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Biomedical subjects

A Kolin

Publications and source records attributed to A Kolin.

82 records · Page 5Linked to original sources
PubMedDate not supplied

Hemodynamic and myocardial effects of long-lasting venodilation in the conscious dog: analysis of molsidomine in comparison with nitrates.

The effect of molsidomine-induced venodilation on cardiac preload was studied in conscious resting dogs, instrumented to analyze left ventricular function and myocardial perfusion. Direct effects on veins were studied during chloralose anesthesia by measuring regional venous capacitance changes with an induction angiometer. Kinetics of molsidomine-induced effects were compared to those induced by nitroglycerin and isosorbide dinitrate. This comparison was restricted to low i.v. dosages, causing only transient threshold effects on peripheral resistance and heart rate. During molsidomine-induced venous pooling, neither any direct effect on the coronary circulation nor any direct cardiac depressant activity of the drug was detected. 100 microgram/kg molsidomine caused a reduction of left ventricular preload by 5 mm Hg, lasting at least 4 hours. This effect was significantly more pronounced than that induced by 1 microgram/kg nitroglycerin or by 25 microgram/kg isosorbide dinitrate, lasting 2 min or 20 min, respectively. However, in raising regional venous capacitance, these nitrate dosages were equi-effective to 100 microgram/kg molsidomine, the effect of which was persistent and with a greater delay in onset. These results indicate that the lasting persistance of venodilation is a decisive factor for the amount of volume pooled in the capacitance system and, consequently, for the extent of preload reduction obtained. It is concluded, that lasting vasodilation, restricted to the veins, is beneficial for ventricular performance in ischemic heart disease.

Animals↗
PubMedDate not supplied

Increased effective vascular compliance and venous pooling of intravascular volume during sustained venodilation in conscious dogs.

The hemodynamic effects of the long-acting antianginal drug molsidomine were studied in 8 chronically instrumented conscious dogs by measuring the partition of the intravascular volume and the effective compliance of the total vascular bed. The blood volume of the resting dogs was varied by +/- 4 ml/kg in a cycle of blood infusion, withdrawal and reinfusion within 12 minutes. Relating the observed alterations in mean right atrial pressure to the induced changes in intravascular volume, an effective compliance of 2.9 +/- 0.4 ml. mm Hg-1 . kg -1 (mean +/- SD) was found. Heart rate, total peripheral vascular resistance and the local capacity of the distal femoral vein did not change significantly during the cycle of volume alterations. Following 0.1 mg/kg molsidomine i.v., mean right atrial pressure was lowered by 1.6 mm Hg and mean left atrial pressure by 3.4 mm Hg; the effective compliance was elevated to 4.7 +/- 0.6 ml . mm Hg-1. kg -1 (p less than 0.001), and the central blood volume was lowered from 17.8 +/- 3.1 to 14.8 +/0 3.3 ml/kg (p less than 0.01), while the total blood volume remained constant. The decline in stroke volume and the reflexly induced increase in heart rate correlated with the control heart rate. Mean arterial pressure declined from 101 +/- 7 to 91 +/- 14 mm Hg (p less than 0.05) and total peripheral vascular resistance remained unaffected. It is concluded that molsidomine exerts exerts its hypotensive effect by dilation within the vascular low-pressure system and that this dilation can be described quantitatively in conscious animals by the analysis of the total effective vascular compliance.

Animals↗
PubMedDate not supplied

Myocardial damage from acute cerebral lesions.

Autopsy findings in 58 patients with intracranial lesions were compared with those in 50 control patients for myocardial damage, characterised by a change from a myofibrillar to a granular staining pattern, using a histochemical method for succinic dehydrogenase. Transmurally scattered foci of damaged myocardial fibres were significantly more common (p less than 0.01) in patients with intracranial lesions (62%) compared to controls (26%). No victims of sudden violent deaths showed these cardiac lesions. Focal myocardial damage required at least six hours to develop after onset of the acute neurological event and was not observed after the second week. It was associated with lesions producing a rapid increase in intracranial pressure and was usually absent in patients with slowly enlarging or small cerebral lesions. Similar myocardial changes were seen in patients in the control group dying from prolonged shock or other forms of acute circulatory or metabolic failure. The postulated mechanism of cardiac damage in these patients is increased levels of plasma catecholamines secondary to rapidly increasing intracranial pressure, irrespective of the cerebral pathology.

Acute Disease↗
PubMedDate not supplied

Cardioprotective effects of sodium gamma-hydroxybutyrate (GHB) on brain induced myocardial injury.

Gamma-hydroxybutyrate (GHB) was evaluated as a protective agent in a gerbil model of non-lethal myocardial injury that follows brain ischaemia. The accumulation of fat droplets in myocardial fibers following brain infarction was measured by electron microscopic morphometry and expressed as a percentage of the area of the sarcoplasm. GHB treatment significantly reduced the area occupied by lipid droplets compared with that found in saline treated controls measured both 10 hours (p less than .005) and 24 hours (p less than 0.05) after unilateral carotid ligation. GHB did not affect the ischaemic swelling of the brain.

Animals↗
PubMedDate not supplied

Arterial resistance to neoplastic invasion.

The relevance of proteinase inhibitors to the resistance of arterial walls against neoplastic invasion was investigated in human and porcine vessels using plasminogen activators as model. No significant differences in the inhibitory potential of extracts from the vascular walls were found between pulmonary and systemic arteries. It is concluded that the proteinase - inhibitor system studied is not responsible for the immunity of arterial walls against neoplastic invasion. The lack of antineoplastic resistance of pulmonary arteries may be explained by lesser intraarterial blood pressure and hence a lower pressure gradient across the vessel wall in pulmonary as opposed to systemic arteries.

Animals↗
PubMedDate not supplied

Antimetastatic effect of amiloride in an animal tumour model.

The diuretic Amiloride competitively inhibits the catalytic activity of the urokinase-type plasminogen activator on plasminogen in vitro. This effect was tested on a rat adenocarcinoma model and its invasive potential in the host lung. While the inhibitory effect on intact cell cultures of the tumour was slight, continuous exposure of tumour-injected animals to the drug completely prevented the formation of lung metastasis.

Adenocarcinoma↗
PubMedDate not supplied

Metastatic carcinomatous arthritis and carcinoma of the lung. A report of two cases diagnosed by synovial fluid cytology.

Arthritis is rarely caused by metastatic carcinomatous deposits in and about joints. Two patients with bronchogenic carcinoma and metastatic carcinomatous arthritis (MCA) are described. The diagnosis was established by the demonstration of malignant cells in the synovial fluid. Histology of the synovium, in 1 case, revealed several metastatic carcinomatous deposits. This report emphasizes the value of synovial fluid exfoliative cytology in the early recognition of MCA so that appropriate palliative therapy can be implemented.

Adenocarcinoma↗