Determination of left ventricular dimensions with ultrasound

Fiedler, Volker B.; Oswald, S.; Göbel, Helmut; Faber, Wladimir; Scholtholt, J

doi:10.1016/0160-5402(80)90002-9

Cited by 11 publications

(2 citation statements)

References 18 publications

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“…and anaesthesia was maintained with chloralose (40 mg (2 g)-I i.v.) S. Oswald VDI, Erkrath, West Germany) and characteristics of the device for the ultrasonic measurement of the dimensions of these small segments has previously been described in detail [9]. Chloralose and urethane were added to when neeed to suppress the medial ocular reflex.…”

Section: Model Bmentioning

confidence: 99%

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On the mechanism of renin release during experimental myocardial ischaemia

Ertl

Meesmann

Kochsiek

1985

Eur J Clin Investigation

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An increase in plasma renin activity (PRA) following experimental coronary occlusion has previously been demonstrated in anaesthetized and conscious dogs. The purpose of the present study was to analyse the mechanism of this renin release. In two distinct models of myocardial ischaemia in anaesthetized dogs--i.e. occlusion of the left-anterior descending coronary artery (model A, n = 21) and atrial pacing in the presence of stenosis of the left-anterior descending coronary artery (model B, n = 23), an increase in arterial PRA was found from 1.68 +/- 0.43 to 3.06 +/- 0.63 ng ml-1 h-1 (model A, mean +/- SEM, P less than 0.025) and from 9.87 +/- 3.59 to 14.96 +/- 4.06 ng ml-1 h-1 (model B, P less than 0.05), respectively. The increase in PRA following coronary occlusion was not blunted by adrenergic beta-receptor blockade with propranolol (3 mg kg-1 i.v.; n = 4). Coronary sinus PRA was lower than arterial PRA and the increase in PRA did not occur in nephrectomized dogs (n = 5). The data suggest that myocardial ischaemia induces a release of renin from the kidney which is not mediated by adrenergic beta receptors.

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Section: Model Bmentioning

confidence: 99%

“…The device (UM3. S. Oswald VDI, Erkrath, West Germany) and characteristics of the device for the ultrasonic measurement of the dimensions of these small segments has previously been described in detail [9]. In fourteen dogs, atrial tachycardia was induced without the presence of coronary stenosis.…”

Section: Model Bmentioning

confidence: 99%

On the mechanism of renin release during experimental myocardial ischaemia

Ertl

Meesmann

Kochsiek

1985

Eur J Clin Investigation

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Molsidomine: Alternative Approaches To Treat Myocardial Ischemia

Nitz¹,

Fiedler²

1987

Pharmacotherapy

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The long-acting antianginal drug molsidomine has been shown experimentally to reduce myocardial infarct size when administered prior to or after cardiac insult. This is due to several drug actions. Dilation of postcapillary capacitance vessels diminishes venous return, preload, heart dimensions, and myocardial oxygen consumption. Relaxation of stenosed conductive coronary arteries increases the perfusion of myocardial areas at risk of infarction due to enhanced collateral circulation. Increased regional blood supply nourishes predominantly subendocardial cardiac muscles as a result of reduction of extravascular coronary pressure, and resistance. The stable heart rate and cardiac contractility favor improved heart performance. The inhibition of platelet aggregation in vivo by molsidomine or its active metabolites, SIN-1 and SIN-1A, is linked to the stimulation of prostacyclin synthesis, inhibition of thromboxane release with induction of thrombosis and vasoconstriction, and enhanced concentrations of cyclic guanosine monophosphate. Dilation of coronary arteries after intracoronary administration of SIN-1, with inhibition of platelet aggregation by restrained release of adenosine diphosphate and stabilization of platelet membranes, facilitates the recanalization of stenosed arteries and reduces coronary muscle tone at the site of thrombosis. Activation of the human fibrinolytic system and drug-induced release of a plasminogen activator favor dysaggregatory effects. The drug's inhibiting actions on lipoxygenase products of arachidonate (e.g., 12-hydroperoxy-eicosatetraenoic acid and leukotrienes) may shift prostaglandin catabolism to cyclooxygenase products (e.g., prostacyclin) that protect against the expansion of ischemia and the induction of coronary spasm. Experimentally, the hemodynamic effectiveness of molsidomine can be antagonized by catecholamines (afterload effects) and dihydroergotamine (preload and afterload effects) respectively. Further clinical investigations will clarify the application of these mechanisms for the therapeutic success of the drug in human myocardial infarction.

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Methods in Cardiovascular Safety Pharmacology

Guth

2006

Drug Discovery and Evaluation

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Determination of left ventricular dimensions with ultrasound

Cited by 11 publications

References 18 publications

On the mechanism of renin release during experimental myocardial ischaemia

On the mechanism of renin release during experimental myocardial ischaemia

Molsidomine: Alternative Approaches To Treat Myocardial Ischemia

Methods in Cardiovascular Safety Pharmacology

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