Efekti HS-3 i HS-6 na kardiovaskularne promene izazvane somanom u pacova

The effects of HS-3 and HS-6 on cardiovascular changes due to poisoning with the LD50 of soman were studied in anaesthetized rats. Both HS-3 and HS-6 were found to antagonize the changes in arterial blood pressure and heart rate. HS-3 was more effective than HS-6 in neutralizing the changes in cardiovascular performance induced by the central action of soman. The two oximes produced an antagonistic effect on some abnormalities in the electrocardiogram caused by soman. The primary haemodynamic effect of soman and its antidotes reflected itself on peripheral vascular resistance, the alteration in cardiac output being secondary, in the course of the homeostatic control of arterial pressure.Dejstvo HS-3 i HS-6 na kardiovaskularne promene izazvane sa LD50 somana ispitivana je u anestetisanih, veštački ventilisanih pacova. Rezultati ovih istraživanja upućuju na to da i HS-3 i HS-6 smanjuju pramene arterijskih pritisaka u pacova tretiranih somanom te da je HS-3 efikasniji od HS-6 u neutralisanju promena u funkciji kardiovaskularnog sistema koje su izazvane centralnim dejstvom somana. HS-3 i HS-6 pokazuju antagonistički efekat na neke poremećaje u EKG-u do kojih dolazi kod trovanja somanom. Primarni hemodinamski efekat somana i njegovih antidota je na perifernom sudovnom otporu, dok su promene u minutnom volumenu srca sekundarne i deo su homeostatske kontrole krvnog pritiska

The effect of acute and chronic hematocrit changes on cardiovascular hemodynamics in spontaneously hypertensive rats

Heparin given over a long term by a subcutaneous route consistently lowers blood pressure in the hypertensive rat models. The decrease in blood pressure is accompanied by a parallel decrease in hematocrit suggesting a causal relationship between hematocrit and blood pressure. The aim of this study was to define the relationships between acute and chronic hematocrit changes and blood pressure in the normotensive and hypertensive states. Nor- motensive Wistar (NWR) and spontaneously hypertensive (SHR) rats were used. Hematocrit was decreased acutely by blood-letting, and chronically by treatment with either heparin (H) or phenylhydrazine (P) for 4 weeks. Acute and chronic hematocrit increase was accomplished by packed cells transfusion. Systolic blood pressure was measured weekly; and at the end of the experimental period, plasma volume, cardiac output, and mean arterial pressure were obtained. Acute hematocrit decrease or increase (hematocrit ranging from 25 to 65%) did not affect blood pressure in either strain of rats; whereas chronic hematocrit changes (hematocrit ranging from 35 to 61%) significantly affected blood pressure only in SHR. Thus, chronic hematocrit decrease induced by H or P resulted in a significant fall in blood pressure compared to control (201 ± 3 v 175 ± 4, 167 ± 4 mm Hg, respectively; P lt .05). Conversely, a chronic hematocrit increase resulted in a significant rise in blood pressure (201 ±3 v 219 ± 4 mm Hg; P lt .05). Similar hematocrit changes produced in NWR, as in SHR, did not affect blood pressure. However, a direct relationships between hematocrit and total peripheral resistance, and an inverse relationship between hematocrit and cardiac output was found in both NWR and SHR. No difference in plasma or blood volume was found among the groups. Therefore, the results of the present study indicate that chronic hematocrit changes, low or high, influence blood pressure only in hypertensive rats, and that this effect of hematocrit on blood pressure is mediated by changes in total peripheral resistance

Regional hemodynamics after chronic nitric oxide inhibition in spontaneously hypertensive rats

Background: Inhibition of nitric oxide (NO) synthase by L-arginine analogs is associated with elevation of blood pressure in rats. Because endothelium-dependent vasomotion in different vascular beds is not homogenous, the aim of this study was to characterize and compare regional hemodynamic responses in carotid, femoral, and renal vascular beds after chronic NO inhibition in spontaneously hypertensive rats. The possible role of circulating endothelin and renin angiotensin systems in mediating the effects of chronic NO inhibition was also studied. Methods: Systemic and regional hemodynamics, left ventricular mass, plasma renin activity, and plasma endothelin-l were determined in control and N-omega-nitro-L-arginine methyl ester (L-NAME)-treated (10 mg/kg/day, 4 weeks) spontaneously hypertensive rats. Results: L-NAME treatment increased arterial pressure and total peripheral and regional vascular resistance and decreased cardiac output, stroke volume, and regional blood flow. An in-crease in blood flow ratio and a decrease in vascular resistance ratio between carotid and renal as well as femoral and renal vascular beds in rats treated with L-NAME was found. Blood flow and vascular resistance ratios between femoral and carotid vascular beds remained unchanged. L-NAME increased plasma renin activity and left ventricular weight/body weight ratio, whereas plasma endothelin-l was not modified. Conclusions: The results of this study showed that the renal circulation seemed to be more sensitive to the effects of chronic NO inhibition than carotid and femoral vascular beds. Simultaneous activation of the renin angiotensin system may further potentiate cardiovascular effects of chronic NO inhibition. No evidence that circulating endothelin-l plays a role in this model of hypertension was found. KEY INDEXING TERMS: Nitric oxide; Regional hemodynamics; Plasma renin activity; Endothelin; Spontaneously hypertensive rats