title: Experimental study on microthrombi and myocardial injuries.
abstract: The experiment was conducted with SD male rats. After they had been each given an intravenous injection of high molecular weight dextran (0.8 ml/100 g body wt) once a day for 4 days, they were brought under the observation of ECG and mesentery microcirculation. Microthrombi were found in the venules and capillaries of each rat of the experimental group, while in the microcirculation of the control group rats, no microthrombi were found. No changes were found in the ECGs of the rats (n = 6) in the control group after the injections, while the rats in the subject group all suffered a rise in the S-T segment of ECG, an indication of myocardial injuries. The rise was significantly in positive correlation to the increase in microthrombi in number (r = 0.944, P < 0.01). The erythrocytes of the rats in the subject group clustered to become rouleau-like, and platelets aggregated by tens and hundreds to form microthrombi. Their blood also showed a significant decrease in number of platelets. The degree of platelet aggregation and the scores of the rise on ECG were significantly in positive correlation as shown by the results: y = 20 + 94x, r = 0.94, P < 0.01. The plasma TXB2 of the subject group increased obviously but the change of 6-K-PGF1 alpha in the blood was not significant. The content of plasma TXB2 and the scores that indicated the rise in the S-T segment of the ECG showed significantly a positive correlation by the analysis of linear regression equation: y = 109.997 +/- 116.25x, r = 0.889, P < 0.05. The activity of Na(+)-K(+)-ATPase on the myocardial cell membranes of the rats with microthrombi was significantly reduced as compared with that of the rats in the control group (P < 0.01). The activity of the Na(+)-K(+)-ATPase was significantly in negative correlation to the rise in the S-T segment of ECG (P < 0.05). This study demonstrates that the above changes are the causes of myocardial injuries in rats with circulatory thrombi.
authors.affiliation: 44th Hospital of PLA, Gui Yang, People's Republic of China.
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Zhen
authors.forename: Y C
authors.initials: YC
authors.lastname: Guo
authors.forename: Z G
authors.initials: ZG
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Yan
authors.forename: P J
authors.initials: PJ
authors.lastname: Ge
authors.forename: H M
authors.initials: HM
authors.lastname: Jin
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D003911:Dextrans / Q000633:toxicity; D004562:Electrocardiography; D004903:Erythrocyte Aggregation; D006331:Heart Diseases / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation; D009206:Myocardium / Q000201:enzymology; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013927:Thrombosis / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D003911:Dextrans; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D000254:Sodium-Potassium-Exchanging ATPase