seven pigs did not have this effect. 3. In five pigs, the magnitude and the duration of the response of increase in coronary blood flow were increased in a graded manner by graded increases in the concentration of the hypertonic saline solution between 2.5, 5 and 7.5%. 4. In nine pigs, the response of increase in coronary blood flow to the bolus infusion of hypertonic saline solution was not affected by the blocking agents atropine, propranolol and phentolamine, but it was completely abolished in the same nine pigs by the subsequent intracoronary administration of N omega-nitro-L-arginine methyl ester (L-NAME) which blocks the synthesis of endothelium-derived relaxing factor (EDRF) and in seven pigs by solely giving L-NAME. 5. These results showed that the intracoronary bolus infusion of hypertonic saline solution in anaesthetized pigs caused a coronary vasodilatation which involved mechanisms dependent on the release of EDRF.

Adrenergic alpha-Antagonists↗

The effect of distension of the stomach on peripheral blood flow in anaesthetized pigs.

The present study was undertaken in anaesthetized pigs to determine the primary reflex effects of gastric distension on the peripheral circulation. Changes in blood flow in the splenic, superior mesenteric, left renal and left external iliac arteries were assessed using electromagnetic flowmeters during distension of a balloon in the stomach, performed at constant aortic blood pressure and heart rate, with 0.6 l of Ringer solution (mean gastric transmural pressure of about 12 mmHg). In fourteen pigs, a decrease in splenic, renal and iliac flows and variable changes in mesenteric flow were obtained. A decrease in mesenteric flow and more marked decreases in the other flows occurred in response to the distension after the administration of propranolol or butoxamine. In five pigs, the vasoconstrictive responses were graded by step increments in gastric distending volume from 0.4 to 0.8 l. The above responses were abolished by the administration of phentolamine (eight pigs) and by bilateral cervical vagotomy (six pigs). The results showed that innocuous distension of the stomach in anaesthetized pigs reflexly caused vasoconstriction in the splenic, renal and iliac vascular beds; vasoconstriction also occurred in the mesenteric vascular bed but only after beta-blockade. These reflex responses were mediated by sympathetic mechanisms which involved both alpha and beta vascular adrenoceptors and their afferent limb was in the vagal nerves.

Analysis of Variance↗

The effects of distension of the stomach and the descending colon on phasic coronary blood flow in the anesthetized pig.

Previous studies in anesthetized animals showed that distension of the stomach or the descending colon primarily caused decreases in mean coronary blood flow. Whether these responses occurred during systole or diastole was not investigated. The present work was planned to study the primary effects of the distension of the two viscera on phasic coronary blood flow in the anesthetized pig. In ten animals, the stomach and the descending colon were distended at constant volume by injecting warm Ringer solution into intravisceral balloons (0.8 and 0.25 l respectively) while preventing changes in heart rate and arterial blood pressure. Distensions of the stomach or the descending colon caused a decrease in mean coronary blood flow in each pig. However, the decrease elicited by gastric distension occurred only during diastole, while the decrease caused by descending colon distension involved both systolic and diastolic coronary blood flows. The same effects on phasic coronary blood flow were observed during experiments in which the decreases in mean coronary blood flow elicited by distension of the stomach or the descending colon were further augmented by adding the distension of the second viscerum. The results indicate that the coronary vasoconstriction caused by gastric distension mainly involves the vessels which supply the subendocardial layers of the myocardium, while that caused by descending colon distension also involves the vessels which supply the subepicardial layers. The vasoconstrictor effect on the subendocardial coronary circulation is enhanced by the combined distension of the two viscera.

Animals↗