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

Vacca, Giovanni; Papillo, B.; Battaglia, A; Grossini, Elena; Mary, D. A. S. G.; Pelosi, G

doi:10.1113/jphysiol.1996.sp021261

Cited by 31 publications

(20 citation statements)

References 16 publications

(10 reference statements)

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“…The increase in coronary blood flow was completely abolished by intracoronary injection of ¬_NAME, which is known to inhibit the formation of nitric oxide (Henderson, 1991). The dose of 100 mg of the blocking agent used has been previously shown in the same experimental model to cause a reduction of the acetylcholine-induced increase in coronary blood flow (Vacca et al 1996b(Vacca et al , 1999 which was considered a reliable marker of the inhibition of the release of nitric oxide (Parent et al 1992). The blocking agent caused an increase in baseline arterial blood pressure and in coronary vascular resistance.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

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The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h−1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h−1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of Nω‐nitro‐L‐arginine methyl ester (L‐NAME) 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. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide.

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Section: Discussionmentioning

confidence: 99%

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

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“…In each of the 29 pigs, the haemodynamic responses to growth hormone were studied without controlling any haemodynamic variables and whilst preventing changes in heart rate and aortic blood pressure. 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].…”

Section: Experimental Protocolmentioning

confidence: 99%

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

Vacca

Battaglia

Chiorboli

et al. 1998

Pfl�gers Archiv European Journal of Physiology

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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.

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“…The dose of 1 mg kg –1 of phentolamine has been shown in anesthetized pigs to abolish the reflex coronary vasoconstriction caused by distension of the gallbladder [21]and has been used previously to block sympathetic α-adrenergic effects [22]. In anesthetized pigs, the intracoronary dose of 100 mg of L-NAME has been shown to significantly reduce (by about 60%) the vasodilatory effect of the intracoronary administration of acetylcholine at a dose of 1 µg [22, 25], a reduction which was considered to be a reliable marker of the inhibition of nitric oxide release [26]. …”

Section: Methodsmentioning

confidence: 99%

Effects of Insulin on Coronary Blood Flow in Anesthetized Pigs

Molinari

Battaglia²,

Grossini³

et al. 2002

J Vasc Res

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Insulin can influence the vasculature by a sympathetically mediated vasoconstriction and a vasodilatation; the latter effect predominates in the renal circulation of anesthetized pigs. We determined the effect of intravenous infusion of insulin on coronary blood flow in pentobarbitone-anesthetized pigs at constant heart rate, arterial pressure and blood levels of glucose and potassium. In 6 pigs, infusion of 0.004 IU kg^–1 min^–1 of insulin decreased coronary flow despite increasing left ventricular dP dt_max^–1; when the latter was abolished by propranolol, the coronary flow response was augmented. The mechanisms of this response were examined in 22 pigs given propranolol. Phentolamine changed coronary flow response to an increase (6 pigs) and this was abolished by intracoronary injection of N^ω-nitro-L-arginine methyl ester (L-NAME; 5 pigs). L-NAME augmented coronary flow response (6 pigs) and this was abolished by phentolamine (5 pigs). In 18 pigs given propranolol, three incremental doses of insulin caused graded coronary flow decreases whether L-NAME was given (6 pigs) or not (6 pigs) beforehand, and caused graded coronary flow increases after phentolamine (6 pigs). Thus insulin caused a coronary vasoconstriction mediated by sympathetic α-adrenergic effects and a vasodilatation related to the release of nitric oxide. The net effect was a coronary vasoconstriction.

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

Cited by 31 publications

References 16 publications

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

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

Effects of Insulin on Coronary Blood Flow in Anesthetized Pigs

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