ABSTRACT
There is currently an imbalance between the need for cadaveric kidneys for transplantation and the supply. The medical criteria for accepting cadaveric donors are changing and organs that were originally thought to be unacceptable have functioned well. Previous reports have discussed the problems with transplanting pediatric allografts less than 4 years old into adult recipients, and the results have not been encouraging. From 1986 to 1991 a total of 50 kidneys ages 11 to 48 months were transplanted as single units into adult recipients (Group A). Ninety-one adult donor cadaveric transplants were used as controls (Group B). The cadaveric transplants were 2nd or 3rd transplants in 7 of the Group A and 12 of the Group B patients. Renal preservation, storage times, and demographics were the same. Prednisone, cyclosporine, and either Minnesota ALG or OKT3 were used for immunosuppression in both groups. Imuran was added in immunologically high-risk patients. The 1-year actuarial patient and allograft survivals for Group A versus Group B were 89.5% versus 94.2% (p=0.49) and 71.3% versus 87.8% (p=0.01), respectively. There was no difference in allograft or patient survival in kidneys from donors 11-24 months of age or 25-48 months (p=0.56). Renal growth, as measured by sonography, occurred while on cyclosporine A. Excretory and hormonal function as measured by creatinine and hematocrit both improved. Seventy percent of the Group A patients and 76% of the Group B patients were free from rejection in the first 2 months post transplantation (p=0.45).(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Kidney Transplantation , Tissue Donors , Adolescent , Adult , Aged , Child , Child, Preschool , Female , Graft Survival , Humans , Immunosuppression Therapy/methods , Infant , Kidney/growth & development , Male , Middle Aged , Organ Preservation , Survival Rate , Tissue and Organ ProcurementABSTRACT
Dopamine increases renal blood flow and dilates isolated afferent and efferent arterioles preconstricted with norepinephrine via dopamine 1 (DA1) receptors. DA1-receptor stimulation also results in dopamine-induced elevation of adenosine 3'5'-cyclic monophosphate (cAMP) in dog and rat renal arteries. The present study was undertaken to determine the effects of dopamine on cAMP accumulation in isolated canine superficial cortical afferent arterioles. The effect of Sch 23390, a specific DA1-receptor antagonist, on dopamine-stimulated cAMP accumulation was also examined. Forskolin (10(-5) M), a potent stimulator of adenylate cyclase, produced a greater than 11-fold increase in cAMP production compared with control. Dopamine produced a dose-dependent increase in cAMP accumulation in afferent arterioles at concentrations of 10(-4) M and 10(-6) M, Sch 23390 (2 x 10(-4) M) abolished dopamine (10(-4) M)-stimulated cAMP accumulation in afferent arterioles. The dopamine-induced increase in arteriolar cAMP accumulation was unaffected by propranolol (10(-4) M). Our results suggest that dopamine increases cAMP production in afferent arterioles via the DA1 receptor. Increased cAMP production may be responsible for dopamine-induced vasodilation in the afferent arteriole.
Subject(s)
Arteries/metabolism , Arterioles/metabolism , Cyclic AMP/metabolism , Dopamine/pharmacology , Receptors, Dopamine/physiology , Renal Circulation/drug effects , Animals , Arterioles/drug effects , Benzazepines/pharmacology , Colforsin/pharmacology , Dogs , Dopamine Antagonists , Propranolol/pharmacology , Receptors, Dopamine/drug effects , Receptors, Dopamine D1 , Reference ValuesABSTRACT
Production of prostaglandin E2 (PGE2) and prostacyclin (PGI2) as 6-ketoprostaglandin F1 alpha (PGF1 alpha) in isolated canine superficial and juxtamedullary afferent arterioles was measured in the basal state and after administration of angiotensin II and bradykinin. Individual afferent arterioles were obtained by microdissection, and pooled collections were incubated at 37 degrees C for two consecutive 30-min periods. Prostaglandin content of the incubation media was measured by radioimmunoassay and expressed as picograms prostaglandin per incubation vial per 30-min period. Bradykinin (10(-7) M) produced significant stimulation of both PGE2 and 6-keto-PGF1 alpha production in superficial (PGE2 from 0.44 +/- 0.32 to 5.46 +/- 3.77 pg/period and 6-keto-PGF1 alpha from 6.5 +/- 5.0 to 104.5 +/- 25.5 pg/period) and juxtamedullary afferent arterioles (PGE2 from 0.31 +/- 0.06 to 7.47 +/- 1.55 pg/period and 6-keto-PGF1 alpha from 12.0 +/- 0.01 to 184.4 +/- 14.8 pg/period). Angiotensin II in concentrations of 10(-12) M to 10(-7) M produced no stimulation of prostaglandin production. Angiotensin II (10(-6) M) produced significant stimulation of 6-keto-PGF1 alpha production only in superficial afferent arterioles (from 4.4 +/- 0.8 to 17.3 +/- 3.1 pg/period). Angiotensin II-stimulated 6-keto-PGF1 alpha production was blocked by saralasin (2 X 10(-6) M). A heterogeneous renal vascular response to angiotensin II is demonstrated, since the latter stimulated PGI2 production in superficial afferent arterioles only. PGI2 could potentially antagonize the vasoactive effect of angiotensin II in superficial afferent arterioles.
