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Biomedical subjects

M Tani

Publications and source records attributed to M Tani.

At least 307 records · Page 17Linked to original sources
PubMed1990

Quantification of human concealed atrioventricular nodal conduction: relation to ventricular response during atrial fibrillation.

We studied the relation between a new quantitative index of concealed atrioventricular nodal (AVN) conduction and the variability of ventricular response during atrial fibrillation in 12 patients without preexcitation. The second atrial extrastimulus (A3) was introduced following the first extrastimulus (A2), which was fixed at a coupling interval 20 to 40 msec longer than the AVN effective refractory period (ERP) during a basic atrial drive (A1) cycle length of 400 to 750 msec. The AVNERP of conducted A2 defined as the longest A2A3 interval at which A3 was not conducted to the His bundle was determined. This pacing sequence was repeated, whereas A2 was fixed at a coupling interval 20 to 40 msec shorter than the AVNERP, which means A2 was concealed within the AVN. Thus AVNERP of blocked A2, defined as the longest A2A3 interval at which A3 was not conducted to the His bundle, was measured. Concealment index (AVNERP of blocked A2/AVNERP of conducted A2) was developed to quantitate the magnitude of concealed penetration into the AVN by A2. During atrial fibrillation induced by premature or rapid atrial stimulation, the coefficient of variation (SD/mean) of R-R intervals and the maximum R-R/minimum R-R interval were significantly correlated with the concealment index (r = 0.838, p less than 0.001; r = 0.678, p less than 0.05). However, neither of these parameters was correlated with AVNERP. Both the minimum R-R and the mean R-R interval were related to the AVNERP (r = 0.946, r = 0.823, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1990

Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart.

Maintenance of low coronary flow (1 ml/min) during 40 or 70 min of anoxia maintained function and prevented Ca2+ overload during reoxygenation in isolated rat hearts. In comparison, recovery from 40 min of global ischemia resulted in only 20% of preischemic function and an increase in end-diastolic pressure (LVEDP) to 39 mmHg. Reperfusion Ca2+ uptake rose from 0.6 to 10.2 mumol/g dry tissue. Intracellular Na+ (Nai+) increased from 13 to 61 mumol/g dry tissue after 40 min of global ischemia, but was unchanged in hearts with low flow anoxia. When glucose and pyruvate were omitted from buffer used for anoxic perfusion, recovery was only 15% of preanoxic values, LVEDP rose to 32 mmHg, and reperfusion Ca2+ uptake was 7.2 mumol/g dry. In addition, Nai+ increased (47.4 mumol/g dry tissue) and ATP was depleted (1.0 mumol/g dry tissue) in the absence of substrate. In anoxic hearts supplied substrate, Nai+ stayed low (12 mumol/g dry tissue) and ATP was preserved (11.6 mumol/g dry tissue). Addition of ouabain (100 or 200 microM) and provision of zero-K+ buffer increased Nai+ and resulted in impaired functional recovery, increased LVEDP, and greater reperfusion Ca2+ uptake. These interventions also decreased energy availability in anoxic hearts. To distinguish between effects of Na+ accumulation and ATP depletion, monensin, a Na+ ionophore, was added during low flow anoxia. Monensin increased Nai+, decreased functional recovery and increased reperfusion Ca2+ uptake in a dose-dependent manner (1-10 microM) without changing ATP content. These results suggested that reduction of Nai+ accumulation by maintenance of Na+, K+ pump activity was the major mechanism of the beneficial effects of low coronary flow on reperfusion injury.

Adenosine Triphosphate↗
PubMed1990

Pacemaker syndrome evaluated by cardiopulmonary exercise testing.

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.

Aged↗
PubMed1990

Vascular washout reduces Ca2+ overload and improves function of reperfused ischemic hearts.

Relationships between myocardial Ca2+ uptake, recovery of ventricular function, and restoration of tissue metabolites were determined during 30 min of reperfusion following ischemic and anoxic perfusion with either zero or low coronary flow, zero flow with intermittent perfusion, and low-flow perfusion without substrates. When zero-flow ischemia was maintained for 30 or 40 min, tissue lactate levels increased approximately 100-fold; with reperfusion of these hearts, developed pressure recovered to only 70 and 40% of preischemic function, respectively, and Ca2+ uptake increased by 7- and 15-fold. In contrast, 30 min of low-flow (1 ml/min) anoxic perfusion resulted in accumulation of less lactate (15-fold increase), less reperfusion Ca2+ uptake, and recovery of developed pressure to the preanoxic level. Omission of energy substrates during the low-flow anoxic perfusion caused a reduced recovery of heart rate with lower high-energy phosphate levels and increased Ca2+ uptake, but contractile function recovered to the same extent as in low-flow perfusion with substrate. Even very low flow rates (0.06-0.16 ml/min) of oxygen-deficient perfusate increased high-energy phosphate content and contractile function and decreased Ca2+ uptake. Intermittent perfusion with either oxygenated or anoxic buffer between four 10-min episodes of ischemia reduced lactate accumulation, maintained function, and left Ca2+ uptake essentially unchanged. Recovery of developed pressure during reperfusion was negatively correlated with the amount of lactate that accumulated during ischemia or anoxia and with reperfusion Ca2+ uptake, regardless of the duration or type of ischemia or anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Mechanisms of reduced reperfusion injury by low Ca2+ and/or high K+.

Mechanisms of the protective effects of low Ca2+ (0.15 mM) and/or high K+ (20 mM) concentrations in the buffer on reperfusion injury were investigated. Intracellular Na+ (Nai+) increased fourfold during 25 min of ischemia. When hearts were reperfused with the standard buffer (1.25 mM Ca2+, 5.9 mM K+), Nai+ increased further during the 1st 2 min (5-fold) and then declined by 30% at 10 min of reperfusion. Ca2+ uptake increased 6- and 12-fold at 10 and 30 min of reperfusion, respectively. Function, which was assessed as the product of developed pressure and heart rate, recovered to 45% of the preischemic value and end-diastolic pressure was elevated (EDP: 31 mmHg). Reperfusion for 10 min with low Ca2+ buffer abolished the increase in Ca2+ uptake during this period, but it increased 10-fold when the perfusate was switched back to the standard buffer. Accelerated Ca2+ influx at this time was probably through Na(+)-Ca2+ exchange because Nai+ did not decline during low Ca2+ reperfusion. Elevation of EDP was suppressed (12 mmHg), but development of pressure did not increase. Reperfusion for 10 min with high K+ buffer accelerated the decline in Nai+ by 70% and reduced the increase in Ca2+ uptake (8-fold). Recovery of function improved (67%, EDP: 18 mmHg). Further improvement in function (78%, EDP: 10 mmHg) was obtained along with less Ca2+ uptake (7-fold) when low Ca2+ and high K+ were combined. Recovery of energy metabolites at 10 and 30 min of reperfusion was not different among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of anti-free radical agents on Na+, Ca2+, and function in reperfused rat hearts.

The purpose of the present study was to determine whether the combined administration of superoxide dismutase (SOD) and catalase (CAT) or efforts to maintain the glutathione redox pathways with sulfhydryl agents could improve Na+ imbalance, reduce Ca2+ overload, and enhance recovery of function and metabolites upon reperfusion in isolated ischemic rat hearts, presumably by scavenging oxygen free radicals. After a 30-min exposure to zero-flow ischemia, left ventricular developed pressure (LVDP) and heart rate recovered to 31 and 81% of the preischemic value, respectively, ATP fell by approximately 40%, and 45Ca2+ uptake rose from 0.8 to 10.4 mumol/g dry tissue. A combination of SOD and CAT at low concentrations (5 X 10(4) and 7.5 X 10(4) U/l, respectively) had a beneficial effect on recovery of LVDP (to 59%), reperfusion 45Ca2+ uptake (to 7.9 mumol/g dry tissue), and recovery of Na+ imbalance. When sulfhydryl donors, such as glutathione, cysteine, N-acetyl-L-cysteine, or dithiothreitol, were administered 20 min before induction of ischemia, no significant protective effects were observed. These results indicated that the extracellular free radical scavengers, SOD and CAT, could attenuate partially the ionic imbalance in ischemic-reperfused myocardium and result in improved recovery of contractile function. Attempts to enhance the intrinsic scavenging system were not successful, suggesting that this system may not play an important role in disposing of free radicals.

Animals↗
PubMed1990

Intermittent perfusion of ischemic myocardium. Possible mechanisms of protective effects on mechanical function in isolated rat heart.

Intermittent restoration of coronary flow during ischemia reduced myocardial damage and improved recovery of function. The mechanisms of the protective effects of intermittent perfusion were investigated in isolated rat hearts. Ventricular function was assessed as the product of developed pressure (left ventricular systolic pressure minus end-diastolic pressure) and heart rate. Recovery of function was calculated by division of the product at the end of reperfusion by that before ischemia. After 40 minutes of sustained global ischemia, intracellular Na+ (Nai) increased from 11 to 74 mumol/g dry wt. During 30 minutes of reperfusion, these hearts took up a large amount of 45Ca2+ (10 mumol/g dry wt), recovered only 24% of preischemic function, and had an increased left ventricular end-diastolic pressure (48 mm Hg). When the 40-minute period of ischemia was interrupted at 10-minute intervals by intermittent perfusion (three periods of 3 minutes) with either oxygenated or hypoxemic buffer, Nai increased to only 12 or 17 mumol/g dry wt, and reperfusion resulted in much lower 45Ca2+ uptake (0.5 and 0.5 mumol/g dry wt, respectively). Recovery of function was 100% of the preischemic value. When hypoxemic buffer without glucose was used for intermittent perfusion, Nai increased to 50 mumol/g dry wt, ATP was depleted, and reperfusion resulted in reduced recovery of function (76%) and moderately increased 45Ca2+ uptake (2.1 mumol/g dry wt). The role of Na(+)-K+ pump activity in maintaining low Nai was assessed by removing K+ from oxygenated or hypoxemic buffers used during intermittent perfusion. Under these conditions, Nai rose to 64 or 102 mumol/g dry wt, 45Ca2+ uptake increased to 4.4 or 9.4 mumol/g dry wt, and recovery of function was poor. There was a highly significant correlation between Nai during ischemia and reperfusion Ca2+ overload (r = 0.87) or impaired recovery of function (r = 0.96). These results indicate that prevention of an increase in Nai by maintenance of Na(+)-K+ pump activity is associated with a reduction of Ca2+ overload through Na+/Ca2+ exchange.

Animals↗
PubMed1990

[Phase 3 and phase 4 block in the accessory pathway].

Pacemaker activity at a site proximal to the area of a conduction disturbance has been postulated as depressing conduction in late diastole (phase 4 block). To elucidate the correlation between the site of phase 4 depolarization and that of a conduction disturbance, we examined seven patients with intermittent Wolff-Parkinson-White syndrome who had tachycardia (phase 3) and bradycardia (phase 4) dependent on block in the accessory pathway. In each patient, antegrade conduction over the accessory pathway was absent at the sinus rate. During premature atrial stimulation a "window" of accessory pathway conduction was identified in each patient. The outer limit of the window ranged from 420 to 670 ms; the inner limit, from 330 to 620 ms. The duration of the window ranged from 20 to 160 ms. Four patients with orthodromic atrioventricular reentrant tachycardia exhibited preserved retrograde accessory pathway conduction. In one patient with unsustained orthodromic atrioventricular reentrant tachycardia, retrograde accessory pathway conduction also exhibited phase 3 and phase 4 blocks. The remaining two patients had no retrograde accessory pathway conduction. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation eliminated a phase 4 block in antegrade accessory pathway conduction. These results suggest that 1) an antegrade phase 4 block may have phase 4 depolarization in the accessory pathway and block at the ventricular insertion of the accessory pathway; 2) a retrograde phase 4 block may have a conduction disturbance at the atrial insertion of the accessory pathway; and 3) a complete retrograde block may occur at the atrial insertion of the accessory pathway.

Adolescent↗
PubMed1990

[Is the clinical course of non-rheumatic aortic regurgitation the same as that of rheumatic aortic regurgitation?].

To determine whether non-rheumatic (NR) aortic regurgitation (AR) has the same clinical and postoperative courses as rheumatic (R) AR, we performed a retrospective study using pre- and postoperative M-mode echocardiograms in 23 patients who underwent aortic valve replacement (AVR) under myocardial protection with hypothermic cardioplegia. The etiology of AR was diagnosed by two-dimensional echocardiography. The NR-AR group consisted of nine patients including four with aortic valve prolapse (AP) and five with bicuspid valve (BV), and the R-AR group included 14 patients. Patients with preoperative end-diastolic dimensions (EDD) of less than 6.0 cm were excluded from this study. The indication for AVR was NYHA functional class III or severer. The severity of preoperative NYHA functional class was similar among these three groups. During the 18-month follow-up period (range 2-32 months), there were no post-operative deaths nor congestive heart failure. Ages at surgery ranged from 17 to 54 years; 10 (71%) of 14 patients with R-AR were 40 years old or older, while seven (78%) of nine with NR-AR were under 39 years old (p less than 0.05). The pre-operative left ventricular end-diastolic pressure (LVEDP) in patients with BV-AR was highest among these three groups (R-AR: 14.5 +/- 3.9 mmHg, AP-AR: 9.5 +/- 4.1 mmHg, BV-AR: 22.0 +/- 2.7 mmHg, p less than 0.05). There was no significant difference in pre-operative M-mode echocardiographic results, except for the end-systolic dimension (ESD) between R-AR (5.20 +/- 0.55 cm) and BV-AR (4.78 +/- 0.18 cm) (p less than 0.05). The EDD one month after AVR was still abnormal (greater than or equal to 5.4 cm) in seven of the 14 patients with R-AR, and three of the four patients with AP-AR but none of the patients with BV-ARs (p less than 0.05 vs AP-AR). All patients with pre-operative ESD of less than 5.2 cm had normal EDD one month after AVR. In conclusion, the clinical course of NR-AR is different from that of R-AR. Furthermore, AP-AR regresses more differently after AVR than does BV-AR. Therefore, it is important to consider the etiology of chronic AR in determining the timing of surgery.

Adolescent↗
PubMed1990

[Lipiodol transcatheter arterial chemoembolization for non-resectable hepatocellular carcinoma--multicenter cooperative study].

A cooperative group study was carried out on the effect of Lipiodol transcatheter arterial chemo-embolization (L-TACE) for non-resectable hepatocellular carcinoma (HCC). Thirty-seven hospitals in Japan participated in this study and a total of 157 eligible patients included 138 males and 19 females with an average age of 60.3 y.o. In the chemo-embolization, Lipiodol mixed with 20-50 mg/m2 of doxorubicin (adriamycin) was given through a catheter, and this was followed by embolization with gelatin sponge. Effect of additional oral 5-FU (150-200 mg/day) was also studied as an open trial. Levels of serum alpha-feto protein decreased at 10 days after L-TACE, and this decrease lasted for 5 weeks. CR was observed in one patient, PR in 33, MR in 24, NC in 66 and PD in 16. The response rate was 24.3%. Cumulative one-year, two-year and three-year survival rates were 56.0%, 30.8% and 26.4%, respectively. It was concluded that higher survival rates after L-TACE were observed when (1) patients had better functional reserves of the liver, (2) HCC was in the less advanced stage and (3) L-TACE was carried out more than twice. A reduction of the tumor size after L-TACE did not necessarily mean a good prognosis for the patients. There was no significant difference in the survival rate between the patients taking or not taking 5-FU.

Adult↗
PubMed1990

[Role of adrenergic-neural regulation in failing heart due to aortic regurgitation in rabbits].

The purpose of this study was to determine the characteristics of the role of adrenergic-neural regulation in the pathophysiology of heart failure, produced by aortic regurgitation (AR), especially in relation to the compensatory process. AR was produced by perforation of the aortic valves in 25 rabbits. Another 6 normal rabbits served as controls. Myocardial beta-adrenoceptors and catecholamines were measured in 17 rabbits with AR after various periods: 1 day (n = 5), 1 week (n = 6), and 4 weeks after production of AR (n = 6). Serial blood samples were taken without anesthesia through a catheter placed in the jugular vein for determination of the serum catecholamine level in 8 rabbits with AR. Left ventricular free wall weight increased 1 week and 4 weeks after AR. Wall thickness didn't increase until 4 weeks had passed. Maximal binding sites of myocardial beta-adrenoceptors were reduced from 67.8 +/- 16.7 fmol/mg. protein in the controls to 37.6 +/- 9.21 day after AR (p less than 0.01). Down regulation persisted for 1 week (37.3 +/- 5.5). This change was reversed in the 4-week group (55.5 +/- 13.9). Myocardial norepinephrine content was preserved at 1 day, but depleted at 1 week after AR. In the 4-week group it was restored. Serum norepinephrine level increased 1 day after AR. However, it returned toward the normal range thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Biphasic effects of a combined administration of SOD and CAT on Ca overload and recovery of function and metabolites].

The present study was performed to clarify whether the combination of superoxide dismutase (SOD) and catalase (CAT) can reduce Ca2+ overload and improve recovery of function and metabolites during reperfusion in isolated globally ischemic rat hearts. In non-treated hearts, left ventricular developed pressure (LVDP) recovered to only 30% of the preischemic value with elevation of left ventricular end-diastolic pressure (LVEDP) after 30 min of reperfusion following 30 min of global zero-flow ischemia. ATP and CP fell by 40% and 60%, respectively with 13 fold increase in Ca2+ uptake. A combined administration of SOD and CAT at low concentrations improved recovery of function (LVDP to 60%), reduced Ca2+ uptake (10 fold) without any improvement in high energy phosphates. However a combination of SOD and CAT at higher concentrations did not improve, or even deteriorate functional and metabolic recovery with increased Ca2+ overload (12 to 14 fold). These results indicated that the extracellular free radical scavengers, SOD and CAT, had a biphasic effect on reperfusion injury and could be partially beneficial at low concentrations.

Animals↗
PubMed1990

[Fall in aortic diastolic pressure immediately after aortic valve destruction can predict severity of regurgitation through the valve and chronic morphological changes in the left ventricle].

Aortic regurgitation (AR) has been studied experimentally, however these reports did not investigate compensatory mechanisms in AR in relation with the severity of regurgitation. If the severity of AR can be changed voluntarily, we can evaluate the pathophysiological response to AR in wide range. The purposes of this study were 1) to see if the extent of fall in aortic diastolic pressure immediately after the production of AR (delta AoDP) was a reliable predictor of the severity of AR and 2) to evaluate the process of adaptation through acute and chronic stage in moderate AR in the rabbit model. AR was produced by perforating the aortic valves in Japanese white rabbits. First, aortic pressure, volume, weight and wall thickness of the left ventricle were measured. Correlations between delta AoDP and body weight-corrected volume (LVV/BW) and weight (LVW/BW) were studied in 18 rabbits soon after, 19 one week after, 23 four weeks after and 10 eight weeks after the production of AR. delta AoDP was closely correlated with LVV/BW after 1 week (1 week: R = 0.667, p less than 0.01, 4 weeks: R = 0.733, p less than 0.01, 8 weeks: R = 0.757, p less than 0.05) and with LVW/BW after 4 weeks (4 weeks: R = 0.484, p less than 0.05, 8 weeks: R = 0.651, p less than 0.05). The slope of these regression equations increased with time (delta AoDP and LVV/BW: 1 week: 0.0138, 4 weeks: 0.0361, 8 weeks: 0.0577 ml/kg.mmHg; delta AoDP and LVW/BW; 4 weeks: 0.0142 8 weeks: 0.0310 g/kg.mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Role of interleukin 2 and interferon gamma in induction of activated natural killer cells by the streptococcal preparation OK432].

The natural killer (NK) cell mediated cytotoxicity to syngeneic tumor cells can be augmented by in vivo priming and subsequent in vitro challenge with the streptococcal preparation OK432. Supernatants of coculture of spleen cells with OK432 contained Interleukin 2 (IL-2) and Interferon (IFN), mainly IFN-gamma. As the anti-mouse IFN-gamma monoclonal antibody but not anti-mouse IFN-alpha antibody inhibited the induction of activated NK cells with OK432, the IFN-gamma participated in this response. The incubated spleen cells with IL-2 receptors increased with OK432 treatment by flow cytometry, and the NK cell and IFN activities of supernatants were also abrogated by the treatment with anti-mouse IL-2 receptor monoclonal antibody to block the interaction between IL-2 and these receptors of effector cells. By panning method, it was clarified that the incubated spleen cells with IL-2 receptors were responsible for the production of IFN-r. These results suggest that IL-2 plays a major role to induce the activated NK cells from murine spleen cells primed in vivo and subsequently challenged in vitro with OK432, by the production of IFN-gamma.

Animals↗
PubMed1989

[Successful adoptive immunotherapy with OK432-inducible activated natural killer cells on tumor-bearing mice].

We had demonstrated that the NK cell mediated cytotoxicity of murine spleen cells could be augmented by in vivo prime and subsequent in vitro challenge with the streptococcal preparation OK432, and the cell surface phenotype of induced killer cells was Thy 1+, asialo GM1+, suggesting the activated NK cells (OK-NK cell). The culture supernatants of spleen cells with OK432 possessed the activity of IL-2 and IFN-gamma, and the IL-2 played a major role to induce the OK-NK cells via the production of IFN-gamma. In this study, we examined the effect of adoptive transfer of OK-NK cells on tumor-bearing mice. The mice were implanted SP2 myeloma cells intraperitoneally (i.p.), or C26 colon adenocarcinoma cells subcutaneously (s.c.) to make the models of peritonitis carcinomatosa or solid tumor, and the OK-NK cells were transferred i.p. or i.t., adoptively. By the adoptive transfer of OK-NK cells, the 92% of mice bearing SP2-tumor had be cured. The tumor growth of C26-solid tumor was inhibited, and the survival rate of mice bearing C26-tumor was increased, significantly. The intratumoral remnants of 125I-labelled OK-NK cells were 61.27 and 8% after intratumoral transfer, respectively. By multiple transfer of OK-NK cells the anti-tumor effect was more augmented than that of a single transfer. Thus we recognized the anti-tumor effect of adoptive transfer of OK-NK cells on tumor-bearing mice, and suggested that OK-NK cells could be useful for the therapy of cancer patients.

Adenocarcinoma↗
PubMed1989

Direct evidence for local generation and release of angiotensin II in human vascular tissue.

A direct measurement of both angiotensins I and II immunoreactive substances was made in the perfusate from isolated human umbilical vein perfused with Krebs-Ringer solution which was free of any component of the renin-angiotensin system. The identity of the immunoreactive peptides was confirmed as angiotensin I and angiotensin II by high-performance liquid chromatography in reference to standard compounds. The rate of release of angiotensins was 41.9 +/- 7.4 and 63.4 +/- 12.0 pg for angiotensins I and II, respectively, during the first perfusion period of 30 min, and it remained stable at least for 3 hours. Angiotensin-converting enzyme inhibitor captopril, added to the perfusion medium (10(-9) to 5 x 10(-6) M), suppressed immunoreactive angiotensin II release in a dose-dependent fashion; the maximal percent inhibition of angiotensin II release evoked by captopril (5 x 10(-6) M) was approximately 56%. These results taken together with the previous observations of presence of essential components of the renin-angiotensin system in vascular tissue provide direct evidence for local generation and subsequent release of angiotensin II in vascular beds of human beings.

Angiotensin I↗
PubMed1989

[Induction of activated natural killer cells by the streptococcal preparation OK432 (I). Induction from spleen cells of normal or tumor-bearing mouse primed in vivo and subsequently challenged in vitro with OK432].

The present study shows that natural killer cell-mediated cytotoxicity of BALB/c mouse spleen cells to syngeneic tumor cells was augmented by in vivo priming or in vitro stimulation with the streptococcal preparation OK432. The augmentation of spleen cell cytotoxicity to syngeneic tumor cells by in vivo priming alone with OK432 was lower than that obtained by in vitro stimulation alone with OK432. When the murine spleen cells primed in vivo with OK432 were rechallenged in vitro with OK432 at various intervals, the natural cytotoxicity was more strongly enhanced than that seen with in vitro stimulation alone. The cell surface phenotype of killer cells activated with OK432 was Thy1+ and asialo GM1+, suggesting the activated natural killer cell. Mice were transplanted with syngeneic colon adenocarcinoma cells, and primed in vivo with OK432, and then their spleen cells were subsequently challenged in vitro with OK432. These cells displayed a strong cytotoxic activity not only to the transplanted adenocarcinoma cells but also to other syngeneic tumor cells.

Animals↗