Search PubMed⌕ Search

Biomedical subjects

J Swies

Publications and source records attributed to J Swies.

7 recordsLinked to original sources
PubMed1992

Cardioprotection by molsidomine and iloprost in myocardial ischemia in anaesthetized cats.

In ten anaesthetized open chest cats the ligation of left descending coronary artery (LLDCA) resulted in 80 percent of mortality with survival time of 40.9 +/- 8.6 min. The death of animals was preceded by premature ventricular contractions which occurred with frequency 7.3 +/- 0.6/min after 2.1 +/- 0.3 min following LLDCA. Molsidomine as a dose of 20 micrograms/kg given i.v. to 10 cats 15 min before LLDCA affected none of the above characteristics of acute myocardial ischemia. The pretreatment with iloprost (2 micrograms/kg given i.v. to 10 cats) diminished frequency of premature ventricular contractions and elongated a period of time required for their occurrence after LLDCA, however, iloprost was also unable to diminish mortality of LLDCA cats. Only a combined administration of molsidomine and iloprost significantly diminished mortality among LLDCA cats down to 20 percent and doubled their survival time as compared to the controls. It is concluded that NO-donors (molsidomine) exert permissive effect towards the cardioprotective action of prostacyclin analogues (iloprost) in cats with myocardial ischemia. LLDCA cats pretreated with molsidomine + iloprost enjoyed a more complete cardioprotection than those pretreated with a high dose (3000 units/kg i.v.) of superoxide dismutase.

Animals↗
PubMed1990

Occlusion and reperfusion-induced arrhythmias in rats: involvement of platelets and effects of calcium antagonists.

The role of blood platelets in ischemia- and reperfusion-induced arrhythmias and the efficacy of three calcium blocking drugs (verapamil, diltiazem, and nicardipine) in preventing the arrhythmias were investigated. Using anesthetized rats, we measured platelet count (Pc) continuously in vivo with a Technicon autocounter. Thromboxane B2 (TxB2) and 6-keto-PGF1 alpha levels in blood from coronary sinus were determined by radioimmunoassay (RIA). Myocardial ischemia and arrhythmias were monitored from lead I ECG during and after occlusion of the left anterior descending coronary artery (LAD) for 7 min. Ischemia-induced arrhythmias were mainly ventricular ectopic contractions (VECs), whereas reperfusion produced VECs, ventricular tachycardia (VT), and reversible and irreversible ventricular fibrillation (VF). Both ischemia and reperfusion decreased platelet count and increased TxB2 level in blood from the coronary sinus. The effects of the CEBs were determined at two dose levels (0.1 and 0.3 mg/kg). Each calcium entry blocker (CEB), at both dose levels, significantly inhibited ischemia-induced arrhythmias. Verapamil and diltiazem significantly reduced reperfusion-induced VECs, prevented VT and irreversible VF, and reduced the number of animals with reversible VF. Nicardipine in preventing arrhythmias was not very effective at either dose. The CEBs also inhibited both ischemia- and reperfusion-induced decreases in PC with a moderate increase (up to 7%) as compared with levels in sham-operated controls. The CEBs also significantly reduced TxB2 levels in blood from the coronary sinus. These results indicate that ischemia and postischemic reperfusion both induce platelet aggregation in rats. Aggregating platelets release biologically active substances including thromboxane A2 (TxA2) which exacerbates existing ischemia and facilitates generation of arrhythmias. CEBs inhibit platelet aggregation and TxA2 release and enhance PGI2 synthesis, thereby preventing arrhythmias.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Kallikrein-thrombolytic and hypotensive action in cats--preliminary results.

An intravenous injection of kallikrein produced hypotensive and thrombolytic effects in anesthetized cats, using the blood superfused tendon technique. The thrombolytic action of kallikrein was mediated by an unstable substance. The generation of this substance was abolished by either acetylsalicylic acid (ASA) or aprotonin and enhanced by captopril. The hypotensive action of kallikrein was only partially inhibited by ASA. It is proposed that both these pharmacological effects of kallikrein are mediated by bradykinin which in turn releases prostacyclin from the endothelium. However, in contrast to the thrombolytic effect of kallikrein which is totally mediated by prostacyclin the hypotensive action of kallikrein depends not only on prostacyclin but also on another endothelium-derived vasorelaxant, e.g. EDRF.

Animals↗
PubMed1978

Lungs as a generator of prostacyclin--hypothesis on physiological significance.

In vivo anti-platelet de-aggregatory activity of exogenous prostacyclin is enhanced after its passage through the pulmonary circulation of anaesthetized cats, probably because of a concomitant generation of endogenous prostacyclin by the lungs. Evidence is also presented that perfused lungs of guinea pigs and rats spontaneously release considerable amounts of prostacyclin. It is therefore postulated that a continuous biosynthesis of prostacyclin by pulmonary endothelium is a general physiological phenomenon, while the generation of thromboxane A2 by lungs occurs in response to pathological stimuli. Coronary and cerebral arteries are supposed to benefit from this hormonal function of the lungs.

Animals↗
PubMedDate not supplied

Haemodynamic changes accompanying lung oedema produced by iv injection of adrenaline or vasopressin into rats.

The blood pressure was investigated in the common left carotid artery (LC), in the left atrium (LA), in the pulmonary artery (PA) and in the right atrium (RA). After adrenaline injection the blood pressure rised rapid and simulatneously in all four regions. After vasopressin injection the blood pressures rised sequence in LC, in LA and PA. The blood pressure in RA in this time was unchanged. These results indicate that primary causes of the lung oedema after adrenaline or vasopressin are different.

Animals↗