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Biomedical subjects

J Manthey

Publications and source records attributed to J Manthey.

At least 19 recordsLinked to original sources
PubMed2002

Genetic toxicity of a standardized mixture of citrus polymethoxylated flavones.

Flavonoids are a ubiquitous family of phytochemicals that display a variety of biological effects, both beneficial and adverse depending on the individual compound. Certain flavonoids are genotoxic while others inhibit the genotoxicity of other mutagens. In the present studies, the mutagenicity of a mixture of polymethoxylated flavones (PMFs) purified from citrus peel oil was evaluated. The mixture consisted of nobiletin (32.5%), 3,3',4',5,6,7,8-heptamethoxyflavone (25.0%), tangeretin (14.0%), trimethylscutellarein (9.1%), sinensetin (3.9%), 5-demethyl-nobiletin (2.8%), hexa-O-methylquercetagetin (3.3%), 5-demethyl-tetramethylscutellarein (0.7%), 5-hydroxy-3,3',4',6,7,8-hexamethoxyflavone (0.7%), and a small quantity of unidentified flavonoid compounds (3.9%). In vitro addition of the PMF mixture over a concentration range that spanned four log doses (0.0005-5.0 mg/plate) did not reveal any evidence of mutagenicity in five bacterial tester strains (Salmonella typhimurium TA98, TA100, TA102, TA1535 and TA1537) either in the absence or presence of S9 activation. The PMF mixture exhibited a statistically significant increase in mutagenicity of L5178Y tk(+/-) mouse lymphoma cells at 0.05 (38.5 x 10(-6); P<0.05) and 0.1 mg/ml (61 x 10(-6); P<0.01) compared with vehicle-treated controls (mutation frequency=19.7 x 10(-6)). However, these responses were within historical values observed in negative control cultures and extremely small compared to the positive control (EMS 0.5 microl/ml; 1685.3 x 10(-6)). Furthermore, in the presence of S9 there was no indication of genetic toxicity in L5178Y tk(+/-) cells. These results demonstrate that the PMF mixture is not genotoxic in in vitro assay systems.

Animals↗
PubMed2001

Immunotoxicity of a standardized citrus polymethoxylated flavone extract.

Polymethoxylated flavones (PMFs) from citrus inhibit production of TNF-alpha and other pro-inflammatory cytokines. As TNF-alpha also modulates NK cell activity, the current studies were conducted to assess the potential for a standardized citrus PMF mixture to suppress humoral and innate immune functions. PMFs were isolated from orange peel oil using a procedure that obtained a consistent mixture of PMFs both in identity and proportion. The mixture consisted of nobiletin (30.7%), 3,3',4',5,6,7,8-heptamethoxyflavone (27.9%), trimethylscutellarein (14.5%), tangeretin (10.4%), sinensetin (5.8%), 5-demethyl-nobiletin (2.0%), hexa-O-methylquercetagetin (1.3%), 5-demethyl-tetramethylscutellarein (0.6%), and other flavonoids (2.7%). To assess the effect of the PMF mixture on humoral immune responses, female B(6)C(3)F(1) mice (n=8) were exposed to the PMF by gavage at 5, 50, 150 and 500 mg/kg/day for 28 days. On day 25, mice were sensitized to sRBC by tail vein injection and AFC response determined 4 days later. Humoral immunity was insensitive to suppression following exposure to all concentrations of the PMF mixture. Suppression of NK cell activity was observed only following 500 mg/kg/day for 28 days. Body weights were not affected by exposure to any concentration of the PMF mixture in sRBC immunized or non-immunized mice. However, in sRBC-immunized mice, higher concentrations of PMF were associated with a statistically insignificant increase in spleen weight (P>0.05). No change in spleen weight was observed in non-immunized mice. As anticipated, based on previously published in vitro observations, long-term, high-dose exposure to a standardized mixture of citrus PMFs caused a mild suppression of NK cell activity; however, humoral immunity was not sensitive to suppression at the same exposure levels.

Animals↗
PubMed1994

[Mechanical recanalization and local thrombolysis in a patient with fulminant pulmonary embolism and craniocerebral trauma].

A 77-year-old female patient presenting with recurrent pulmonary embolism and shock had a severe craniocerebral trauma after collapsing at home 2 days before admission. Since systemic thrombolytic therapy appeared hazardous in this patient, percutaneous fragmentation and distal dispersion of the proximal pulmonary emboli was performed using a pigtail catheter. This procedure improved cardiac output immediately by 15%, whereas the mean pulmonary artery pressure dropped only slightly from 48 to 46 mmHg. Thereafter, a streptokinase infusion of 100,000 IU during 1 h was instituted through the pigtail catheter into the pulmonary artery. 12 hours after the treatment was started, cardiac output was raised by 70% and mean pulmonary artery pressure was decreased from 48 to 25 mmHg. 14 days after admission, control ventilation-perfusion scan showed a markedly improved pulmonary perfusion, and right heart catheterization revealed normal right heart pressures. The patient recovered rapidly and there was no evidence of recurrent pulmonary embolism 18 months later. This report demonstrates that a percutaneous catheter fragmentation of proximal pulmonary emboli combined with local intermediate-dose infusion of streptokinase may be a helpful therapeutic option in patients with massive pulmonary embolism in whom systemic thrombolytic therapy is contraindicated.

Aged↗
PubMed1994

[Capillary hemangioma of the heart: a case report].

In a 52-year-old man, within the left ventricle, a globular mass 1.5 cm in diameter was detected incidentally by echocardiography. Selective coronary angiography showed a mobile patch of hypervascularity suggesting the vascular nature of the cardiac mass. The patient was operated and a pedunculated tumor originating from the anterolateral papillary muscle was removed. Histological examination revealed a benign capillary hemangioma. Six months after surgery the patient was reevaluated by echocardiography. There was no evidence of tumor recurrence.

Coronary Angiography↗
PubMed1994

Popliteal venous aneurysm with pulmonary and paradoxical embolization.

A 31-year-old woman was admitted with recurrent pulmonary emboli. The patient subsequently developed right sided hemiplegia. A mobile left atrial mass attached to the interatrial septum was detected and paradoxical embolization was assumed to be the underlying cause of the cerebral event. Leg phlebography and B-mode ultrasonographic imaging showed that the most probable source of embolization was a right popliteal venous aneurysm containing thrombi adherent to the vein wall. The immediate treatment was restricted to full dose heparin therapy and supportive measures. Thirteen days after admission, the aneurysm was excised. Recovery was rapid and the patient was discharged for further rehabilitation with an only minimal neurological deficit 3 weeks after admission.

Adult↗
PubMed1992

Baroreceptor-mediated release of vasopressin in patients with chronic congestive heart failure and defective sympathetic responsiveness.

In patients with congestive heart failure (CHF), overactivity of the sympathetic nervous system may be accompanied by an impairment of the baroreflex control mechanism. To evaluate the reflex responses of the sympathetic nervous system, the renin-angiotensin system and vasopressin release to baroreceptor unloading, 38 patients with left ventricular dysfunction were studied. Hemodynamic data, and plasma norepinephrine, renin activity and vasopressin concentrations were measured before and 60 minutes after administration of high-dose hydralazine (0.4 mg/kg intravenously). On the basis of blood pressure response to vasodilator administration, patients were divided arbitrarily into those with a decrease in mean arterial blood pressure greater than or equal to 15 mm Hg (group A; n = 12) and those with a decrease less than 15 mm Hg (group B; n = 26) compared with control values. In response to hydralazine, heart rate decreased in group A from 100 to 92 beats/min (p less than 0.001) and increased in group B from 90 to 96 beats/min (p less than 0.05). In group A, hemodynamic changes induced by hydralazine were accompanied by a decrease in plasma norepinephrine from 822 to 518 pg/ml (p less than 0.01) and an increase in plasma vasopressin from 8.4 to 45.2 pg/ml (p less than 0.001). In group B, plasma norepinephrine and vasopressin did not change significantly (407 vs 447, and 8.4 vs 8.3 pg/ml, respectively). Plasma renin activity remained unchanged in group A and increased in group B (p less than 0.001). The data show that baroreceptor-mediated release of vasopressin is not impaired in patients with CHF and a defective sympathetic reflex control mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

ACE inhibition improves vagal reactivity in patients with heart failure.

The deranged autonomic control of heart rate was studied in 34 patients with heart failure (New York Heart Association [NYHA] functional class II to III) by examining the carotid sinus baroreflex. The carotid sinus baroreceptors were stimulated by graded suction. The slope of the regression line between increases in cycle length and the degree of neck suction was taken as an index of baroreflex sensitivity. The reflex response is mediated by a selective increase of vagal efferent activity. Baroreflex sensitivity therefore represents a measure of vagal reactivity. Using multiple regression analysis, baroreflex sensitivity (BS) correlated positively to stroke volume index (SVI) and inversely to plasma renin activity (PRA) and to age: BS = 0.47 SVI - 0.38 PRA - 0.23 age + constant (r = 0.74; p less than 0.0005). In addition to digitalis and diuretics, angiotensin-converting enzyme (ACE) inhibitors (captopril or enalapril) were given to 16 patients for a mean of 17 +/- 3 days. The patients with hemodynamic improvement (group A) exhibited improved baroreflex sensitivity (1.4 +/- 0.4 to 3.6 +/- 1.2 msec/mm Hg; p less than 0.01). Baroreflex sensitivity remained unchanged (3.1 +/- 0.8 to 2.4 +/- 1.0 msec/mm Hg; n.s.) in the patients without hemodynamic improvement (group B). The increase in reflex sensitivity did not correlate with hemodynamic alterations. Baroreflex sensitivity during ACE inhibition (BSD) was only related to the baseline baroreflex sensitivity (BSB): BSD = 2.8 BSB - 0.46 (r = 0.84; p less than 0.005). In patients with heart failure, reflex bradycardia decreases with age and with PRA and increases with stroke volume. Chronic therapy with ACE inhibitors enhances vagal reactivity in patients with hemodynamic improvement.

Adult↗
PubMed1990

Haemodynamic changes caused by alteration of autonomic activity in patients with heart failure.

In 14 patients with heart failure (New York Heart Association class 2-3) and sinus rhythm the carotid sinus baroreceptors were stimulated to induce a reflex mediated decrease of sympathetic efferent activity and a simultaneous increase in vagal tone. Five patients were in severe heart failure (New York Heart Association class 3) with raised plasma concentrations of noradrenaline at rest (2.99 (0.86) nmol/l (mean (SD)) and nine patients had less severe heart failure (class 2.2 (0.2)) and normal plasma concentrations of noradrenaline at rest. The haemodynamic responses during arterial baroreceptor stimulation were different in both groups. In all five patients with severe heart failure cardiac output increased whereas in the nine patients with less severe heart failure it was unchanged or decreased. The increase of cardiac output in the group with severe heart failure was solely the result of a significant increase of stroke volume index (by 9 (2) ml/m2). In the nine patients with less severe heart failure stroke volume remained unchanged but heart rate decreased significantly by 7 (2) beats/min during baroreceptor stimulation. These data show that an integrated change of autonomic activity consisting of a decrease in sympathetic tone and an increase in vagal activity leads to an increase of stroke volume in patients with severe heart failure and hence to haemodynamic improvement.

Adult↗
PubMed1989

Four-year follow-up study in patients with angina pectoris and normal coronary arteriograms ("syndrome X")

In patients with typical stress-induced anginal pain, normal coronary arteries, and unimpaired left ventricular performance at rest ("syndrome X"), a reduced coronary dilatory capacity, abnormal lactate metabolism during stress, and reduction of left ventricular functional reserve have been described. A group of 40 patients with syndrome X was followed for several years to determine their long-term prognosis. In 27 patients pulmonary artery pressure and in 19 patients left ventricular ejection fraction were reassessed during rest and exercise approximately 4 years after the initial examination. In patients with stress-induced ST-segment depression, these variables did not change during the observation period. In patients with constant or rate-dependent left bundle branch block, however, there was significant deterioration of left ventricular performance during rest (pulmonary artery mean pressure, 16 +/- 3 vs. 17 +/- 4 mm Hg, p = NS; left ventricular ejection fraction, 62 +/- 5% vs. 55 +/- 5%, p less than 0.05) and exercise (pulmonary artery, 30 +/- 6 vs. 39 +/- 10 mm Hg, p less than 0.005; left ventricular ejection fraction, 59 +/- 6% vs. 49 +/- 5%, p less than 0.01). These findings suggest that in syndrome X two subgroups with distinctly different prognoses may be defined: In patients with stress-induced ST-segment depression during exercise, left ventricular performance remains well preserved; however, in patients with either constant or rate-dependent left bundle branch block, there is significant deterioration of left ventricular function within several years.

Angina Pectoris↗
PubMed1988

Humoral adaptation mechanisms and clinical outcome during vasodilator therapy.

Administration of hydralazine and isosorbide dinitrate leads to a reduction of one-year mortality by 38%. However, a major disappointment has been the inability to predict the individual patient's response to these drugs. The aim of the present study, therefore, was to evaluate possible predictors for a favourable response to hydralazine treatment on the basis of the acute humoral and haemodynamic response to the drug. Stroke volume increased in all 37 patients with severe left ventricular dysfunction in response to acute intravenous hydralazine (0.4 mg kg-1). However, when re-investigated after 2 months of chronic oral hydralazine therapy, sustained haemodynamic and clinical improvement was observed in only 16 patients. Pretreatment values of either left ventricular filling pressure, cardiac index or systemic vascular resistance were not useful in predicting the outcome of treatment. However, when patients were subdivided on the basis of their heart rate response to acute hydralazine, better discrimination for a beneficial response, was possible. It is concluded that the haemodynamic and humoral responses to acute intravenous hydralazine allow discrimination between patients not responding to chronic vasodilator treatment and those who are likely to benefit. A reflex excitation of sympathetic outflow in response to acute vasodilation (indicated by a reflex acceleration of heart rate and increase in plasma noradrenaline levels) characterised best those patients who did not benefit from oral hydralazine. The data indicate a detrimental role of reflex sympathetic stimulation which may blunt at least part of the direct beneficial drug-induced effect in chronic vasodilator therapy.

Atrial Natriuretic Factor↗
PubMed1988

Influence of captopril on the arterial baroreceptor reflex in patients with heart failure.

In 16 male patients with heart failure (NYHA II-III), the influence of a single dose of 25 mg captopril on the carotid sinus baroreceptor reflex was examined. Blood pressure fell significantly by 11 +/- 1.7 mm Hg (P less than 0.001), whereas heart rate remained unchanged (85 +/- 3 vs. 83 +/- 3 beats min-1). Carotid sinus baroreceptors were stimulated by means of an airtight neck chamber. Two indices of baroreflex sensitivity were calculated. (1) The sensitivity to reflex heart rate slowing was increased by captopril from -2.9 +/- 0.7 to -5.0 +/- 1.3 ms mmHg-1 (P less than 0.02). The higher the initial sensitivity the more pronounced was the change after captopril with an increase of sensitivity by 46% (y = 1.46x -0.17, P less than 0.01). This increase in sensitivity cannot be explained by haemodynamic changes induced by captopril. (2) In eight patients the sensitivity of the baroreflex to increased transmural pressure gradients of the carotid sinus was evaluated by registration of the blood pressure response to neck suction; this demonstrated an unchanged responsiveness following captopril administration. From these data it can be concluded that captopril selectively augments a reflex bradycardia which is mediated by an increase in vagal efferent tone. The change in the reflex response depends on the initial reflex sensitivity and cannot be explained by haemodynamic changes caused by captopril.

Adult↗
PubMed1988

Congestive heart failure: how to evaluate efficacy of treatment.

Vasodilators are widely used in the therapy of congestive heart failure. Different mechanisms responsible for a failure of vasodilator therapy are discussed. Tolerance and/or diminished reabsorption or a less than optimal choice of the drug may be responsible for the lack of acute response. In addition, counter-regulation, mainly by the sympathetic nervous system, may decrease the drug effect. Furthermore, the initial beneficial effect of each vasodilator can be diminished with long-term therapy. Based on a clinical assessment and on invasive and noninvasive techniques a proposal is made as to how to treat an individual patient efficaciously.

Heart Failure↗
PubMed1988

[Comparison of captopril with enalapril in the therapy of heart failure: effect on hemodynamics and kidney function].

24 patients with severe heart failure (NYHA III) were randomly assigned to an additional therapy with captopril or enalapril. The mean daily dose of captopril was 56 +/- 2 mg and of enalapril, 9.6 +/- 0.9 mg. After a mean of 9 days, the influence of both inhibitors of the angiotensin converting enzyme (ACE-inhibitors) on hemodynamics and renal function was evaluated. The mean arterial pressure in the group treated with captopril (group A) fell by 11 +/- 2 mm Hg (p less than 0.001), with enalapril (group B) by 13 +/- 3 mm Hg (p less than 0.01), the difference between the groups not being significant. Heart rate decreased in both groups to a similar degree. The change was significant only in the patients treated with enalapril (13 +/- 4/min; p less than 0.05 vs. 11 +/- 5/min in group A). Stroke volume index increased by 10 +/- 2 ml/m2 in group A vs. 12 +/- 2 ml/m2 in group B; both increases were highly significant (p less than 0.001). Mean decreases in pulmonary artery and right atrial pressure were comparable in both groups. The hemodynamic improvement was not different with both ACE-inhibitors. Serum sodium and potassium before therapy were 137 +/- 1 mmol/l and 4.1 +/- 0.2 mmol/l in group A and 139 +/- 1 mmol/l and 3.8 +/- 0.1 mmol/l in group B and serum creatinine was 1.2 +/- 0.1 mg/dl in both groups. Neither serum electrolytes nor serum creatinin were changed significantly by therapy with captopril or enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[5-year survival rate in acute transmural heart infarct following thrombolysis and immediate coronary angioplasty].

Two-hundred-eighty-six patients with acute transmural myocardial infarction underwent thrombolytic treatment (Streptokinase) between 1980 and 1986. In the earlier years patients were treated by thrombolysis only (n = 158) and in more recent years by thrombolysis followed by immediate percutaneous transluminal coronary angioplasty (n = 128). Age, sex, incidence of previous infarction and incidence of multivessel disease were comparable between groups. Patency of the infarct vessel (TIMI 3) was higher after thrombolysis combined with angioplasty than after thrombolysis alone (87% vs. 70%, p less than 0.001), and the residual stenosis of the infarct vessel was lower (46% vs. 84%, p less than 0.05). Hospital mortality (thrombolysis combined with angioplasty vs. thrombolysis alone) was 6% vs. 13%; one-year mortality was 8% vs. 21%, and five-year mortality was 18% vs. 31% (p less than 0.02). We conclude that treatment of patients with acute transmural myocardial infarction by thrombolysis combined with angioplasty is followed by a better long-term prognosis than treatment by thrombolysis only.

Angioplasty, Balloon↗
PubMed1987

Ramipril and captopril in patients with heart failure: effects on hemodynamics and vasoconstrictor systems.

Fifteen patients with congestive heart failure (New York Heart Association III) were randomly assigned to treatment with either captopril or ramipril, a newly developed angiotensin converting enzyme inhibitor. Both groups were similar with respect to baseline hemodynamic measurements and plasma levels of norepinephrine, renin and vasopressin. The group receiving ramipril showed hemodynamic changes comparable to the group receiving captopril on the seventh day of treatment. The stroke volume index increased by 20% versus 21%, respectively, and the total peripheral resistance decreased by 13% versus 20%, respectively. The decrease in blood pressure and the tendency to decrease heart rate were similar in both groups. All patients had reactive hyperreninemia during therapy with the converting enzyme inhibitor. The resting elevated plasma norepinephrine decreased in both groups significantly, whereas vasopressin did not change. The hemodynamic improvement was more pronounced and comparable in both groups during exercise. Thus, ramipril is equally effective compared with captopril in the treatment of patients with severe congestive heart failure.

Adult↗
PubMed1987

[Thrombolysis in acute myocardial infarct. An improved long-term prognosis following balloon dilatation].

UNLABELLED: A systemic and intracoronary thrombolytic treatment was carried out in 217 patients with acute transmural myocardial infarction between March 1980 and March 1985. 141 patients were only treated with thrombolysis, and 76 were additionally treated by balloon dilation in the same session. Indications for additional balloon dilation were unsuccessful thrombolysis as well as a residual stenosis of more than 50% after primarily successful thrombolysis. Age, sex, proportion of patients with anterior and posterior wall infarction as well as with 1, 2 and 3-vessel disease did not significantly differ in the two groups. The result of therapy (complete reperfusion) was less after thrombolysis than after thrombolysis with balloon dilation (63% as compared to 88%, P less than 0.0003). The patients who were only treated with thrombolysis had a more unfavorable three-year actuarial survival than those in whom thrombolysis and balloon dilation were carried out (70% as compared to 90%, P less than 0.02). CONCLUSION: additional balloon dilation in thrombolytic treatment of acute transmural myocardial infarction improves the long-term prognosis.

Angioplasty, Balloon↗
PubMed1986

[Reinfarction after initially successful thrombolysis in acute myocardial infarct].

UNLABELLED: In 24 of 77 patients (31%, group A), successfully treated by intracoronary streptokinase infusion in the acute stage of a transmural myocardial infarction, reocclusion of the infarct artery occurred within four weeks, in 15 patients with, in the remaining nine without re-infarction symptoms. The age of the patients, frequency of single, double or triple-vessel disease, number of anterior and posterior wall infarcts, creatine-kinase activity before and during treatment, and degree of stenosis at first contrast-medium injection were all comparable in the patients with or without re-occlusion (53 patients, group B). At the end of the acute treatment, in five patients of group A (21%) and in 17 of group B (32%) combined with balloon dilatation at the same time as the infusion, residual stenosis was significantly higher in group A than group B (75%) and 62%, respectively; P less than 0.001). No patient with a residual stenosis of less than 50% (18, of whom 12 had balloon dilatation) had a re-occlusion. CONCLUSION: A residual stenosis of at least 50% after initially successful thrombolysis presents a marked re-infarction risk and should lead to a second intervention in such cases.

Adult↗