Biomedical subjects

H C Herrmann

Publications and source records attributed to H C Herrmann.

78 records · Page 5Linked to original sources

PubMed1983

Q-T prolongation and torsades de pointes ventricular tachycardia produced by the tetracyclic antidepressant agent maprotiline.

Tricyclic antidepressant drugs such as imipramine and desipramine have long been known to produce cardiovascular side effects including sinus tachycardia, prolongation of the P-R, QRS, and Q-T intervals, and decreased T-wave amplitude. Life-threatening ventricular ectopic activity has occurred after tricyclic drug overdose. Recently, maprotiline (Ludiomil), a tetracyclic anthracene-derivative antidepressant, has become available for the treatment of affective disorders. It appears as effective as the tricyclic drugs in relieving unipolar depression. Although several studies have reported a low incidence of cardiovascular side effects, others show little difference between the tetracyclic and tricyclic drugs. This report describes a patient in whom maprotiline treatment caused Q-T prolongation and life-threatening torsades de pointes ventricular tachycardia (VT).

Aged↗

PubMed1983

The feedback regulation of angiotensinogen production by components of the renin-angiotensin system.

The in vivo generation of angiotensin appears to be dependent on both plasma renin and angiotensinogen concentrations. Much less is known about the control of hepatic angiotensinogen synthesis and release, as compared to that of renin. In this study, we examined the feedback regulation of angiotensinogen synthesis and release by various components of the renin-angiotensin system, using an in vitro rat liver slice system. Livers were removed for study from rats which were subjected to various systemic infusions or physiological perturbations. Infusion of angiotensin II has been reported to increase angiotensinogen release rate. However, infusion of angiotensin I (with simultaneous suppression of plasma renin by antirenin antibody infusion and angiotensin II production by captopril administration) had no effect on the angiotensinogen release rate. Direct infusion of renin in rats treated with captopril resulted in further suppression of the angiotensinogen release rate, compared with those given captopril alone. We postulate that renin (or des-angiotensin I-angiotensinogen) inhibits the angiotensinogen release rate, whereas angiotensin II stimulates it. Angiotensin I has no effect on angiotensinogen release rate. This hypothesis was evaluated further in rats with various physiological states. Indeed, when conditions were such that the renin-angiotensin system was completely suppressed, such as binephrectomy and antirenin antibody infusion, angiotensinogen release rate was markedly stimulated. When angiotensin II production was prevented by captopril treatment, angiotensinogen release rate declined. This appeared to be the case for all states of sodium balance. Thus, angiotensinogen release rate is subject to a complex feedback control by other components of the renin-angiotensin system.

Angiotensin I↗

PubMed1981

The association of a hearing deficit with Larsen's syndrome.

A retrospective study of 45 cases of Larsen's syndrome reported since 1950 reveals a prevalence of cleft palate in this disease of about 30 per cent. Although cleft palate abnormalities in infancy invariably cause otitis media, which may result in hearing loss, only rarely have hearing deficits been reported in association with Larsen's disease. This paper reports the occurrence of a bilateral conductive hearing loss secondary to otitis media, and possible ossicular abnormality in a five-year-old with cleft palate and Larsen's disease and considers the possibility that this otologic problem may be more prevalent than currently suspected.

Abnormalities, Multiple↗

PubMed1980

Effect of angiotensin II and sodium depletion on angiotensinogen production.

An in vitro preparation of liver slices was used to study the effect of angiotensin II and sodium depletion on the synthesis of angiotensinogen in rats. Two other treatments known to increase plasma angiotensinogen concentration in vivo, viz., intraperitoneal administration of dexamethasone or ethinyl estradiol, resulted in an increase in the rate of release of angiotensinogen by liver slices; this increase was inhibited by adding actinomycin D or vincristine to the incubation medium. Intravenous infusion of angiotensin II (33 ng/min for 3 days) also produced a marked increase in the release of angiotensinogen concentration and a decrease in plasma renin activity. In contrast, no change in the rate of release of angiotensinogen was observed in rats depleted of sodium for 7--14 days, even though these animals exhibited a marked increase in plasma angiotensin II concentration. Plasma angiotensinogen concentration decreased by 30%, presumably as a consequence of the accompanying increase in renin secretion. These results provide further evidence that the synthesis of angiotensinogen may be increased by angiotensin II, but indicate that the circulating level of angiotensin II in sodium-deficient animals is not sufficiently high to produce this response.

Angiotensin II↗

PubMedDate not supplied

Hormonal control of angiotensinogen production.

The renin-angiotensin-aldosterone system appears to be under neural and hormonal control. Plasma angiotensinogen concentration is elevated in Cushing's disease, during pregnancy and in women taking oral contraceptives. An in vitro liver slice system was used to study the hormonal control of angiotensinogen synthesis and release in the rat. Dexamethasone administration in vivo resulted in increase in the in vitro rate of release of angiotensinogen by liver slices into the incubation media. This increase was inhibited by actinomycin D, an inhibitor of protein synthesis and vincristine which blocks secretion. Similarly, ethinyl estradiol treatment resulted in a 50% increase in angiotensinogen production. Hyperthyroid state was achieved by injecting rats with L-thyroxine daily for seven days. Hepatic production rate of angiotensinogen rose 21/2-fold above control and was accompanied by increases in plasma angiotensinogen concentration and plasma renin activity. In contrast, plasma angiotensinogen concentration and plasma renin activity were reduced in thyroidectomized rats. The rate of angiotensinogen production by liver slices of these rats decreased by five-fold below that of intact animals. These changes were largely corrected when thyroidectomized rats were treated with replacement doses of L-thyroxine. We conclude that hepatic angiotensinogen biosynthesis is under hormonal control. Glucocorticoid, estrogen and thyroid hormones all stimulate angiotensinogen production. These results may in part explain the pathogenesis of hypertension associated with certain disease states.

Angiotensinogen↗

PubMedDate not supplied

Percutaneous balloon aortic valvuloplasty as a bridge to heart transplantation.

Despite high rates of restenosis and recurrent symptoms, percutaneous aortic balloon valvuloplasty may be a useful alternative therapy to surgery in certain patients with aortic stenosis. In this case report, we describe a potentially new indication for this procedure, namely to reduce symptoms and stabilize a patient before heart transplantation. Our patient with class IV heart failure benefited from valvuloplasty with fewer symptoms and was able to be discharged while awaiting transplantation, which was successfully performed 2 months later. Percutaneous aortic balloon valvuloplasty should be considered as a palliative procedure in patients with severe aortic stenosis who are awaiting heart transplantation.

Aortic Valve↗