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

The Journal of Physiology

Grossini

et al. 2002

This work was undertaken to study the effects of testosterone on the coronary, mesenteric, renal and iliac circulations and to determine the mechanisms of action involved. In prepubertal pigs of both sexes anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary, superior mesenteric, left renal and left external iliac blood flow caused by intra‐arterial infusion of testosterone were assessed using electromagnetic flowmeters. Changes in heart rate and arterial blood pressure were prevented by atrial pacing and by connecting the arterial system to a pressurized reservoir containing Ringer solution. In 12 pigs, intra‐arterial infusion of testosterone for 5 min to achieve a stable intra‐arterial concentration of 1 μg l−1 increased coronary, mesenteric, renal and iliac blood flow without affecting the maximum rate of change of left ventricular systolic pressure (left ventricular dP/dtmax) and filling pressures of the heart. In a further five pigs, a concentration‐response curve was obtained by graded increases in the intra‐arterial concentration of the hormone between 0.125 and 8 μg l−1. The mechanisms of these responses were studied in the 12 pigs by repeating the experiment after haemodynamic variables had returned to the control values before infusions. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the responses caused by intra‐arterial infusion of testosterone performed to achieve a stable intra‐arterial concentration of 1 μg l−1. In the same pigs and in the remaining six pigs, the increases in coronary, mesenteric, renal and iliac blood flow caused by intra‐arterial infusion of testosterone performed to achieve a stable intra‐arterial concentration of 1 μg l−1 were prevented by intra‐arterial injection of Nω‐nitro‐L‐arginine methyl ester. The present study shows that intra‐arterial infusion of testosterone dilated coronary, mesenteric, renal and iliac circulations. The mechanism of this response involved the release of nitric oxide.

Section: Discussionmentioning

confidence: 99%

The effect of testosterone on regional blood flow in prepubertal anaesthetized pigs

Molinari

The Journal of Physiology

Grossini

et al. 2002

“…The dose of atropine has been shown to abolish the vagally-mediated component of the reflex decrease in coronary blood flow caused by urinary bladder distension in anaesthetized dogs [6] and has been used previously in anaesthetized pigs to block coronary cholinergic receptors [27]. The phentolamine dose abolishes the reflex increase in aortic blood pressure to descending colon distension in anaesthetized dogs [7]; in anaesthetized pigs this dose prevents the reflex increase in aortic blood pressure and the reflex coronary vasoconstriction caused by gallbladder distension [25,28] and by uterine distension [29]. The propranolol dose prevents the reflex increases in heart rate caused by gallbladder [25] and uterine distension [29] in anaesthetized pigs and has been used previously in anaesthetized pigs and dogs to block coronary β-adrenoceptors [4,27,28].…”

Section: Experimental Protocolmentioning

confidence: 99%

“…The phentolamine dose abolishes the reflex increase in aortic blood pressure to descending colon distension in anaesthetized dogs [7]; in anaesthetized pigs this dose prevents the reflex increase in aortic blood pressure and the reflex coronary vasoconstriction caused by gallbladder distension [25,28] and by uterine distension [29]. The propranolol dose prevents the reflex increases in heart rate caused by gallbladder [25] and uterine distension [29] in anaesthetized pigs and has been used previously in anaesthetized pigs and dogs to block coronary β-adrenoceptors [4,27,28]. The atenolol dose blocks β 1 -adrenergic effects in conscious dogs [30] and 2.5 mg kg -1 butoxamine were used previously to block β 2adrenoceptors in anaesthetized rats [31] and in anaesthetized pigs [26].…”

Section: Experimental Protocolmentioning

confidence: 99%

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

Vacca

Pfl�gers Archiv European Journal of Physiology

Chiorboli

et al. 1998

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.

“…This contribution was about 45 %, 41 % and 52 %, respectively. As in the case of the stomach, stimulation of other mechanoreceptors, such as those located in the gallbladder or uterus, has been shown to cause reflex regional vasoconstriction through efferent sympathetic mechanisms (Vacca et al 1996a(Vacca et al , 1997aMolinari et al 2000). This peripheral vasoconstriction response was shown to be significantly contributed to by a concomitant activation of the renin-angiotensin system (Molinari et al 2000(Molinari et al , 2001.…”

Section: Figurementioning

confidence: 99%

Activation of the Renin‐Angiotensin System Contributes to the Peripheral Vasoconstriction Reflexly Caused by Stomach Distension in Anaesthetized Pigs

Molinari

Experimental Physiology

Grossini

et al. 2003

Gastric distension in anaesthetized pigs reflexly elicits peripheral vasoconstriction and an increase in plasma renin activity (PRA), with vagal afferent and sympathetic efferent limbs. The aim of the present study was to quantify the contribution of the renin‐angiotensin system to the peripheral vasoconstriction. In pigs anaesthetized with α‐chloralose, changes in anterior descending coronary, superior mesenteric and left external iliac blood flow caused by stomach distension before and after blockade of angiotensin II receptors with losartan were assessed using electromagnetic flowmeters. Gastric distension for periods of 30 min was performed by injecting 0.8 l warm Ringer solution into balloons positioned within the viscus. Changes in heart rate and renal blood flow were prevented by atrial pacing and injection of phentolamine into the renal arteries, and changes in regional perfusion pressure and in baroreceptor activity were minimized by aortic constriction and denervation of the carotid sinuses. PRA was assessed by radioimmunoassay of angiotensin I. Before blockade of angiotensin II receptors by administration of losartan, stomach distension decreased coronary blood flow by 14.2% in six pigs and mesenteric and iliac blood flow by 11% and 17.3%, respectively, in another six pigs. After administration of losartan, these decreases were significantly reduced to 7.4%, 6.8% and 8.7%, respectively. The above responses were abolished by bilateral section of the subdiaphragmatic vagal nerves. These results show that the peripheral vasoconstriction reflexly caused by stomach distension was significantly contributed to by the concomitant activation of the renin‐angiotensin system.