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Biomedical subjects

U Tönnesmann

Publications and source records attributed to U Tönnesmann.

At least 19 recordsLinked to original sources
PubMed2002

[Blood coagulation in normotensives and hypertensives in relation to their body mass index].

UNLABELLED: BACKGROUND AND PERSPECTIVE: Various parameters of the coagulation cascade and fibrinolysis are important predictors of myocardial infarction and stroke, for which hypertension is a risk factor. It is unclear whether an elevated blood pressure by itself can produce activated clotting. PATIENTS AND METHODS: Coagulation tests were done on overweight hypertensive (n=40); aged 49 +/- 8 years; group 3), overweight normotensives (n=19; aged 51 +/- 8 years; group 2) and normal-weight normotensives (n=20; aged 51 +/- 8; group 1). RESULTS: Plasminogen-activator-inhibitor 1 (PAI-1), a measure of impaired fibrinolysis, was elevated in group 2 (20.5 +/- 11 U/ml; p < 0.001), compared with group 1 (11.6 +/- 6 U/ml), and was even higher in group 3 (27.5 +/- 9 U/ml; p < 0.05). Fibrinogen and factor VIII, parameters that promote clotting, were elevated in group 2 (360 +/- 61 mg/dl and 143 +/- 15 %, respectively; p < 0.001), and in group 3 (368 +/- 63 mg/dl and 146 +/- 18%; p < 0.001) compared to group 1 (304 +/- 40 mg/dl and 127 +/- 17%). Correspondingly, fibrin monometers, a measure of intravascular coagulation, were elevated in group 3 (p < 0.05) and partial thromboplastin time (PTT) decreased (p < 0.001). Pearson correlation showed a significant (p < 0.001) positive relationship between PAI-1 and body mass index (BMI) (0.539), triglycerides (0.512), blood pressure (0.388 to 0.534), fibrinogen (0.404, and a negative one with HDL-cholesterol (0.625). BMI also correlated with fibrinogen (0.509; p < 0.001) and factor VIII (0.337; p < 0.01). CONCLUSIONS: Fibrinolysis and activated coagulation are reduced in hypertensive subjects: this favours the occurrence of myocardial infarction and stroke. In addition to the level of blood pressure, the extent of the changes are effected especially by BMI and metabolic risk factors.

Adult↗
PubMed1998

Time course of complete normalization of left ventricular hypertrophy during long-term antihypertensive therapy with angiotensin converting enzyme inhibitors.

Metaanalyses have indicated that ACE inhibitors are more effective than other first-line therapies in reducing left ventricular hypertrophy (LVH). The average treatment period, however, was only approximately 6 months. The aim of the present study, therefore, was to clarify the time course and degree of reversal, and primarily to find out in how many patients a complete normalization of LVH can be achieved. Secondly, we sought to determine whether atrial enlargement can be reduced. Previously untreated hypertensive patients (mean age 46.3 +/- 9 years, eight women, 15 men) with echocardiographically confirmed LVH (left ventricular mass index ([LVMI] > 125 g/m2 for men; > 110 g/m2 for women) were prospectively treated over a 3-year treatment period with quinapril. Nine patients received 10 mg quinapril, 12 received 20 mg of quinapril daily, and five patients additionally received 25 mg hydrochlorothiazide. The time course of changes in LVMI, relative wall thickness, left atrial size, fractional shortening, and diastolic function was evaluated and ambulatory blood pressure monitoring (ABPM) and an exercise test were performed every 6 months. After a mean treatment period of only 7.5 months, there was a significant (P < .001), 17.5% decrease in LVMI with a further continuous and significant (P < .001) decrease of 38.6% after 38.3 +/- 3 months of therapy. In 90.5% of the patients a complete reversal of LVH was achieved. Fractional shortening increased significantly, the maximum being 14.6% after 38.3 +/- 3 months. The peak early/atrial velocity (E/A) ratio increased significantly (P < .01) after just 7.5 +/- 3.1 months with no further changes during follow-up. There seemed to be a parallel change with the decrease in left atrial dimension, where the most important decrease occurred after only 7.5 +/- 3.1 months (P < .01), with a further continuous reduction. Our study clearly shows that maximum reversal of LVH is a time-consuming process and that an essential goal of antihypertensive therapy should be not only a reduction in LVH but also a normalization in LV mass, left atrial size, and in diastolic dysfunction.

Adult↗
PubMed1998

Enalaprilat improves the impaired left ventricular pump function during exercise in hypertensives with coronary microangiopathy and with coronary artery disease.

BACKGROUND: The pump function during exercise can be disturbed not only in hypertensives with coronary artery disease (CAD), but also in those with a normal angiogram. METHODS: In 10 hypertensive patients (group 1; aged 52+/-4 years, 1 men, 9 women) with ST segment depression during exercise and concomitant angina pectoris but normal coronary angiograms (microangiopathy) and without left ventricular hypertrophy (LVMI <110 g/m2), the left ventricular function at rest and during exercise was studied by cardiac catheterization and compared with 10 hypertensives with CAD (group 2; aged 57.6+/-4 years, 7 men, 3 women) and 10 hypertensives without ST segment depression (group 3; aged 51.8+/-5 years, 10 men) before and after intravenous administration of 1.25 mg enalaprilat. RESULTS: The pulmonary capillary wedge pressure (PCWP) was normal at rest and pathologically increased at 60+/-13 W only in groups 1 and 2 (27.2+/-3 and 32.2+/-8 mm Hg, respectively), but not in group 3 (12.2+/-4 mm Hg; p<0.001). At the identical load level, the PCWP in patients with microangiopathy (group 1) was significantly (p<0.01) reduced after enalaprilat (-21.7%) and even normalized in 5 of 10 patients. This was accompanied by a significant (p>0.01) decrease in ST segment depression (-73.9%) and in the occurrence of angina pectoris, despite the fact that the rate-pressure product as a measure of myocardial oxygen consumption was significantly (p<0.05) increased. Also in patients with CAD enalaprilat had a significant effect on PCWP (p<0.01), ST segment depression (p<0.01), occurrence of angina pectoris (p<0.001), cardiac index (p<0.05), and stroke index (p<0.05) during exercise. In group 3 there were no significant changes in PCWP, cardiac index, and stroke index after enalaprilat either at rest or during exercise. CONCLUSION: The functional improvement under the action of enalaprilat suggests that the advantages of the drug may be mediated mainly through an increase in myocardial blood flow and that angiotensin II might be involved in the restricted increase in coronary blood flow during dynamic exercise in hypertensives with coronary microangiopathy.

Angina Pectoris↗
PubMed1997

[Exercise hemodynamic in hypertension associated with coronary microangiopathy, coronary heart disease and without ischemic syndrome effect of nifedipine].

OBJECTIVE: Is heart function during exercise impaired in hypertensive patients with effort angina and ST-segment depression but normal coronary angiograms? METHODS AND RESULTS: In 12 hypertensive patients (group 1; aged 53 +/- 4 yrs), who had ST-segment depression during exercise, concomitant angina pectoris but normal coronary angiograms, and no LVH, left ventricular function at rest and during exercise was studied by cardiac catheterization and compared with 12 hypertensives with CAD (group 2; aged 56 +/- 5 yrs) and 12 hypertensives without ST-segment depression (group 3; aged 56 +/- 7 yrs) after discontinuation of all cardiac medications. PCWP was normal at rest and pathologically increased at 79.2 +/- 17.9 watts only in group 1 and 2 (30.2 +/- 6 mm Hg; 31.5 +/- 5 mm Hg, respectively) but not in group 3 (18.5 +/- 3 mm Hg; p < 0.001). Repeated measurements during exercise and 30 min after 10 mg nifedipine orally, showed a significant (p < 0.001) and nearly identical fall in MAP, an increase in CI (p < 0.01), and an unchanged HR x SBP in all groups. However there were significant differences in decrease of PCWP (group 1: -41.4%; group 2: -22.9%, p < 0.01; group 3: -25.4%, p < 0.01) with concomitant reduction in ST-segment depression (p < 0.01) in group 1 and 2 (-43.7% and -36% respectively). CONCLUSIONS: ST-segment depression during exercise ECG with concomitant angina pectoris is not a false-positive finding in hypertensive patients with normal angiograms and without LVH but demonstrates myocardial ischemia, resulting in an impaired left ventricular heart function. This seems to be mainly caused by a functional changeable disorder of the coronary vascular bed as heart function is improved after nifedipine.

Coronary Disease↗
PubMed1996

[Decreasing the antihypertensive dosage during longterm treatment and complete regression of left ventricular hypertrophy].

AIM OF STUDY: To discover whether in hypertensives with left ventricular hypertrophy (LVH) the increased muscle mass will completely regress under antihypertensive treatment and drug dosage can in consequence be reduced. PATIENTS AND METHOD: Prospectively 22 previously untreated hypertensives (20 men, 2 women; mean age 43.6 +/- 9 years) with echocardiographically confirmed LVH were investigated. The observation period was 102 +/- 5 months. All patients initially received metoprolol, 100 mg daily, after 14 days 200 mg daily (additionally hydrochlorothiazide in five patients). In all patients the blood pressure became normal at rest and on exercise within 6 weeks. RESULTS: After one year the mean left ventricular muscle mass index (LVMI) had fallen from 151 +/- 29 to 117 +/- 26 g/m2 (P < 0.001), and after 7 years to 82 +/- 14 g/m2 (P < 0.001; - 45.7%). Complete remission of LVH was demonstrated in 21 Patients. The drug dosage could either be reduced or the drug completely discontinued in 11 patients (group 1): after 102 +/- 5 months four patients took no drug, while seven were on 100 mg metoprolol. This was not possible in the other 11 patients (group 2), five of whom had been on both metoprolol and hydrochlorothiazide. The two groups differed with respect to loss of body weight (group 1: from 81.+/- 12 to 79.1 +/- 13 kg; P < 0.05; group 2: 85.7 +/- 8 to 88.1 +/- 10 kg; P < 0.05), but not regarding reduction of LVMI and blood pressure. CONCLUSION: Antihypertensive treatment for several years leads to regression in LVH in nearly all patients. In half of them the drug dosage can be reduced or the drug even discontinued. Weight loss may play an important part in this development.

Adult↗
PubMed1994

Time course of reduction in left ventricular mass during long-term antihypertensive therapy.

Left ventricular mass sometimes decreases during treatment of hypertension but the effects are inconsistent and the response to long-term treatment is unknown. Therefore the long-term effects of antihypertensive therapy on echocardiographically-proven left ventricular hypertrophy (LVH) were prospectively investigated in 117 previously untreated hypertensive patients (mean age 46 +/- 9 years; 15 women and 102 men). Twenty-two patients received 100 mg of gallopamil daily, 24 patients received 200 mg of metoprolol, 35 patients received both 50 mg of atenolol and 20 mg of nifedipine (follow-up five years), 14 patients received 200 mg of acebutol plus 20 mg of nifedipine, and 21 patients received 50 mg of atenolol and 10 mg of enalapril daily (follow-up of four years). For the entire population, there was a significant (P < 0.001) decrease in left ventricular mass index (LVMI; measurements were performed blind by two observers) of 24.5% after one year, with a further continuous and significant (P < 0.001) reduction of 44.1% after five years of treatment. There was a significant (r = 0.61, P < 0.001) correlation between the extent of LVMI before therapy and the percentage of regression of LVMI after five years of treatment. In 82% of the patients, almost complete regression of LVH was achieved. Nevertheless, there was no significant change in ventricular end-diastolic dimension but fractional shortening increased by 16% (P < 0.001). It can be concluded that achieving maximum regression of LVH by antihypertensive therapy in previously untreated hypertensives takes a long time and depends not only on the drug regimen chosen but especially on the duration of treatment and the extent of pretreatment left ventricular mass.

Adult↗
PubMed1992

[Disordered 24-hour blood pressure rhythm in normotensive and hypertensive asthma patients].

Asthmatic patients typically show a nocturnal increase in bronchial obstruction. In 100 asthmatic patients, we investigated if there is also a reduced decline of blood pressure; we used 24-h blood-pressure monitoring. The whole group consisted of 50 hypertensive asthmatic patients (group 1, 48.8 +/- 11 years, 30 females, 20 males), 25 normotensive asthmatic patients (group 2, 49.6 +/- 10 years, 22 females, 3 males) and 25 antihypertensive-treated asthmatic patients (group 3, 50.2 +/- 8 years, 15 females, 10 males). 52% of group 1, 52% of group 2, and 44% of group 3 patients showed no sufficient nocturnal systolic and diastolic blood pressure decline (less than - 15%). When we looked only for systolic blood pressure that was also the case in 82%, 92%, and 64% of the patient groups', respectively. There was no significant difference in daytime blood pressure between hypertensives (group 1) without (142 +/- 9/93 +/- 5 mmHg) and with 142 +/- 12/92 +/- 6 mmHg) sufficient nocturnal blood pressure decline, however, nighttime blood pressure (135 +/- 14/84 +/- 5 mmHg versus 123 +/- 14/72 +/- 6 mmHg) was significantly (p less than 0.0001) different. This was also true for the normotensive asthmatic patients (group 2). The results cannot be explained by differences in heart rate, degree of asthma, or in anti-obstructive medication.

Asthma↗
PubMed1991

Long-term studies on regression of left ventricular hypertrophy.

The long-term effects of antihypertensive therapy on echocardiographically proven left ventricular hypertrophy (LVH) were investigated in 117 previously untreated hypertensive patients (mean age of 46 +/- 9 years; 15 women, 102 men). Twenty-two patients (group 1) received daily 100 mg of gallopamil, 25 (group 2) received 200 mg of metoprolol, 35 (group 3) received both 50 mg of atenolol and 20 mg of nifedipine (follow-up of 5 years), 14 (group 4) received 200 mg of acebutolol and 20 mg of nifedipine, and 21 (group 5) daily received 50 mg of atenolol and 10 mg of enalapril (follow-up of 4 years). For the entire population, there was a significant (p less than 0.001) decrease in left ventricular mass index (LVMI) of 24.5% after 1 year, which increased further to 44.1% after 5 years of treatment. In addition, fractional fiber shortening increased by 16% (p less than 0.001). In 82% of the patients, almost complete regression of LVH was achieved. However, the time course of regression of LVMI differed significantly between the five treatment groups, despite similar blood pressure reduction under resting conditions.

Adult↗
PubMed1991

Impaired left ventricular function during exercise in hypertensive patients with normal coronary arteriograms.

Patients with left ventricular hypertrophy (LVH) often exhibit manifestations of myocardial ischemia. In 17 hypertensive patients (group 1, mean age of 56 +/- 4 years, 10 females, 7 males) with ST-segment depression during the exercise electrocardiogram (ECG) and effort angina and normal coronary arteriograms, the left ventricular function at rest and during exercise was studied by heart catheterization. The results were compared with 17 hypertensive patients (group 2, mean age of 56 +/- 6 years, 6 females, 11 males) with coronary artery disease (CAD). The normal pulmonary wedge pressure at rest (group 1, 8.9 +/- 3 mm Hg; group 2, 8.9 +/- 3 mm Hg) was pathologically increased (p less than 0.001) in both groups (group 1, 27.1 +/- 5 mm Hg; group 2, 28.8 +/- 7 mm Hg) even at a work load of 50 W with a further increase at 75 W to 31 +/- 4 and 29.7 +/- 4 mm Hg, respectively. Cardiac output was normal. There was no significant correlation between ST-segment depression, pulmonary wedge pressure, LVH, and Holter ECG. Hypertensive patients without CAD may reveal a disturbed pump function due to ischemia even at low work loads, which does not differ significantly from patients with CAD. This may provoke subendocardial fibrosis and thereby contribute to the development of heart failure.

Blood Pressure↗
PubMed1990

[Regression of left ventricular hypertrophy in hypertensive patients under long-term therapy with antihypertensive agents].

The effect of long-term therapy of hypertension with antihypertensive drugs was investigated in 117 previously untreated patients (15 women, 102 men; mean age 46.4 +/- 9 years) with echocardiographically proven left-ventricular hypertrophy. 22 patients (group 1) received 100 mg/d Gallopamil, 25 (group 2) received 200 mg/d Metoprolol, 35 daily received both 50 mg Atenolol and 20 mg Nifedipine (group 3), 14 received daily 200 mg Acebutolol plus 20 mg Nifedipine (group 4), and 21 (group 5) 50 mg Atenolol plus 10 mg Enalapril daily. The treatment period lasted a mean of 38 (36.2-42.3) months. Left-ventricular muscle mass index (LVMI) as well as septal and posterior-wall thickness decreased significantly after 12.8 and 38.5 months (P less than 0.001). After a mean of 38.5 months LVMI had decreased by 36.7% in group 1, 35.1% in group 2, 42.3% in group 3, 45% in group 4 and 39.6% in group 5. LVMI was within normal range (less than or equal to 95 g/m2) in 81 of the 117 patients (69.2%) at the end of the treatment period. There was, however, no significant increase of the end-diastolic dimension of the left ventricle, but a significant increase of "fractional shortening" as a measure of myocardial contractility.

Acebutolol↗
PubMed1989

Regression of left ventricular hypertrophy by acebutolol and nifedipine.

Fourteen patients with previously untreated essential hypertension and left ventricular hypertrophy were treated with a fixed-dose combination of acebutolol 200 mg and nifedipine 20 mg once daily for a followup of 25.6 +/- 1.8 months. Echocardiography showed a significant decrease after a mean period of 6.6 months in interventricular septal thickness (14.8%, p less than 0.001), posterior wall thickness (14.8%, p less than 0.001), and left ventricular mass index (21.3%). After 25.6 months, the reductions were 29% (p less than 0.001), 28.1% (p less than 0.001), and 38.7% (p less than 0.001), respectively. Left wall thickness was significantly reduced, but left ventricular end-systolic and end-diastolic dimensions and fractional shortening remained unchanged. Treatment reduced resting blood pressure from 161/102 mmHg to 132/87 mmHg (p less than 0.001) and reduced exercise blood pressure at 100 W from 208/113 mmHg to 170/94 mmHg (p less than 0.001). Thus, nifedipine in combination with acebutolol produces significant blood-pressure reduction accompanied by regression of left ventricular hypertrophy without noticeable changes in left ventricular function.

Acebutolol↗
PubMed1989

[Regression of left heart hypertrophy in hypertensive patients as a result of antihypertensive therapy].

In a previous study (1) we could show a significantly more pronounced reversal of LVH with metoprolol than with gallopamil, whereas the combined therapy with atenolol and nifedipine was even more effective. We now report in 121 previously untreated hypertensive patients the longterm effect of the beta-blocker metoprolol (200 mg/die); 25 patients, mean age 43.6 yrs., follow-up 32.1 +/- 3.5 months, group A); the calcium antagonist gallopamil, 26 patients, mean age 49.7 yrs., follow-up 36.2 +/- 2.6 months, group B); the combined therapy with 50 mg atenolol and 20 mg nifedipine, 35 patients, mean age 44.5 yrs., follow-up 31.7 +/- 1.1 months, group C); 200 mg acebutolol and 20 mg nifedipine, mean age 52.1 yrs., follow-up 31.8 +/- 1.8 months, group D); 50 mg atenolol and 10 mg enalapril, mean age 43.3 yrs., follow-up 31.9 +/- 1.3 months, group E). Similar results were obtained for intraventricular septal and posterior wall thickness. Left ventricular enddiastolic dimensions remained unchanged but fractional shortenings were significantly (p less than 0.05-p less than 0.01) increased after 32 months of treatment.

Acebutolol↗
PubMed1988

Regression of left ventricular hypertrophy during combined atenolol and nifedipine treatment.

36 patients with previously untreated essential hypertension and left ventricular hypertrophy were treated with a fixed dose combination of atenolol 50 mg and sustained release nifedipine 20 mg once daily for a mean period of 12.1 months. Echocardiography showed a significant decrease after a mean period of 7.9 months in interventricular septal thickness (13.6%, p less than 0.01), posterior wall thickness (12.6%, p less than 0.001) and left ventricular mass index (18.3%). After 12.1 months the reductions were 20.7% (p less than 0.001), 22.5% (p less than 0.001) and 30.8% (p less than 0.001), respectively. Posterior wall thickness was significantly reduced, but left ventricular end-systolic and end-diastolic dimensions and fractional shortening remained unchanged. Treatment significantly reduced resting blood pressure from 153/105 mm Hg to 122/79 mm Hg (p less than 0.001), and exercise blood pressure at 100W from 189/109 to 157/93 mm Hg (p less than 0.001). Thus, nifedipine in combination with atenolol produces significant blood pressure reduction accompanied by regression of left ventricular hypertrophy without noticeable changes in left ventricular function.

Adult↗
PubMed1987

Long-term effect of antihypertensive therapy on left ventricular hypertrophy.

We studied a total of 88 previously untreated hypertensives in order to determine the long-term effect of antihypertensive therapy on echocardiographically confirmed left ventricular hypertrophy. The drugs tested were the beta-blocker metoprolol (200 mg/day; 26 patients; mean age 43.9 years; follow-up 32 months), the calcium antagonist gallopamil (100-150 mg/day; 26 patients; mean age 49.7 years; follow-up 23 months) and a combination of 50 mg atenolol and 20 mg nifedipine (36 patients; mean age 44.2 years; follow-up 18 months). Despite similar reductions in resting blood pressure, each of the three therapeutical regimens had a different effect on the left ventricular mass index after 1 year of treatment: gallopamil reduced the index by 13.2% (170 +/- 49 to 148 +/- 41 g/m2, P less than 0.001), metoprolol by 21.9% (150 +/- 27 to 117 +/- 27 g/m2, P less than 0.001) and atenolol + nifedipine by 30.8% (148 +/- 33 to 103 +/- 21 g/m2, P less than 0.001). Similar results were obtained for interventricular septal (9.9, 15.4 and 20.7%, respectively) and posterior wall thicknesses (10.4, 16.7 and 24.1%, respectively). During the follow-up there was a further significant reduction in ventricular hypertrophy under all three treatments, but no significant changes in ventricular end-diastolic and end-systolic dimensions or in fractional shortening.

Adult↗
PubMed1986

Effects of single oral doses of bisoprolol and atenolol on airway function in nonasthmatic chronic obstructive lung disease and angina pectoris.

A randomized, placebo-controlled, double-blind crossover investigation in 12 patients with non-asthmatic chronic obstructive lung disease and co-existing stable angina pectoris was done to compare two beta 1-selective adrenoceptor blocking agents, atenolol 100 mg and bisoprolol 20 mg. Systolic and diastolic blood pressures (SBP, DBP), heart rate (HR) as well as airway resistance (AWR, and less frequently forced expiratory volume in 1 s (FEV1) and intrathoracic gas volume (ITGV) were measured in the sitting position before and at various times up to 24 h after drug intake. During the first 4 h both beta-blockers produced a significant reduction in HR in comparison to placebo (p less than 0.01). Atenolol 100 mg significantly increased AWR relative to placebo and bisoprolol (p less than 0.05). After 24 h, a significant reduction in HR (p less than 0.01) could only be demonstrated after bisoprolol, whereas atenolol alone led to a significant elevation in AWR relative to placebo and bisoprolol (p less than 0.05) at that time. It is concluded that bisoprolol appears to have a high degree of beta 1-selectivity, thus providing a wide split between beta 1- and beta 2-adrenoceptor blockade. Bisoprolol in its therapeutic dose range is expected to be relatively safe as regards bronchoconstriction in patients suffering both from hypertension and/or angina pectoris and chronic obstructive lung disease.

Adrenergic beta-Antagonists↗
PubMed1984

Dose-response relationship of the beta-adrenoceptor antagonist bisoprolol in patients with coronary heart disease and chronic obstructive bronchitis.

The effects of single, consecutively increased, oral doses of the beta-adrenoceptor antagonist bisoprolol (5, 10, 15, 20, 30 and 40 mg) on blood pressure, heart rate and bronchomotor tone were investigated in an open acute trial with 16 patients suffering from angina pectoris due to coronary heart disease and reversible chronic obstructive bronchitis. Even the lowest dose of bisoprolol (5 mg) caused a marked, long-lasting reduction in blood pressure and heart rate. After doses exceeding 20 mg, the incidence of an exaggerated pharmacodynamic effect on heart rate (beta 1-blockade) increased with dose. At doses above 30 mg, bisoprolol showed incipient impairment of bronchomotor function (beta 2-blockade) in individual patients. It is concluded that bisoprolol exhibits high beta 1-selectivity, i.e. a wide beta 1/beta 2 split, since blockade of bronchial beta 2-receptors only occurred at doses well above the therapeutically relevant dose range. The results may not be applicable to chronic treatment.

Adrenergic beta-Antagonists↗
PubMed1981

Acute poisoning with pine oil - metabolism of monoterpenes.

A patient attempting suicide ingested 400-500 ml pine oil and was admitted to the clinic. Since more than the lethal dose had been ingested hemoperfusions with activated charcoal and amberlite and a hemodialysis were performed. The composition of the ingested pine oil was determined by gaschromatography/mass spectrometry. Four monoterpenes were identified: 57% alpha-pinene, 8% beta-pinene, 26% carene, 6% limonene and 3% other hydrocarbons. The blood and urine monoterpene concentrations were continuously monitored. The data suggest that monoterpenes are poorly resorbed in the gastrointestinal tract. The resorbed portion of the hydrocarbons cumulates in the lipophilic body compartments and is slowly metabolized and then excreted by the kidneys. The main metabolic pathways are hydratation, hydroxylation, rearrangement, and acetylation. Five metabolites were identified.

Bicyclic Monoterpenes↗