The effect of distension of the urinary bladder on coronary blood flow in anesthetized dogs

Cevese, Antonio; Drinkhill, Mark J.; Mary, D. A. S. G.; Patel, Priya; Schena, Federico; Vacca, Giovanni

doi:10.1113/expphysiol.1991.sp003508

Cited by 21 publications

(17 citation statements)

References 11 publications

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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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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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show abstract

“…This method has been previously shown in anaesthetized dogs and pigs to allow the aortic blood pressure to be maintained at steady levels without significant changes in left ventricular pressures or the haematocrit (e.g. Cevese et al 1991;Vacca et al 1996aVacca et al , 1999. Coagulation of the blood was avoided by the intravenous injection of heparin (Parke-Davis; initial dose 500 i.u.…”

Section: Methodsmentioning

confidence: 99%

The Role of Nitric Oxide in the Coronary Vasoconstriction Caused by Growth Hormone in Anaesthetized Pigs

Molinari

Battaglia

Bona

et al. 2000

Experimental Physiology

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Intravenous injection of growth hormone in anaesthetized pigs has been shown to cause coronary vasoconstriction by antagonizing the vasodilatory effects of β2‐adrenergic receptors. Because nitric oxide is believed to modulate or mediate β2‐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 Nω‐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 β2‐adrenergic vasodilatory effect, was mediated by inhibition of nitric oxide release.

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“…One possible explanation for the variable inotropic responses to bladder distension is that two or more factors are involved. It has been shown previously that, when heart rate is controlled by cardiac pacing, distension of the bladder causes a reflex decrease in coronary blood flow (Cevese et al 1991). It is possible that this reflex coronary vasoconstriction could have a secondary negative inotropic effect which would oppose any direct positive inotropic effect on the left ventricle in response to bladder distension.…”

Section: Responses To Distension Of the Bladdermentioning

confidence: 98%

Urinary bladder distension: its effects on carotid baroreceptor reflex left ventricular inotropic response in the dog.

Ward¹,

Daly²,

Wood³

1995

The Journal of Physiology

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1. The effects of distension of the urinary bladder on heart rate, maximum rate of change of left ventricular pressure (dP/dt max) and hindlimb vascular resistance together with their modulation at different carotid sinus pressures were studied in dogs anaesthetized with a mixture of chloralose and urethane and artificially ventilated. 2. When the carotid sinus mean perfusion pressure was raised in randomly selected steps from 60 to 210 mmHg, it caused a progressive bradyeardia, and a reduction in left ventricular dP/dt max and in arterial blood pressure, together with vasodilatation in the perfused hindlimb. Distension of the bladder at each level of carotid sinus pressure resulted in tachyeardia, a small but significant increase in left ventricular dP/dt max (160 + 30 mmHg s-') and hindlimb vasoconstriction.3. When heart rate and arterial blood pressure were held constant to exclude these secondary effects on left ventricular dP/dt max, raising the carotid sinus pressure caused a progressive reduction in left ventricular dP/dt max and hindlimb vasodilatation. Superimposition of tests of bladder distension at each level of sinus pressure resulted in variable responses, but overall there was a significant increase in left ventricular dP/dt max of 190 + 54 mmHg s-. Hindlimb vasocontriction, however, was a consistent finding. 4. The gain of the relationship between the carotid sinus perfusion pressure and left ventricular dP/dt max was unaffected by distension of the bladder. 5. It is concluded that, when changes secondary to increases in heart rate and blood pressure are prevented, distension of the bladder causes a small but significant reflex increase in left ventricular dP/dt max. The responses, however, are variable and the possible reasons for this are discussed.

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The effect of distension of the urinary bladder on coronary blood flow in anesthetized dogs

Cited by 21 publications

References 11 publications

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

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

The Role of Nitric Oxide in the Coronary Vasoconstriction Caused by Growth Hormone in Anaesthetized Pigs

Urinary bladder distension: its effects on carotid baroreceptor reflex left ventricular inotropic response in the dog.

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