Neutrophilia and granulocyte colony-stimulating factor levels after cardiopulmonary bypass.

PURPOSE: The precise mechanism of neutrophilia after cardiac surgery is unknown. Granulocyte colony stimulating factor (G-CSF) can increase the number of leukocytes. The purpose of this study was to evaluate the relationship between serum G-CSF levels and peripheral blood leukocyte counts after cardiac surgery. METHODS: We prospectively studied 10 patients undergoing cardiac surgery (coronary artery bypass grafting) using cardiopulmonary bypass (CPB). Plasma G-CSF levels and neutrophil count were measured before induction of anaesthesia, at the end of surgery, and on the first postoperative day. These changes were compared with those in patients undergoing non-cardiac major surgery (control group). RESULTS: At the end of surgery, G-CSF levels increased (P < 0.01) in both groups, but were higher in the control than in the cardiac group (3,250 +/- 690 vs 194 +/- 29.5 pg ml(-1), respectively, mean +/- SEM, P < 0.01). On the first postoperative day, G-CSF levels were still high in both groups, and were still higher in the control (710 +/- 179 vs 122 +/- 19.9, respectively, P < 0.01). However, neutrophilia was greater in the cardiac group than in the control. G-CSF response correlated positively with neutrophilia in the control group (r = 0.656, P < 0.05) but not in the cardiac group. CONCLUSIONS: Our results indicate that changes in leukocyte count following cardiac surgery are unique to patients undergoing CPB. G-CSF plays an important role as the mediator of neutrophilia after non-cardiac surgery, but not after cardiac surgery with CPB.

Effects of zinc acetate on splenocytes of endotoxemic mice: enhanced immune response, reduced apoptosis, and increased expression of heat shock protein 70.

Immune function is markedly attenuated in endotoxemia. Zinc is involved in the regulation of cellular functions and maintenance of immune function, and its level in the serum is low in endotoxemia. We mainly investigated the effects of zinc acetate (ZA) on splenocytes in mice with endotoxemia. After we confirmed increased plasma zinc level by ZA treatment, C57BL/6 mice were randomly divided into four groups: 10 control mice received 500 microL saline solution as vehicle; 10 control mice received ZA at 3 mg/kg body weight; 20 endotoxemic mice received a 40 mg/kg lethal dose of lipopolysaccharide (LPS); 20 mice received ZA followed by LPS as the above dose. In vivo, we confirmed that ZA pretreatment did not significantly affect the plasma cytokine level in endotoxemic mice. In vitro, splenocytes from ZA-plus-LPS mice showed drastic effects, in that ZA abrogated LPS-induced suppression of cellular proliferation and production of interleukin-2 and interferon-gamma. The percentage of apoptotic splenocytes was significantly reduced in ZA-plus-LPS mice (23.4%) as compared with LPS mice (41.6%). Furthermore, the expression of HSP-70 mRNA in splenocytes was strongly enhanced in both ZA and ZA-plus-LPS mice, especially in the latter group. Finally, studies monitoring survival rates for 6 days showed that LPS caused 100% mortality while ZA-plus-LPS mice showed 75% survival. Our results suggest that zinc normalized the immune response and reduced apoptosis of splenocytes. These changes were probably caused by increased synthesis of HSP-70 by splenocytes, which might enhance survival of mice with LPS-induced endotoxemia.

[Hemodynamic effects of propofol as an anesthesia induction agent in hyperthyroidism patients on chronic beta-blocker].

This study was designed to investigate the effect of propofol on the heart rate and blood pressure in the patients on chronic beta-blocker. Seventy two hyperthyroidism patients scheduled for subtotal thyroidectomy were enrolled. Thirty six patients who were on chronic beta-blocker received either propofol (group beta-P) or thiamylal (group beta-T) as an anesthesia induction agent. In control groups, patients who were not on beta-blocker also received either propofol (group C-P) or thiamylal (group C-T). Anesthesia was maintained with nitrous oxide in oxygen and sevoflurane. Heart rate and systolic blood pressures were monitored and recorded before and during anesthesia. Heart rate decreased significantly in group beta-P compared to three other groups through this study. Significant decreases in systolic blood pressure were observed in the groups beta-P and beta-T compared to group C-P. These results suggest that careful attention should be paid to the patients on chronic beta-blocker when propofol was selected as an anesthesia induction agent.

[Effects of loprinone hydrochloride on hemodynamics and respiratory oxygenation in patients after cardiac surgery].

Loprinone hydrochloride (Lop), a phosphodiesterase fraction III inhibitor and positive inotrope, was recently released in Japan. We evaluated its dose-related effects on hemodynamics and oxygenation as as well as on plasma levels of Lop in ten patients after cardiac surgery. Immediately after admission to the intensive care unit, baseline hemodynamics and arterial blood gas data were obtained; patients with inotropic support, were given 0.1, 0.2, 0.3 microgram.kg-1.min-1.lop over 1 hour incrementally, and additional data were obtained. CI increased significantly from baseline (2.1 +/- 0.3 l.min-1.m-2) to 3.2 +/- 0.8 at 0.3 microgram.kg-1.min-1. Systemic vascular resistance decreased significantly from baseline (2853 +/- 439 dynes.sec.cm-5.m-2) to 1554 +/- 440 at 0.3 micrograms. kg-1.min-1, and mean arterial pressure also decreased significantly from baseline. There were no significant changes in heart rate (HR), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), or PaO2.FIO2(-1) in patients over the period evaluated. Plasma levels of Lop rapidly increased to 27.8 ng.ml-1 (effective level; 20 ng.ml-1) at 0.3 microgram.kg-1.min-1. In this study, Lop was shown to effectively increase CI in patients after cardiac surgery with no significant changes in HR, CVP, PAOP or PaO2/FIO2. Thus, Lop has a beneficial effect in the treatment of patients with low cardiac output immediately after cardiac surgery.