Urinary excretion of polyamines: importance of circadian rhythm, age, sex, menstrual cycle, weight, and creatinine excretion.

The urinary excretion of putrescine, spermidine, spermine, and N1- and N8-acetylspermidines was measured in 95 volunteers. The 24-h excretion, split in four consecutive periods, was analyzed for circadian rhythm in eight volunteers. Circadian rhythm was observed in total polyamine and in N1- and N8-acetylspermidine excretions. The excretion rates of these polyamines were highest in the morning. The normal values for 24-h urinary excretion of polyamines were determined in 87 volunteers. Men excreted significantly more spermidine (P less than 0.001), N8-acetylspermidine (P less than 0.05), and spermine (P less than 0.001) than did women; putrescine excretion was higher in women (P less than 0.001). This variation was only partially explained by differences between sexes in body or muscle mass because most differences remained significant even after normalization for creatinine excretion and body weight. No correlation between the polyamine excretions and age or menstrual cycle was found.

Urinary excretion of polyamines in patients with surgical and accidental trauma: effect of total parenteral nutrition.

Excretion of polyamines first increases and then decreases in patients with multiple trauma receiving total parenteral nutrition (TPN). To separate the effects of trauma and TPN on polyamine excretion, we studied 12 patients with multiple trauma and 14 patients after surgery for colorectal malignancy. Patients were randomized to receive either TPN or hypocaloric glucose infusion. Urinary excretion of total and free polyamines, putrescine (PU), spermidine (SPD), and spermine (SP), and their metabolites, N1-acetylspermidine (N1-AcSPD) and N8-acetylspermidine (N8-AcSPD), and energy and nitrogen balance were measured. Polyamine excretion, excluding SP, markedly increased after trauma and surgery, exceeding the normal values by twofold to 10-fold. In patients receiving TPN, the excretion of total polyamines was 48% higher (P < .01), PU was 34% higher (P < .05), SPD was 35% higher (P < .05), and SP was 350% higher (P < .05) than in patients receiving hypocaloric glucose. Urinary excretion of SP was only 17% of the reference value during hypocaloric glucose (P < .05), but was normal during TPN. The difference in polyamine excretion between nutrition groups was more pronounced when normalized for nitrogen or energy balance. Patients receiving TPN were more hypermetabolic than patients receiving hypocaloric glucose (resting energy expenditure, 1.36 +/- 0.06 [SE] and 1.16 +/- 0.04 times predicted values, respectively; P < .025). Statistically, energy expenditure could explain the difference in polyamine excretion between nutrition groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential effects of sepsis and trauma on urinary excretion of polyamines.

Urinary excretion of polyamines increases in patients with trauma and infection. To separate the effect of infection from the general metabolic response to sepsis, we studied 7 patients with sepsis and 13 patients with multiple trauma in the intensive-care unit. Urinary excretion of total and free polyamines, putrescine, spermidine, spermine, and their metabolites N1-acetylspermidine (N1-AcSPD) and N8-acetylspermidine (N8-AcSPD), and energy and nitrogen balance were measured. The patients were randomized to receive either hypocaloric glucose alone or with amino acids for 2 days. The excretion of individual polyamines, except spermine, significantly exceeded normal values in both patient groups; the excretion of total polyamines was 530 and 323% higher than normal in patients with sepsis and trauma, respectively. The excretion of N1-AcSPD and total spermidine was 141 and 74% higher in patients with sepsis than in patients with trauma, respectively (p < 0.05), whereas the excretion of N8-AcSPD was equal in both patient groups. This was also reflected as a significantly increased urinary ratio of N1-AcSPD to N8-AcSPD in septic patients (6.37 +/- 1.61; mean +/- SE) compared with patients after injury (2.69 +/- 0.27, p < 0.01) or a healthy population (1.08 +/- 0.04, p < 0.001). Amino acid infusion had no effect on polyamine excretion. The mean energy balance was -17.0 +/- 1.1 and -19.1 +/- 1.1 kcal.kg-1.day-1, and the mean nitrogen balance was -0.17 +/- 0.03 and -0.15 +/- 0.02 g.kg-1.day-1 in patients with sepsis and trauma, respectively (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Polyamine excretion in depleted patients with gastrointestinal malignancy: effect of perioperative nutrition and tumor removal.

Polyamines, synthesized by all mammalian cells, are involved in protein and energy metabolism. We measured urinary excretion of polyamines, putrescine, spermidine, spermine, and their metabolites N1-acetylspermidine and N8-acetylspermidine, resting energy expenditure, and nitrogen excretion in 12 depleted patients with gastrointestinal malignancy during preoperative and postoperative parenteral nutrition and in 7 patients with multiple trauma receiving similar parenteral nutrition. During preoperative nutrition support, the excretion of putrescine (p less than .05) and total polyamines (p less than .01) increased by 420% and 60%, respectively. Increases in energy balance and resting energy expenditure during nutrition could entirely explain the observed changes in polyamine excretion. Preoperatively, the excretion of N1-acetylspermidine (p less than .05), N8-acetylspermidine (p less than .001) and total polyamines (p less than .05) was higher in patients with a surgically noncurable tumor than in those with a surgically curable tumor. The energy balance and resting energy expenditure could also explain the differences in polyamine excretion between patients with surgically curable and noncurable disease, excluding the increased N8-acetylspermidine. Postoperatively, the excretion of N8-acetylspermidine in patients with multiple trauma without malignancy and in patients with palliative operation was similar, and was higher than in patients with a totally resected malignancy (p less than .01). Our results suggest that the excretion of polyamines reflects the activity of energy metabolism in general and that polyamine excretion is not specific for any particular disease.

Procaine and timing of aortic declamping affect ventricular reperfusion fibrillation.

Both ventricular fibrillation and electric defibrillation are detrimental to the myocardium. Therefore, we studied the effect of procaine hydrochloride during crystalloid cardioplegia and the effect of performing all central anastomoses before aortic declamping in an attempt to prevent ventricular reperfusion fibrillation during coronary bypass operation. Seventy-four patients were randomised, first to receive procaine hydrochloride or saline during cardioplegia, and secondly, to have central anastomoses performed before and after aortic declamping. In patients receiving procaine in cardioplegic solution (n = 37), the mean ventricular fibrillation time was shorter (27 +/- 79 sec. vs 205 +/- 161 sec., P < 0.0001), the proportion of patients spontaneously achieving stable rhythm was higher (67.6% vs 13.5%, P < 0.0001) and the mean number of defibrillations was lower (0.3 +/- 0.7 vs 2.4 +/- 1.7, P < 0.0001) than in patients receiving placebo (n = 37). Although the aortic occlusion time was longer (112 +/- 28 min vs 91 +/- 26 min, P = 0.0015) in patients with central anastomoses made during cardiac arrest (n = 35) and the mean fibrillation time was shorter (53 +/- 87 sec. vs 173 +/- 179 sec., P = 0.0006) than compared with patients with central anastomoses made after declamping the aorta (n = 39), the mean number of defibrillations (1.2 +/- 1.7 vs 1.4 +/- 1.7, P = 0.59) and the cardiopulmonary bypass time (138 +/- 29 min vs. 132 +/- 34 min, P = 0.47) were not statistically different between these groups. There were no differences in arrhythmias, conduction defects or postoperative recovery between the study groups. We conclude that both procaine hydrochloride during cardioplegia and the performance of central anastomoses of vein grafts during aortic occlusion effectively reduce reperfusion ventricular fibrillation.