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Biomedical subjects

G Autenrieth

Publications and source records attributed to G Autenrieth.

At least 19 recordsLinked to original sources
PubMed1992

Cholinergic baroreflex vasodilatation: defect in heart transplant recipients due to denervation of the ventricular baroreceptor.

Afferent denervation of the ventricular baroreceptor may impair reflex vasodilatation after heart transplantation. This may alter the regulation of blood pressure and contribute to arterial hypertension. A baroreceptor-loading procedure was performed in 23 heart transplant recipients with cyclosporine A immunosuppression and 11 control subjects using a continuous infusion of increasing doses of angiotensin II (15 and 30 ng/kg.min). After m-cholinoceptor blockade the procedure was repeated in order to study the contribution of cholinergic effects on vasodilatation in humans. Instantaneous vascular resistance was calculated as the ratio of mean blood pressure to stroke volume as evaluated by echocardiography. When heart transplant recipients were compared with control subjects, infusion of 30 ng/kg.min of angiotensin II resulted in an increase in mean blood pressure of 43 +/- 20 vs 31 +/- 13 mm Hg (p less than 0.05) and an increase in instantaneous resistance of 1.21 +/- 0.61 vs 0.65 +/- 0.38 mm Hg/ml (p less than 0.01), respectively. M-cholinoceptor blockade with atropine (0.015 mg/kg) did not produce any change in blood pressure or resistance response to angiotensin II in heart transplant recipients. However, m-cholinoceptor blockade resulted in a significantly increased blood pressure and resistance response to angiotensin II in control subjects, which was similar to the response in heart transplant recipients to angiotensin II alone: The increase in mean blood pressure during administration of 30 ng/kg.min angiotensin II amounted to 47 +/- 11 mm Hg, and the increase in instantaneous resistance to 1.13 +/- 0.48 mm Hg/ml (for both, p less than 0.001 vs control subjects without atropine; p = not significant vs heart transplant recipients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Antiadrenergic effect of M-cholinoceptor stimulation on human ventricular contractility in vivo.

The relevance of an indirect negative inotropic effect of pharmacological or vagally mediated M-cholinoceptor stimulation in the human ventricle in vivo is unknown. The inotropic response induced by isoproterenol (isoprenaline, 20 ng.kg-1 x min-1), measured by m-mode echocardiography as the increase of fractional shortening in seven healthy subjects, was reduced from 17.1 +/- 4.3 to 9.1 +/- 3.9% (P < 0.01) by M-cholinoceptor stimulation using intravenous injection of 3.6 micrograms/kg carbachol. However, the inotropic response of increasing doses of isoprenaline (5-20 ng.kg-1 x min-1) did not differ in 13 healthy subjects without and after M-cholinoceptor blockade (atropine, 0.015 mg/kg i.v.); the increase of fractional shortening amounted to 17.4 +/- 4.0 vs. 19.5 +/- 4.8% (NS) in response to 20 ng.kg-1 x min-1 isoprenaline. It is concluded that pharmacological M-cholinoceptor stimulation of the human ventricle significantly reduces the inotropic response of beta-adrenoceptor stimulation. This may offer a new therapeutic approach to attenuate an increased cardiac sympathetic tone. However, M-cholinoceptor blockade, i.e., interruption of parasympathetic influences, does not augment the inotropic response to beta-adrenoceptor stimulation. Therefore, in healthy resting humans a physiological role of the parasympathetic nervous system in mediating an indirect negative inotropic effect on ventricular contractility seems to be absent.

Adult↗
PubMed1992

Isolated presynaptic inotropic beta-adrenergic supersensitivity of the transplanted denervated human heart in vivo.

BACKGROUND: The regulation of contractility of the transplanted heart depends on circulating catecholamines resulting from cardiac denervation. Supersensitivity to circulating catecholamines may result from loss of presynaptic neuronal uptake or upregulation of postsynaptic beta-adrenergic receptors. METHODS AND RESULTS: Dose-response curves using the beta-adrenergic receptor agonists isoprenaline (no neuronal uptake) and epinephrine (neuronal uptake) were performed in vivo. The inotropic response was measured echocardiographically as the increase of fractional shortening (delta FS) and the increase of the systolic pressure/dimension ratio (delta P/D). The inotropic response to increasing doses of isoprenaline (5-20 ng/kg.min) was identical in 36 heart transplant recipients compared with 13 control subjects: delta FS during 20 ng/kg.min isoprenaline amounted to 18.2 +/- 6.2% versus 17.4 +/- 4.0% (NS) and delta P/D to 2.3 +/- 1.2 mm Hg/mm versus 2.2 +/- 0.5 mm Hg/mm (NS), respectively. A vagally mediated indirect negative inotropic effect in the innervated hearts was excluded by identical inotropic responses to isoprenaline in control subjects without and after atropine pretreatment. The inotropic response to increasing doses of epinephrine (10-40 ng/kg.min) was significantly augmented in 13 heart transplant recipients compared with 11 control subjects: delta FS during 40 ng/kg.min epinephrine amounted to 19.9 +/- 2.6% versus 8.6 +/- 2.0% (p less than 0.001) and delta P/D to 2.3 +/- 0.9 mm Hg/mm versus 0.6 +/- 0.3 mm Hg/mm (p less than 0.001), respectively. Pretreatment with desipramine (blockade of neuronal uptake) in control subjects resulted in a significantly increased inotropic response: delta FS during 40 ng/kg.min epinephrine amounted to 17.6 +/- 3.6% (p less than 0.001 versus untreated controls, NS versus heart transplant recipients) and delta P/D to 1.7 +/- 0.8 mm Hg/mm (p less than 0.001 versus untreated controls, NS versus heart transplant recipients). CONCLUSIONS: These findings provide evidence against a postsynaptic inotropic supersensitivity or subsensitivity of the beta-adrenergic receptor-effector system of the transplanted denervated human heart in vivo. However, a marked presynaptic inotropic supersensitivity is present because of denervation-associated loss of neuronal catecholamine uptake.

Adult↗
PubMed1991

Contractility of the transplanted, denervated human heart.

The purpose of the study was to characterize the contractility of the transplanted human heart and to evaluate possible adverse effects of denervation or structural changes of the myocardium or coronary vessels. As an index of contractility, the linear slope k of the end-systolic pressure/dimension relationship during afterload increase with angiotensin II was determined by M-mode echocardiography in 34 heart transplant recipients and 20 healthy control subjects. Baseline findings for end-systolic diameter and systolic blood pressure were normal and similar in both groups, but the transplanted hearts performed at a significantly lower end-systolic wall stress (40.4 +/- 12 gm/cm2 vs 49.9 +/- 11 gm/cm2, p less than 0.001). Comparable increase of afterload was achieved in heart transplant recipients with significantly (p less than 0.001) less angiotensin II, which indicates increased vasoconstrictor sensitivity. Contractility index k did not differ between heart transplant recipients (12.95 +/- 4.9 mm/100 mm Hg) and control subjects (12.78 +/- 2.8 mm/100 mm Hg). This finding is consistent with a normal contractility of the transplanted, denervated human heart. Normal baseline contractility therefore is an intrinsic property of the intact heart, which is independent of autonomic neural control. Contractility was not compromised by increasing interval from transplantation or the presence of mild acute rejection or mild interstitial fibrosis. Mildly impaired contractility (k greater than 2 SD of k in control subjects) in four heart transplant recipients (12%) was neither associated with structural myocardial or coronary changes nor with rejection episodes or graft ischemic time. One may speculate that impaired contractility, which is present in a minority of heart transplant recipients, results from pretransplantation damage.

Adult↗
PubMed1990

[2 year interferon therapy of metastatic carcinoid tumor].

A 39 year old male patient was treated with daily 5 X 10(6) IU interferon alpha 2b s.c. for 22 months because of advanced carcinoid tumor. Objective response was achieved with greater than 50% reduction of 5-HIAA-excretion. Multiple metastases (liver, lung, bones, thyroid gland) were not progressing in size. An unintentional omission of treatment resulted in a rapid biochemical and morphological tumor progression. Reversibility was achieved with reinstitution of effective interferon therapy. Thus, interferon therapy of advanced carcinoid tumor is able to induce a long-term objective response. It seems to be superior to conventional chemotherapy.

Adult↗
PubMed1989

[Echocardiography with angiotensin administration in the diagnosis of adriamycin-induced cardiomyopathy].

Noninvasive assessment of early cardiotoxicity of doxorubicin is still a problem of clinical concern. We studied whether echocardiography during afterload stress induced by angiotensin II (1,000-3,000 ng/min) allows earlier detection of left ventricular impairment than echo at rest. We compared 30 normals (N) to 30 patients with carcinoma, who had received doxorubicin at a cumulative dose of at least 360 mg/sqm. At rest echocardiograms of patients were either normal (P1; n = 24) or abnormal (P2; n = 6; fractional shortening less than 28%, distance of mitral E-point to septum greater than 7 mm). Best parameter for separation of P1 vs N was the slope K of the regression line of the relation between endsystolic diameter and systolic blood pressure (cuff-method). 38% of P1 and 100% of P2 had K-values below the range of N (less than 4.7 mm Hg/mm). Four of five patients with reduced ejection fraction assessed by scintigraphy (less than 55%) after continued therapy with doxorubicin have had, in previous echocardiographic studies, normal resting parameters but abnormal K-values. We conclude that afterload-stress increases the sensitivity of echocardiography in detecting cardiotoxicity due to doxorubicin.

Adolescent↗