Cardiovascular Effects of Diethylcarbamazine Citrate

Abaitey, A.K.; Parratt, J. R.

doi:10.1111/j.1476-5381.1976.tb07445.x

Cited by 12 publications

(11 citation statements)

References 14 publications

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“…In contrast, increasing the dose of D4975 resulted in further elevations in arterial blood pressure. These, together with the changes in heart rate, are summarised in Table 1 One of the problems with using LV dP/dt..10, as an index of myocardial contractility is its partial dependence upon changes in preload and afterload, although the effect of the latter has been disputed (Schaper, Lewi & Jageneau, 1965 (Mason, 1969;Abaitey & Parratt, 1976). This involves recording left ventricular pressure (and dP/dt) using very fast paper speeds (in this case 1000 mm/s) and plotting isovolumic pressure against dP/dt at 10 mmHg intervals.…”

Section: Reultsmentioning

confidence: 99%

The Cardiovascular Pharmacology of 7‐propyl‐theophylline‐dopamine (D4975); Comparison With Dopamine and Dobutamine

McCaig

Parratt

1979

British J Pharmacology

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I The effects of a newly developed dopamine-xanthine derivative, 7-propyl-theophylline-dopamine (D4975), have been examined in cats anaesthetized with sodium pentobarbitone. When administered intravenously (in doses as low as 0.5 to 1.0 tg/kg) it increased systemic arterial pressure, left ventricular (LV) dP/dt,,,x, dP/dt at fixed ventricular isovolumic pressures and cardiac output. Heart rate effects were minimal.2 D4975 was about 5 times more active than dopamine or dobutamine in elevating LV dP/dt,... or dP/dt at common peak isovolumic pressures (CPIP) and about 10 times more active than dopamine at increasing systemic arterial blood pressure. The effects of D4975 were also more prolonged than those of the other two agents.3 The effects of D4975 on LV dP/dt,,,,, were greatly reduced by the prior administration of propranolol. D4975 has no effect on peripheral fJ2-adrenoceptors.4 It is suggested that the effects of D4975 on the myocardium involve both fl1-adrenoceptor stimulation and inhibition of phosphodiesterase and that the marked and prolonged pressor response is due to resistance to enzymatic breakdown by monoamine oxidase.5 The results suggest that D4975 might prove valuable in the treatment of the hypotension and reduced myocardial contractility of shock, especially as it is possible to select a dose that increases LV dP/dt,,.l without increasing either heart rate or systemic arterial pressure.

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Section: Reultsmentioning

confidence: 99%

The Cardiovascular Pharmacology of 7‐propyl‐theophylline‐dopamine (D4975); Comparison With Dopamine and Dobutamine

McCaig

Parratt

1979

British J Pharmacology

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“…Pig coronary artery strips. In view of the increases in local myocardial blood flow observed when DECc was administered to anaesthetized cats (Abaitey & Parratt, 1976), experiments were made to see whether the drug relaxed isolated coronary arteries in vitro.…”

Section: Rat Portal Veinmentioning

confidence: 99%

“…It is also the drug of choice in destroying the microfilariae of Onchocerca volvulus in man. More recently, the drug has been used, with varying results, in the treatment of bronchial asthma (Mallen).In a recent study of the cardiovascular effects of DECC in anaesthetized cats (Abaitey & Parratt, 1976) we concluded that the drug has marked effects on sympathetic ganglia. The present study was designed to examine the effects of DECC on a variety of isolated smooth muscle preparations, including some which contain parasympathetic ganglia.…”

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confidence: 92%

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The effects of diethylcarbamazine citrate on smooth muscle

Abaitey

Parratt

1977

Journal of Pharmacy and Pharmacology

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The effect of the anthelmintic drug diethylcarbamazine citrate (DECC) was examined on the guinea‐pig isolated ileum, rabbit duodenum, chick oesophagus, rat portal vein and pig coronary artery. DECC contracted all the gastrointestinal smooth muscle preparations. The contractions were antagonized by hexamethonium and atropine but they were not affected by mepyramine or methysergide in concentrations that abolished, or markedly reduced, responses to histamine and 5‐hydroxytryptamine. DECC inhibited the responses of the guinea‐pig ileum to other spasmogens, namely, acetylcholine, histamine and nicotine. Physostigmine markedly potentiated the responses of the chick oesophagus and the rabbit duodenum to DECC. DECC relaxed the potassium chloride‐induced contractions of the pig coronary artery strips; these relaxations were not modified by propranolol or calcium chloride. There was no evidence that DECC released histamine from skin or muscle.

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“…DECC has been used in the treatment of filarial infections. It has been demonstrated that intravenous DECC administration into anaesthetized cats induces hypotension, bradycardia and a reduction in +dP/dt max (the maximum rate of increase in the left ventricular pressure) followed by hypertension and an increase in +dP/dt max and the myocardial blood flow (2). It is possible that DECC affects cardiovascular functions, but little is known about its mechanisms of action during these cardiac effects.…”

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The effects and mechanisms of action of diethylcarbamazine citrate in isolated rat hearts

Kaygisiz¹,

Kaygisiz²,

Özkurt³

et al. 2013

Anadolu Kardiyol Derg

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Scientific Letter Bilimsel Mektup 589The anthelmintic drug, diethylcarbamazine citrate (DECC), is a piperazine derivative (1). DECC has been used in the treatment of filarial infections. It has been demonstrated that intravenous DECC administration into anaesthetized cats induces hypotension, bradycardia and a reduction in +dP/dt max (the maximum rate of increase in the left ventricular pressure) followed by hypertension and an increase in +dP/dt max and the myocardial blood flow (2). It is possible that DECC affects cardiovascular functions, but little is known about its mechanisms of action during these cardiac effects. In isolated rat hearts, the possible action of DECC on the left ventricular developed pressure (LVDP), +dP/dt max , the heart rate, the coronary flow, -dP/dt min (the maximum rate of decrease in the left ventricular pressure) and the left ventricular end-diastolic pressure (LVEDP) has not been investigated, and the signal transduction pathways mediating the actions of DECC are not known. Therefore, we studied the possible cardiovascular effects of DECC in isolated rat hearts. We postulated that the activation of sarcoplasmic reticulum Ca 2+ ATPase inhibitor (SERCA) and the muscarinic receptors, as well as nitric oxide (NO) generation, may be responsible for the cardiac effects of DECC, and we also studied whether SERCA, muscarinic receptors or NO mediate the effects of DECC.All procedures were approved by the local research ethics committee. Male and female Sprague-Dawley rats weighing 300-400 g were used. One hour after the administration of 1000 IU heparin ip., the heart was rapidly excised under the administration of light ether anesthesia. The aorta was immediately attached to a stainless steel cannula of the perfusion system and the hearts were perfused under a constant pressure. The perfusion solution was Modified Krebs-Henseleit solution and this solution was continuously oxygenated with 95% O 2 and 5% CO 2 (pH=7.4). The temperature was maintained at 37°C.A liquid-filled latex balloon was connected to a pressure transducer (Isotec, Hugo Sachs Electronic, March-Hugstetten, Germany) and inserted into the left ventricle via the mitral valve. The peak systolic pressure and LVEDP were measured. LVDP (an index of cardiac contractility) was calculated as the difference between the systolic and the diastolic pressures, and this pressure was accepted as the contractile force. Furthermore, +dP/dt max (other index of contractility), heart rate and -dP/dt min (an index of relaxation) were determined from the left ventricular pressure signal using the data acquisition software. The coronary flow, which is an index of the coronary vascular tone, was measured from the timed collection of the coronary effluent in a graduated cylinder. The hearts were allowed to equilibrate for 30 minutes to establish a stable baseline. After the stabilization period, DECC (20, 100 and 500 µM) was infused to the hearts for 30 minutes using an infusion pump (Graseby Medical, Model 3400, Watford Herts, England). Ten nM tha...

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Cardiovascular Effects of Diethylcarbamazine Citrate

Cited by 12 publications

References 14 publications

The Cardiovascular Pharmacology of 7‐propyl‐theophylline‐dopamine (D4975); Comparison With Dopamine and Dobutamine

The Cardiovascular Pharmacology of 7‐propyl‐theophylline‐dopamine (D4975); Comparison With Dopamine and Dobutamine

The effects of diethylcarbamazine citrate on smooth muscle

The effects and mechanisms of action of diethylcarbamazine citrate in isolated rat hearts

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