Acute effects of dibutyryl cyclic AMP on renal circulation in congestive heart failure.

Hoshino, Yumiko

doi:10.1536/ihj.29.771

Cited by 1 publication

(1 citation statement)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…release of intracclluDBcA M P in Skeletal M uscle R ep erfu sio n In ju ry As a result, cAMP increases, and in the same way as endogenous cAMP enters the metabolic pathway, to be transformed into nucleic acids or free nucleotides providing an energy source for the cell [21]. Since DBcAMP has positive inotropic and chronotropic effects on the heart [22,23], it enhances systolic contrac tion and increases cardiac output [24,25]. DBcAMP also lowers intracellular Ca concen trations and inhibits capillary smooth muscle constriction, resulting in dilatation of blood vessels and reduced vascular resistance [25,26], In this way the cardiac aftcrload is re duced and at the same time the peripheral cir culation enhanced [24,27], In the present study, blood flow was measured, and since the standard deviation was large the results were shown as the percent change in blood flow, DBcAMP was administered as a continuous infusion from 1 h prior to the induction of ischemia, and in the DBcAMP group the per cent change in blood flow was found to be sig nificantly increased at 15 and 30 min after reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dibutyryl Cyclic Adenosine Monophosphate on Skeletal Muscle Reperf usion Injury in the Rat

Ohshima¹,

Yabe²,

Ishiguro³

et al. 1997

Eur Surg Res

View full text Add to dashboard Cite

To clarify the action of dibutyryl cyclic adenosine monophosphate (DBcAMP) on reperfused ischemic muscle, experiments were conducted using the hindlimbs of 18 male Lewis rats. At the midportion of the thigh all tissues except for the femoral artery and vein were transected, and a route for continuous intravenous infusion was secured in a contralateral limb vein. After inducing total ischemia by clamping the femoral artery and vein with a vascular clamp for 4 h, the limb was reperfused for 1 h. Blood flow was then compared using the hydrogen gas clearance method in a group in which DBcAMP 10 mg was continuously infused from a vein in the contralateral hindlimb from 1 h prior to the induction of ischemia to 1 h after the completion of ischemia (DBcAMP group), a group in which saline was infused in the same manner (control group), and a group which was subjected to biopsy alone (biopsy group). The percent change in blood flow was significantly higher in the DBcAMP group than in the control group at 15 and 30 min after the release of the clamp. Adenosine triphosphate (ATP), phosphocreatine (PCr), and lipid peroxide (LPO) were measured in tissue samples obtained 1 h after reperfusion. Serum LPO was measured in blood samples collected at the same time. ATP values were higher in the DBcAMP group than in the control group. PCr was significantly higher in the DBcAMP group than in the control group. LPO levels in skeletal muscle tissue did not differ significantly between the DBcAMP and control groups. In contrast, serum LPO levels were significantly lower in the DBcAMP group than the control group. On morphologic analysis the control and DBcAMP groups showed normal vascular endothelial cells and absence of the ‘no-reflow’ phenomenon. These data confirm that in this reperfusion model the administration of DBcAMP enhances the viability of skeletal muscle cells. Moreover, mediated by an effect on vascular endothelial cells this agent is thought to be of help in mitigating the vascular endothelial cell injury occurring in acute ischemic injury. DBcAMP may be a useful agent in mitigating skeletal muscle ischemia-reperfusion injury.

show abstract