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D Gattullo

Publications and source records attributed to D Gattullo.

82 records · Page 5Linked to original sources
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Transient effects of quick changes in myocardial metabolism and perfusion pressure on coronary vasomotor responses.

The effects of transient changes in coronary transmural pressure on the coronary vasomotor tone were studied in 23 anesthetized dogs. Increases and decreases of the coronary transmural pressure were obtained by constrictions of various duration (2 to 20 s) of the descending thoracic aorta. The maneuvers were performed in animals with intact cardiac innervation, with the vagi sectioned and with vagal section together with beta-blockade. In the absence of beta-blockade the increase in the transmural pressure caused a transient increase in the coronary vasomotor tone attributable to a myogenic contractile response and the extravascular compression. This contractile response was not observed when the transmural pressure was increased in the presence of high vasomotor tone after beta-blockade. In all animals a transient hyperemia was seen with its peak 8 to 12 s after the release of the aortic constriction. Since its timing and amplitude were independent of the duration of the constriction, the metabolic effect of the increased ventricular afterload, although it may have contributed to the decrease of the coronary resistance, cannot be considered entirely responsible for the hyperemia, which was otherwise compatible with a myogenic vasodilatory response triggered by the sudden fall of the transmural pressure at the release of the constriction. It is concluded that, in the coronary circulation of the intact dog, transient changes in transmural pressure can induce vasomotor responses in which myogenic and metabolic mechanisms combine together in regulating the coronary flow. Changes in extravascular compression can also affect the flow when the experimental maneuver implies changes in the diastolic left ventricular pressure and volume. With the present experimental procedure the myogenic responses have been evidenced when the metabolic factors would have been expected to produce opposite changes in the vasomotor tone.

Animals↗
PubMedDate not supplied

Ventricular distension and diastolic coronary blood flow in the anaesthetized dog.

There appears to be no agreement as to whether or not an increase in diastolic left ventricular pressure and/or volume can cause a decrease in diastolic coronary blood flow. We investigated the problem in the anaesthetized dog using a flaccid freely distensible latex balloon inserted into the left ventricle with the animal on extracorporeal circulation and the coronary perfusion pressure constant at about 45 mm Hg. Maximal vasodilatation and suppression of autoregulation in coronary vasculature was obtained by the intracoronary infusion of dipyridamole (10-40 mg/h). Ventricular volume was changed in steps of 10 ml from 10 to 70 ml and back to 10 ml, whilst recording coronary blood flow and left ventricular pressure in the left circumflex coronary artery. Over a range of ventricular volumes from 20 to 50 ml and a concomitant rise in diastolic ventricular pressure to about 20 mm Hg there was no change in the diastolic coronary flow. Only when the ventricular volume was more than two times the control value (i.e. exceeded 50 ml) and left ventricular pressure was more than 20 mm Hg, was there a decrease in coronary flow. During the return of the volume to the control level there was a fall in diastolic flow and ventricular contractility with respect to the values obtained when the volume was increased; these two effects were transient lasting less than 10 min. It was not considered that any of the three models of the coronary circulation, waterfall, intramyocardial pump or varying elastance model could explain our results.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMedDate not supplied

[Effect of Bunaftine on the ventricular tachycardia due to aconitine in the dog].

Suppression of aconitine-induced ventricular tachycardia in the dog with various doses of Bunaftine was attempted. Stable re-establishment of the sinus rhythm was achieved in only 3/15 cases, whereas in 3 tachicardia was unchanged, and in 9 fibrillation appeared, due, it is thought, to the effect of the drug on myocardial conductivity, since fibrillation was the most frequent outcome when high doses were used.

Aconitine↗
PubMedDate not supplied

[Effect of Bunaftine on the aconitine-induced atrial arrhythmias in the dog].

Bunaftine has a quinidine-like vagolytic effect and does not act as a beta-blocking agent. Its effect on aconitine-induced atrial fibrillation in the dog was examined. It led to suproventricular tachycardia in all cases, but re-established the sinus rhythm in only 5/15. It is felt that this lack of success is attributable to the slowing of the frequency of the primary pacemaker on the part of the drug. Slowing down of atrioventricular and intraventricular conduction by Bunaftine was revealed by lengthening of the P-R interval and widening of the Q-RS complex. Decreased blood pressure following administration of the drug appears to be due to reduction of heart rate rather than altered myocardial inotropism or peripheral resistance.

Aconitine↗
PubMedDate not supplied

Integration between myogenic response and neurovegetative activity in the regulation of the coronary flow.

In the anaesthetized dog a 10 s increase in the coronary perfusion pressure was obtained by constriction of the descending thoracic aorta. At the release of the constriction, the pressure fell abruptly below the control and about 10 s later was followed by a transient myogenic reduction of the coronary vascular resistance. The reduction occurred to about the same extent in the animals with the intact vagi, after vagotomy and after vagotomy plus beta blockade, showing that changes in the basal vasomotor tone do not affect the amplitude of the myogenic vasodilation.

Animals↗
PubMedDate not supplied

Heart rate decrease after inhibition of nitric oxide release in the anaesthetized dog.

In 5 anaesthetized vagotomized dogs the administration of an inhibitor of the synthesis of nitric oxide (NO) was seen to reduce the heart rate, although the arterial pressure was prevented from increasing. Such a finding suggests that the inhibition of nitric oxide release can produce bradycardia without the involvement of baroreceptor reflexes. Since NO inhibition is known to increase the concentration of adenosine in the myocardium, in 3 additional dogs, dipyridamole, which also potentiates the effect of adenosine, was infused: a reduction in heart rate was observed also in these animals. In both groups of animals, before and after the administration of the relevant compound, the increase in ABP obtained with aortic constriction caused the same reduction in heart rate, which which was attributed to a reduction of the basal sympathetic discharge, which was shown not to be affected by NO inhibition. It is concluded that NO inhibition can cause bradycardia without the intervention of any nervous mechanism but with the possible intervention of an increase in myocardial adenosine concentration.

Adenosine↗
PubMedDate not supplied

Endothelium and coronary reactive hyperaemia.

The effect of the inhibition of the endothelial release of nitric oxide (NO) on the hyperaemia which follows a 10 s coronary occlusion was studied in 5 anaesthetized dogs, keeping aortic blood pressure constant. The left circumflex coronary artery was occluded before and after the intracoronary infusion of an inhibitor of NO (LNNA). After LNNA, the peak amplitude of the hyperaemia was the same but the duration was reduced almost to a half of the control value; it is suggested that a myogenic vasodilatation is involved in the amplitude of the reactive hyperaemia, while the reduction in the duration of the hyperaemia after the inhibitor could result from the shear stress being less effective in causing the release of NO during the first part of the hyperaemia.

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