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.


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within the gallbladder was distended with volumes of Ringer's solution equal to the volumes of bile previously withdrawn (mean vol: 62 mL; mean gallbladder pressure: 12 mm Hg).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.
Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia di Novara, Università di Torino, Italy.
G
G
Vacca
A
A
Battaglia
E
E
Grossini
D A
DA
Mary
C
C
Molinari
D000759:Adjuvants, Anesthesia / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000344:Afferent Pathways / Q000502:physiology; D000758:Anesthesia; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000294:innervation / Q000502:physiology*; D004525:Efferent Pathways / Q000502:physiology; D005704:Gallbladder / Q000294:innervation / Q000502:physiology*; D007552:Isotonic Solutions; D010276:Parasympatholytics / Q000494:pharmacology; D010424:Pentobarbital / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D012018:Reflex / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D000077325:Ringer's Lactate; D013153:Splanchnic Nerves / Q000601:surgery; D013552:Swine; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology / Q000601:surgery; D014661:Vasoconstriction / Q000502:physiology*
D000759:Adjuvants, Anesthesia; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D007552:Isotonic Solutions; D010276:Parasympatholytics; D011942:Receptors, Adrenergic, alpha; D000077325:Ringer's Lactate; D001285:Atropine; D011433:Propranolol; D010424:Pentobarbital; D010646:Phentolamine