Subsensitivity to noradrenaline and isoprenaline in rabbits acutely pre-treated with morphine

Bhargava, Hemendra N.; Kasabdji, D; Thompson, Emmanuel B.

doi:10.1016/0306-3623(77)90023-4

Cited by 3 publications

(1 citation statement)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…62 Bradycardia has been frequently observed in STZ diabetic rats 63 as well as in ISO-induced rats. 64 The development of STZ-induced bradycardia has been attributed to a downregulation of myocardial beta adrenoceptors, hypothyroidism, 65 depression of myocardial calcium metabolism, 66 reduced uptake of calcium by the sarcoplasmic reticulum and concomitantly depression of SR-calcium ATPase activity. 67 It is well established that Ang II exerts an inhibitory influence on baroreceptor reflex control of heart rate after either intravenous administration in several species.…”

Section: Discussionmentioning

confidence: 99%

Perindopril protects against streptozotocin-induced hyperglycemic myocardial damage/alterations

Patel

Bhadada

2012

Hum Exp Toxicol

View full text Add to dashboard Cite

High blood pressure, obesity, abnormal lipid profile, which often coexist with diabetes, tend to be associated with preclinical cardiovascular abnormalities and may contribute to the association of diabetes with cardiovascular events. Many studies have proved that streptozotocin (STZ) is responsible for type-2-diabetes-induced cardiovascular complications. Long-term perindopril therapy in patients with hypertension and diabetes has been observed to correct carotid remodeling by reducing hypertrophy. We studied the effect of perindopril (1 mg/kg/d orally [po]) on cardiovascular complications in neonatal model of rats, which was induced by administering STZ (90 mg/kg, intraperitoneally [ip]), in 5-d-old wistar rats and cardiac hypertrophy induced by isoprenaline (ISO; 5 mg/kg, ip) for 10 d. Various biochemical, cardiac, and hemodynamic parameters were measured at the end of 8 weeks of treatment in diabetes model and 10 d in hypertrophy model. STZ produced hyperglycemia, hyperinsulinemia, dyslipidemia, hypertension, bradycardia, increased creatinine kinase (CK-MB), lactate dehydrogenase enzymes (LDH) and C-reactive protein (CRP) levels, cardiac hypertrophy, and oxidative stress. Chronic treatment with perindopril significantly prevented STZ-induced hyperglycemia and hyperinsulinemia and controlled dyslipdemia in diabetic rats. Further, perindopril produced a significant reduction in elevated levels of CRP, LDH, and CK. STZ-induced hypertension and bradycardia were also prevented by perindopril treatment. Perindopril also produced beneficial effect by preventing cardiac hypertrophy as evident from cardiac hypertrophy index and left ventricular hypertrophic index. Perindopril also prevented STZ-induced oxidative stress. Similar results were obtained in ISO-induced cardiac hypertrophic model, which confirms the beneficial role of perindopril in cardiac hypertrophy. In conclusion, our data from both studies suggest that perindopril produced beneficial effect on cardiac complications.

show abstract