Functional carotid body tumor: report of a case and a review of the literature.
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3-Iodobenzylguanidine↗
Biomedical subjects
S Takeo
Publications and source records attributed to S Takeo.
Effects of delayed treatment with nafronyl oxalate on microsphere embolism-induced changes in monoamine levels of rat brain regions.
1. The present study was undertaken to examine the effects of delayed treatment with nafronyl oxalate (nafronyl), a cerebral vasodilator, on monoamine neurotransmitters of brain regions in the microsphere-embolized rat. 2. Microsphere embolism was induced by injecting 900 microspheres with a diameter of 48 microns into the right internal carotid artery of rats. Microsphere-embolized rats were treated with nafronyl, 15 mg kg-1, i.p., twice daily from the first to the 5th day. Levels of monoamines and their metabolites in the cerebral cortex, striatum, and hippocampus were measured on days 3 and 5 after the operation by a high-performance liquid chromatograph with electrochemical detection. In vivo tyrosine or tryptophan hydroxylation was estimated by measurement of the accumulation of 3, 4-dihydroxyphenylalanine or 5-hydroxy-1-tryptophan after administration of 3-hydroxybenzylhydrazine dihydrochloride, an inhibitor of aromatic L-amino acid decarboxylase. 3. Microsphere embolism induced decreases in dopamine, noradrenaline and 5-hydroxytryptamine in three brain regions of the right hemisphere on days 3 and 5. In the left hemisphere, the monoamines were reduced, but to a lesser degree than in the right hemisphere. On days 3 and 5, the decrease in the monoamines of the right hemisphere was attenuated by nafronyl treatment except for noradrenaline on day 3. The decrease in the monoamines levels in the left hemisphere was almost completely prevented by nafronyl treatment. 4. On day 3 after microsphere embolism, in vivo tyrosine and tryptophan hydroxylation was lower than the pre-embolic value in all three brain regions. Treatment of the embolized rats with nafronyl significantly attenuated the decrease in in vivo tyrosine and tryptophan hydroxylation in the ipsilateral hemisphere, but not hippocampal tryptophan hydroxylation. 5. The results suggested that treatment with nafronyl improves or attenuates changes in monoamine neurotransmitter metabolism of the brain regions impaired by microsphere embolism. The mechanisms underlying this effect may be attributed to preservation of the ability to synthesize monoamines when the brain is ischaemic or oligaemic.
3,4-Dihydroxyphenylacetic Acid↗
The role of accumulation of sodium and calcium on contractile failure of the hypoxic/reoxygenated heart.
The present study was undertaken to determine whether myocardial energy or ion levels are related to oxygen-replenishment-induced recovery of cardiac contractile force after hypoxia. Isolated rat hearts were perfused for 3 to 40 min under hypoxic conditions, followed by 45 min of reoxygenation. Hypoxia induced a cessation of cardiac contractile force, a rise in resting tension, a decrease in high energy phosphates, and an increase in lactate. Myocardial ATP, creatine phosphate (CP) and lactate reached steady-state levels after 15, 10 and 5 min of hypoxia, respectively. Hypoxic conditions in the present study also caused an increase in sodium content and a decrease in potassium content, but not changes in calcium content, along with a prolonged hypoxic period. When the hearts were perfused for more than 25 min under hypoxic conditions, no recovery of contractile force was observed following 45-min of reoxygenation. Hypoxic perfusion for more than 25 min induced an accumulation of tissue sodium content approximately 3 fold higher than the pre-hypoxic value at the end of hypoxia, and also induced a marked increase in myocardial calcium content upon reoxygenation. When tissue sodium content accumulated by less than 300% of the pre-hypoxic value, cardiac contractile function was partially reversed by reoxygenation and calcium-overload was not observed. The recovery of post-hypoxic cardiac contractility correlated with tissue sodium content during hypoxia rather than with myocardial high energy phosphate content at the end of hypoxia. These results suggest that accumulation of tissue sodium content in the hypoxic myocardium and calcium content in the reoxygenated myocardium may be indicative of hypoxia/reoxygenation-induced cardiac contractile failure.
Adenosine Triphosphate↗
Long-term treatment with angiotensin I-converting enzyme inhibitors attenuates the loss of cardiac beta-adrenoceptor responses in rats with chronic heart failure.
BACKGROUND: Cardiac contractile force in response to beta-adrenoceptor agonists and beta-adrenergic receptor density are decreased in failing human hearts. The effects of angiotensin I-converting enzyme (ACE) inhibitor on cardiac responsiveness to beta-adrenergic stimulation in failing hearts are not established. The present study was undertaken to determine whether ACE inhibitor may improve cardiac beta-adrenergic responsiveness in animals with chronic heart failure (CHF). METHODS AND RESULTS: CHF was induced by left coronary artery ligation in rats. Cardiac output and stroke volume indices decreased 12 weeks after the operation. In sham-operated rats, dobutamine and isoprenaline increased cardiac output and stroke volume indices. In contrast, cardiac output and stroke volume responses to dobutamine and isoprenaline were severely blunted in the CHF rat. Cardiac beta 1-adrenergic receptor density was decreased while its dissociation constant (Kd) was not altered in the viable tissue of the left ventricle of the CHF rat, which is consistent with beta-adrenergic receptor downregulation. Cardiac norepinephrine content decreased in the CHF rats. Rats were treated orally with ACE inhibitors, 3 mg/kg trandolapril or 10 mg/kg enalapril once daily, or 5 mg/kg captopril twice daily from the 2nd to the 12th weeks after the operation. Treatment with ACE inhibitors attenuated the reduction in cardiac output and stroke volume indices and improved the inotropic response to dobutamine and isoprenaline and reversed partially the cardiac norepinephrine content in the CHF rat. ACE inhibitor treatment also attenuated the reduction in beta 1-adrenergic receptor density in the viable tissue of the left ventricle of the CHF rat. CONCLUSIONS: The results suggest that ACE inhibitor treatment attenuates the blunting of cardiac responses to beta-adrenergic agonists in the CHF rat and that one of the mechanisms underlying this effect is prevention of cardiac beta 1-adrenergic receptor downregulation.
Adrenergic beta-Agonists↗
Mexiletine and lidocaine reduce post-ischemic functional and biochemical dysfunction of perfused hearts.
The present study was undertaken to determine whether class Ib antiarrhythmic agents, mexiletine and lidocaine, exert beneficial effects on ischemia/reperfusion-induced cardiac contractile dysfunction. Isolated rat hearts were subjected to 35-min global ischemia, followed by 60-min reperfusion and the functional and metabolic alterations were examined with and without mexiletine or lidocaine treatment. Ischemia/reperfusion resulted in a lack of recovery of contractile function, a sustained rise in left ventricular end-diastolic pressure and increased coronary perfusion pressure of the perfused heart during reperfusion. Contractile dysfunction was associated with increases in tissue Na+ and Ca2+ levels, decreases in K+ and Mg2+ levels, and release of creatine kinase and purine nucleosides and bases (ATP metabolites) from the heart. Treatment of the perfused heart with either 10-100 microM of either mexiletine or lidocaine during pre-ischemia resulted in an enhancement of post-ischemic contractile recovery, a suppression of changes in tissue Na+, K+, Ca2+ and Mg2+ contents and an attenuation of the release of creatine kinase and ATP metabolites in an almost concentration-dependent manner. Tissue sodium accumulation was observed at the end of ischemia, which was also attenuated by pretreatment with these agents. The prevention of Na+ overload and accompanying Ca2+ overload in cardiac cells may be the mechanism underlying the improvement of post-ischemic contractile function of perfused hearts by these agents.
Adenosine Triphosphate↗
Hypoxic preconditioning in isolated rat hearts: non-involvement of activation of adenosine A1 receptor, Gi protein, and ATP-sensitive K+ channel.
Activation of the adenosine A1(A1) receptor, Gi protein, and ATP-sensitive K+ (KATP)-channel system has been shown to play an important role in the cardioprotective effects of ischemic preconditioning in dogs. The present study was undertaken to elucidate the possible involvement of this system in hypoxic preconditioning, which ameliorates injury induced by prolonged ischemia and subsequent reperfusion in perfused rat hearts. Ten minutes of hypoxic preconditioning resulted in an appreciable improvement of post-ischemic cardiac contractile recovery. This was associated with a significant reduction in the release of creatine kinase (CK) from reperfused hearts. Hypoxic preconditioning shortened the time to ischemic contracture onset and prevented a further rise in left ventricular end-diastolic pressure (LVEDP) during reperfusion. Neither the selective A1 receptor antagonist, 8-cyclopentyltheophylline (CPT) nor the KATP channel blocker, glibenclamide, altered the beneficial effects of hypoxic preconditioning. In vivo pretreatment with an inhibitor of Gi protein, pertussis toxin (PTX), also did not diminish the preconditioning effect. The results suggest that, although hypoxic preperfusion ameliorates post-ischemic contractile dysfunction, neither the activation of the A1 receptor, nor the opening of the KATP-channel, nor transduction through Gi protein are involved in the post-ischemic functional recovery of hypoxic preconditioning in the perfused rat heart.
Adenosine Triphosphate↗
The effects of long-term treatment with eicosapentaenoic acid and docosahexaenoic acid on hypoxia/rexoygenation injury of isolated cardiac cells in adult rats.
N-3 polyunsaturated fatty acids have been epidemiologically demonstrated to decrease the incidence of ischaemic heart disease. The present study was undertaken to examine the effects of long-term treatment with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on hypoxia/reoxygenation injury of isolated adult rat cardiomyocytes. Rats, fed with standard rat chow, were treated with 100 to 1000 mg/kg/day EPA or 1000 mg/kg/day DHA for 4 weeks and their cardiomyocytes were isolated by collagenase treatment. The cardiomyocytes, approximately 90% of which were rod-shaped, were subjected to 150-min hypoxia/15-min reoxygenation, and their survivals at the ends of hypoxia and reoxygenation were determined. Treatment with either 1000 mg/kg/day of EPA or DHA resulted in a significant increase in the survival of the cardiomyocytes (39.9 +/- 1.1 and 38.3 +/- 3.0%, n = 14 and 8, respectively v 26.7 +/- 1.6%, n = 8, for untreated group). Treatment with EPA increased eicosapentaenoic (377% increase), oleic (25% increase) and linoleic acid (37% increase) contents in the myocardial total phospholipids without changes in the total phospholipid content, whereas treatment with DHA did not increase DHA incorporation into the myocardial phospholipids. The results suggest that EPA and DHA protect the myocardial cells against hypoxia-reoxygenation-induced injury. Although alterations in myocardial phospholipid composition were observed by treatment with EPA or DHA, the primary mechanism underlying the benefit of EPA or DHA intake is unlikely to be related to increased incorporation of their own fatty acids into the myocardial phospholipids, or the mechanism may be different in each n-3 unsaturated fatty acid employed.
Animals↗
Biliary secretion of antibody to dextran following oral immunization with dextran B512.
Anti-dextran in bile was induced to high levels by oral immunization with dextran B512. IgM anti-dextran were dominant in serum, whereas IgG anti-dextran was dominant in bile. The binding properties of these IgM and IgG antibodies were different, as determined by ELISA with several dextrans. Splenocytes produced equal amounts of IgG and IgM antidextran but cells from mesenteric lymph nodes (MLN) and Peyer's patches produced mainly IgG anti-dextran. Differences were observed among different strains of mice in their ability to produce anti-dextran in serum and bile upon immunization with dextran. BALB/c mice, which are intermediate responders in terms of their serum antibody levels, produced high levels of anti-dextran in bile. C3H/He and C57BL/6, which are high responders in terms of serum antibody levels, had intermediate responses in bile. DBA/2, which are low responders in terms of serum antibody levels, showed low responses in bile. The results provide further evidence of the existence of anti-dextran producing cells. These results indicate that B cells in systemic and mucosal-associated lymphoid tissues from BALB/c, C3H/He, C57BL/6 and DBA/2 mice respond differently to oral immunization with dextran B512.
Administration, Oral↗
Effects of long-term therapy with ACE inhibitors, captopril, enalapril and trandolapril, on myocardial energy metabolism in rats with heart failure following myocardial infarction.
Although pharmacological therapy with angiotensin converting enzyme (ACE) inhibitors has proved to be effective in patients with heart failure (HF), the experimental basis of this effect has not yet been addressed. In the present study, animals with HF were treated with an oral administration of 10 mg/kg/day captopril, 10 mg/kg/day enalapril and 3 mg/kg/day trandolapril from the 2nd to 12th week after the operation. HF was induced by permanent occlusion of the left coronary artery of the rat at 2 mm from its origin. Treatment of the HF rats with the ACE inhibitors enhanced the decrease in mean arterial blood pressure, attenuated the rise in left ventricular end-diastolic pressure, an indirect marker of preload, and diminished the reduction in cardiac output and stroke volume indices of the HF animal. Treatment also reversed the reduction in ATP, creatine phosphate, creatine and the mitochondrial oxygen consumption rate of the viable left and right ventricles of the HF animal. The improvement of the cardiac output index and high-energy phosphate levels of the HF rat by the ACE inhibitors was associated with the recovery of the mitochondrial oxygen consumption rate. In sham-operated animals, treatment with the ACE inhibitors reduced mean arterial pressure and left ventricular systolic pressure, but not metabolic variables concerning myocardial energy metabolism. The present results provide evidence that ACE inhibitor therapy improves cardiac function and myocardial energy metabolism of experimental animals with chronic heart failure. The mechanism underlying the benefit of long-term treatment with ACE inhibitors is probably attributable to recovery or preservation of the mitochondrial function and reduction in preload.
Adenine Nucleotides↗
Reperfusion at reduced flow rates enhances postischemic contractile recovery of perfused heart.
The effects of reperfusion at reduced flow rates on postischemic cardiac contractile function were examined in perfused rat hearts. Isolated hearts were subjected to 35-min ischemia followed by reperfusion at the preischemic flow rate (9.0 ml.g-1.min-1; ordinary flow rate) or at reduced flow rates (0.9-8.1 ml.g-1.min-1). Reperfusion at ordinary flow rate did not generate any left ventricular developed pressure (LVDP), whereas reperfusion at reduced flow rates (0.9-7.2 ml.g-1.min-1) elicited 13-57% of initial contractile force at reperfusion's end; optimal recovery occurred at 3.6 ml.g-1.min-1 (reduced flow rate). Reduced flow rate reperfusion attenuated ischemia-reperfusion-induced increase in left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP), alteration in tissue Na+, K+, Ca2+, and Mg2+, release of creatine kinase and ATP metabolites, and development of triphenyltetrazolium chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely related to higher coronary PP at the initial stage (4 min) of reperfusion (r = -0.763). The benefit of reduced flow rate reperfusion could not be attributed to rate of calcium delivery to the heart, formation of oxygen free radicals in myocardium, endothelium-dependent coronary artery dilation, or LVDEP reduction. Enhancement of postischemic LVDP recovery was associated with attenuation of ischemia-reperfusion-induced increases in myocardial sodium and calcium; failure of postischemic LVDP recovery was accompanied by an increase. Reduction in sodium and calcium overload may underlie the beneficial effects of reduced flow rate reperfusion in ischemic-reperfused heart.
Adenosine Triphosphate↗
Changes in striatal dopamine metabolism after microsphere embolism in rats.
BACKGROUND AND PURPOSE: Dopamine plays an important role in striatal function. The present study was undertaken to elucidate the pathophysiological changes in striatal dopamine metabolism after microsphere embolism. METHODS: Microspheres (48 microns) were injected into the right internal carotid artery of rats. Extracellular levels of dopamine and its metabolites were measured by in vivo microdialysis with the aid of high-performance liquid chromatography. In vivo striatal tyrosine hydroxylation and turnover (catabolism) rate of dopamine were estimated on the first and third days after the embolism. These were estimated by measuring tissue dopa or dopamine content in the presence of either an aromatic L-amino acid decarboxylase inhibitor or a tyrosine hydroxylase inhibitor, respectively. RESULTS: In the microdialysis study, a 190-fold increase in the release of dopamine from the right striatum was observed 40 minutes after microsphere embolism, whereas the striatal dopamine metabolites decreased during the first 180 minutes after the embolism. Microsphere embolism decreased the striatal dopamine content throughout the experiment (28 days), whereas it increased tissue dopamine metabolites on the first day, followed by a decline in the metabolites on the third day or later. The in vivo turnover rate of dopamine decreased both on the first and third days, whereas the in vivo tyrosine hydroxylation decreased only on the third day after the embolism. CONCLUSIONS: The results suggest that microsphere embolism induces severe damage to striatal dopaminergic metabolism 3 to 28 days after the embolism. Dopamine synthesis may be more resistant to the embolism-induced ischemic insults than its catabolism.
3,4-Dihydroxyphenylacetic Acid↗
Diminished responsiveness to cardiac beta 1-adrenoceptor agonists in rats with chronic heart failure following myocardial infarction.
The present study was undertaken to determine whether cardiac response to beta 1-adrenergic agonists is altered in rats with chronic heart failure (CHF), and whether this alteration is related to beta-adrenergic receptor down-regulation in the viable tissue of the left ventricle of these rats. For this purpose, the cardiac response to denopamine, a selective beta 1-adrenergic agonist, and the change in cardiac beta-adrenoceptor density were examined in rats with CHF. A non-selective beta-adrenergic agonist, isoprenaline, was also examined as a comparison. Cardiac output and stroke volume indices were reduced 12 weeks after left coronary artery ligation, suggesting that CHF had developed at this time. Denopamine (2, 4 and 8 micrograms/kg i.v.), and isoprenaline (0.01 microgram/kg i.v.) increased the cardiac output and stroke volume indices in sham-operated rats, whereas such increases were attenuated in the CHF rat. The cardiac beta-adrenergic receptor density, measured by [3H]CGP-12177 binding assay, was reduced in homogenates and microsomal membranes in the viable tissue of the left ventricle of the CHF rat (homogenates: 29% reduction, microsomal membrane: 23% reduction). These results suggest that the cardiac responsiveness to denopamine is diminished in the CHF rat and this alteration is accounted for, in part, by a decrease in cardiac beta-adrenoceptor density.
Adrenergic beta-1 Receptor Agonists↗
Effects of trandolapril on cardiac angiotensin I converting enzyme activity in rats with chronic heart failure following myocardial infarction.
The effects of long-term treatment with a novel angiotensin I converting enzyme (ACE) inhibitor, trandolapril, on ACE activity and cardiac function in rats with chronic heart failure (CHF) were examined and compared with those of captopril and enalapril. Left coronary artery ligation of rats resulted in decreases in mean arterial pressure, left ventricular systolic pressure, dP/dt, cardiac output and stroke volume indices, and increases in left ventricular end-diastolic pressure and systemic vascular resistance 12 weeks after the operation. A significant increase in ACE activity of the myocardium, but not that of serum or other tissues, was detected in the CHF rat 12 weeks after the operation. Oral treatment with ACE inhibitors (10 mg/kg/day captopril, 10 mg/kg/day enalapril or 3 mg/kg/day trandolapril) from the 2nd to 12th week, attenuated the changes in cardiac output and stroke volume indices, left ventricular end-diastolic pressure and systemic vascular resistance of the CHF rat. Treatment also attenuated the increase in the cardiac. ACE activity of CHF rats. A close relationship between the decrease in cardiac output index and the increase in cardiac ACE activity was detected. The results suggest that trandolapril, like other ACE inhibitors, exerts a beneficial effect on cardiac function in the CHF rat and that one of the mechanisms for this effect is attenuation of elevated cardiac ACE activity.
Angiotensin-Converting Enzyme Inhibitors↗
Effects of NKH477, a water-soluble forskolin derivative, on cardiac function in rats with chronic heart failure after myocardial infarction.
Our study was designed to determine whether NKH477, a novel, potent and water-soluble forskolin derivative, may exert a positive inotropic effect in rats with chronic heart failure (CHF) after myocardial infarction. Cardiac output and stroke volume indices were decreased and systemic vascular resistance was increased 12 wk after left coronary artery ligation, suggesting that CHF has developed at this time. Dobutamine (4 micrograms/kg i.v.) increased the cardiac output and stroke volume indices in sham-operated rats (22.7 +/- 1.9 and 15.1 +/- 2.0% increase, respectively), whereas such increases were attenuated in rats 12 wk after the induction of myocardial infarction (cardiac output index: 4.0 +/- 1.4% increase and stroke volume index: 2.2 +/- 1.8% increase, respectively). In contrast to beta-adrenoceptor agonist, NKH477 (3, 10 and 30 micrograms/kg i.v.) increased cardiac output and stroke volume indices in the rats with CHF. The beta-adrenergic receptor density, measured by [3H] CGP-12177 binding assay, was reduced in homogenates of the failing heart. These results suggest that the decrease in cardiac beta-adrenergic receptor density may account, in part, for the reduction in the responsiveness to beta-adrenoceptor agonists. The primary defects in the signal transduction from beta-adrenergic receptor to adenylate cyclase, such as the receptor down-regulation and the failure in signaling from adenylate cyclase, may be present in the CHF heart. It may be possible to reverse the cardiac dysfunction associated with CHF with NKH477.
Animals↗
A possible involvement of sodium channel blockade of class-I-type antiarrhythmic agents in postischemic contractile recovery of isolated, perfused hearts.
The present study was undertaken to test the hypothesis that the degree of sodium channel blockade by class-I-type antiarrhythmic agents accounts for enhancement of postischemic contractile recovery of ischemic/reperfused hearts. Electrophysiological studies showed that the class-I-type antiarrhythmic agents quinidine, disopyramide, procainamide, lidocaine, mexiletine, flecainide and pilsicainide suppressed the Vmax value of the rat left ventricular muscle cell, a marker of sodium channel blockade, in a concentration-dependent manner. Isolated rat hearts were subjected to 35 min of ischemia and 60 min of reperfusion. Postischemic contractile recovery, which was never detected in untreated hearts, was enhanced in hearts pretreated with these antiarrhythmic agents during the last 3 min before ischemia at concentrations ranging from 3 to 300 microM. Tissue Na, but not Ca, accumulation was also detected in the ischemic heart, and tissue Na and Ca accumulation was observed in the reperfused heart, which suggests that sodium overload occurs during ischemia, followed by sodium and calcium overload during reperfusion. The degree of postischemic contractile recovery seen in the presence of these antiarrhythmic agents was inversely related to tissue Na or Ca accumulation after reperfusion, which suggests that class-I-type antiarrhythmic agents inhibit sodium overload occurring in ischemic/reperfused myocardial cells. A close relationship between postischemic contractile recovery of the perfused heart and depression in the Vmax value of the ventricular muscle was also observed. These results suggest that the ability class-I-type antiarrhythmic agents to inhibit myocardial sodium channels plays a significant role in the enhancement of postischemic contractile recovery of the ischemic/reperfused heart.
Animals↗
Effects of naftidrofuryl oxalate on microsphere-induced changes in acetylcholine and amino acid content of rat brain regions.
Effects of naftidrofuryl oxalate (naftidrofuryl) on neurotransmitter, acetylcholine, and amino acid content of brain regions following microsphere-induced cerebral embolism were examined to elucidate its possible therapeutic effects on ischemic brain. Rats received 900 microspheres (48 microns in diameter) via the right internal carotid artery, followed by ligation of the right common carotid artery; and histological and biochemical alterations were examined on the 3rd, 5th, and 28th days after embolism. The embolism induced increases in triphenyltetrazolium chloride- (TTC)-unstained areas and decreases in acetylcholine, glutamate, aspartate, and gamma-aminobutyric acid (GABA) contents in the cerebral cortex, striatum, and hippocampus of the right hemisphere, suggesting that microsphere embolism causes severe damage to these brain regions. Hematoxylin-eosin staining of the right cortical sections after embolism showed degeneration and necrosis of nerve cells with chromatolytic nuclei and eosinophilic cytoplasm. Changes in neurotransmitters of the left hemisphere were relatively small. Treatment with naftidrofuryl of the embolized rats with stroke-like symptoms took place from postoperative day 1 to 28. Treatment resulted in a reduction in TTC-unstained areas, less morphological damage to cerebral cortex on the 3rd and 5th days, and an appreciable restoration of acetylcholine content of three brain regions of the right hemisphere throughout the experiment, but restoration of neurotransmitter amino acids was observed to a smaller degree. The results suggest that naftidrofuryl is capable of preventing the development of ischemia-induced, sustained damage to brain regions vulnerable to oxygen deficiency, particularly by improving impaired acetylcholine metabolism.
Acetylcholine↗
Analysis of effector T cells against the murine syngeneic tumor MethA in mice orally administered antitumor polysaccharide SPR-901.
The growth of MethA tumor was significantly inhibited by oral administration of the alpha-glucan SPR-901 in BALB/c (+/+) mice but not in nude mice. Mice treated orally with SPR-901 exhibited an augmentation of antigen-specific resistance against rechallenge with the tumor cells. The tumor-neutralizing activity of regional lymph node cells from MethA-bearing mice against the tumor was augmented by oral administration of SPR-901. The tumor-neutralizing activity of lymph node cells from SPR-901-treated mice mainly appeared in Lyt2+ cells. Furthermore, lymphokine-activated killer activity of these cells was enhanced by administration of SPR-901. The antitumor effect of SPR-901 was abrogated in mice depleted of either L3T4+ or Lyt2+ cells, and in cyclosporin-A-treated mice. These results suggest that Lyt2+ cells are important effector cells in MethA-bearing mice orally administered SPR-901 and that functional exertion of both Lyt2+ and L3T4+ T cells is necessary for the antitumor effect of orally administered SPR-901 in vivo.
Adjuvants, Immunologic↗
Subclavian venipuncture: a reliable technique.
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Catheterization, Central Venous↗