Showing papers by "Joseph L. Izzo published in 1989"
TL;DR: This review examines the evidence that damage to the kidneys, eyes, and brain can be grouped under the basic heading of hypertensive vasculopathy and hypothesis is put forward that norepinephrine is a major contributor and an overlooked cardiovascular risk factor.
24 citations
TL;DR: Preliminary studies investigate hormonal effects of NE on blood elements and found a consistent increase in hematocrit during NE infusion, reasoned that if circulating NE is a true "stress hormone," then stress-related increases in platelet and leukocyte counts could also be NE-dependent.
Abstract: In the past, norepinephrine (NE) has generally been considered to serve more as a neurotransmitter than as a a hormone. 1 This notion has been based largely on studies of intermediary metabolism and glucose counterregulation. However, from the point of view of the cardiovascular system, the potential humoral role of NE may have been underestimated. We 2 and others 3 have demonstrated that circulating NE is important in regulating renal renin release. We have also found a consistent increase in hematocrit during NE infusion, 2 and have reasoned that if circulating NE is a true "stress hormone," then stress-related increases in platelet and leukocyte counts could also be NE-dependent. The obvious implications for cardiovascular morbidity and mortality prompted these preliminary studies to investigate hormonal effects of NE on blood elements.
21 citations
TL;DR: Unrecognized warm ischemia during conventional MOR is a plausible cause of DGF in kidneys from multiple-organ donors and is unrelated to other differences in donor, preservation, or recipient characteristics in the comparative groups.
Abstract: From 1984 to 1987, 110 locally retrieved cadaveric kidneys were transplanted into 108 local recipients, including 50 kidneys from multiple-organ retrieval (MOR) procedures and 60 from kidney-only (KO) donors. Conventional multiple organ retrieval technique, iced Euro-Collins storage, and cyclosporine-prednisone immunosuppression were employed. Delayed graft function (DGF), defined as dialysis dependence after transplantation, was twice as high in the MOR allografts as in the KO allografts, 46% vs. 22%, P less than 0.01. DGF was associated with longer hospitalization postoperatively and reduced eventual allograft function. The greater concordance of DGF in allograft pairs from the MOR group (25% vs. 7% in the KO group) and the increased incidence of DGF when more complex forms of MOR were used (40% with liver or heart retrieval, 55% with liver and heart retrieval) suggested that retrieval-related factors influenced allograft function. DGF in the MOR allografts was unrelated to other differences in donor, preservation, or recipient characteristics in the comparative groups. Unrecognized warm ischemia during conventional MOR is a plausible cause of DGF in kidneys from multiple-organ donors.
14 citations
TL;DR: The differential effect of alpha-agonists on PRA defines an important humoral effect of NE, which should be considered to be a "cardiovascular hormone."
6 citations
TL;DR: It is concluded that ACE inhibition does not acutely impair K homeostasis in men with normal renal function and enalapril treatment.
Abstract: The effect of angiotensin-converting enzyme (ACE) inhibition on renal and extrarenal potassium (K) regulation was examined. Six healthy men were studied in double-blinded crossover fashion on placebo or enalapril, 80 mg/day. On day 4, the subjects were given an intravenous infusion of KCI and on day 5 an oral dose of 10% NH4Cl. Treatment with enalapril decreased plasma aldosterone and increased plasma renin activity (PRA), epinephrine and norepinephrine, but did not affect serum glucose, plasma insulin or basal plasma K. Maximal increases in plasma K during K infusion or NH4Cl ingestion were similar during enalapril and placebo treatment. With enalapril treatment urinary K excretion was unchanged following K loading but moderately reduced following NH4Cl loading. We conclude that ACE inhibition does not acutely impair K homeostasis in men with normal renal function.
3 citations
TL;DR: As suggested by these authors, both the excretion of cystine and the effect of a vasoactive drug such as captopril on that excretion is probably multifactorial.
Abstract: In Reply .—We are most encouraged to see that our findings 1 have prompted other investigators to research the effects of captopril therapy on cystine excretion in cystinuria. The individual case study performed by Dahlberg and Jones demonstrates a close correlation between urinary cystine determinations as quantitated both by the ion exchange–triketohydrindene hydrate (Ninhydrin) method and the phosphotungstic method that we used. The reason for the discrepancy between their results and those we obtained is unclear. As suggested by these authors, both the excretion of cystine and the effect of a vasoactive drug such as captopril on that excretion is probably multifactorial. Genetic subtypes of cystinuria could account not only for differing renal tubular handling of cystine, dibasic amino acid, and, possibly, captopril, but also for intestinal transport of these substances. 2 Alternatively, their patient, who had such high levels of urinary cystine, may not have received enough captopril to
1 citations