Decrease In Total Peripheral Vascular Resistance Research Articles

Reduced Systolic Volume: Main Pathophysiological Mechanism in Patients with Orthostatic Intolerance?

BackgroundOrthostatic intolerance patients' pathophysiological mechanism is still obscure, contributing to the difficulty in their clinical management.ObjectiveTo investigate hemodynamic changes during tilt test in individuals with orthostatic intolerance symptoms, including syncope or near syncope.MethodsSixty-one patients who underwent tilt test at - 70° in the phase without vasodilators were divided into two groups. For data analysis, only the first 20 minutes of tilting were considered. Group I was made up of 33 patients who had an increase of total peripheral vascular resistance (TPVR) during orthostatic position; and Group II was made up of 28 patients with a decrease in TPVR (characterizing insufficient peripheral vascular resistance). The control group consisted of 24 healthy asymptomatic individuals. Hemodynamic parameters were obtained by a non-invasive hemodynamic monitor in three different moments (supine position, tilt 10' and tilt 20') adjusted for age.ResultsIn the supine position, systolic volume (SV) was significantly reduced in both Group II and I in comparison to the control group, respectively (66.4 ±14.9 ml vs. 81.8±14.8 ml vs. 101.5±24.2 ml; p<0.05). TPVR, however, was higher in Group II in comparison to Group I and controls, respectively (1750.5± 442 dyne.s/cm5 vs.1424±404 dyne.s/cm5 vs. 974.4±230 dyne.s/cm5; p<0.05). In the orthostatic position, at 10', there was repetition of findings, with lower absolute values of SV compared to controls (64.1±14.0 ml vs 65.5±11.3 ml vs 82.8±15.6 ml; p<0.05). TPVR, on the other hand, showed a relative drop in Group II, in comparison to Group I.ConclusionReduced SV was consistently observed in the groups of patients with orthostatic intolerance in comparison to the control group. Two different responses to tilt test were observed: one group with elevated TPVR and another with a relative drop in TPVR, possibly suggesting a more severe failure of compensation mechanisms.

Toxic Damage to the Myocardium and Systemic Hemodynamic Disorders in Acute Propranolol Poisoning in the Experiment

Objective: to clarify the mechanisms underlying the development of systemic hemodynamic disorders in acute propranolol poisoning and possible ways of their correction. Materials and methods. The experiments were carried out on 40 male rats in 4 groups: 1) intact animals (n=10); 2) animals receiving propranolol in a dose of 1 mg/100 g body weight (n=10); 3) those receiving the drug in a dose of 2 mg/100 g body weight (n=10); 4) animals given noradrenaline in a single dose of 0.006 mg/100 g body weight 20 min after acute poisoning by propranol (2 mg/100 g body weight) (n=10). After administration of calypsol in a dose of 100 mg/kg body weight, the investigator catheterized the carotid artery to measure blood pressure (BP) (mm Hg) and the jugular vein to estimate central venous pressure (CVP) (cm H2O). An integral rheogram was recorded and stroke output (^l), cardiac output (CO) (ml/min), and total peripheral vascular resistance (TPVR) (103 din^s^cm-5) were calculated during 60 min. ECG was recorded. At min 60 of poisoning, blood samples were taken and estimated for the levels of glucose, lactate, pyruvate, and uric acid to determine the level of metabolic changes. The serum activity of enzymes, such as aspartate aminotransferase, lactate dehydrogenase, and cre-atine kinase MB fraction, was evaluated. The rate of free radical oxidation processes was estimated by the plasma chemilumines-cence technique. After the end of the experiment, the rats were killed by decapitation under calypsol anesthesia. The hearts were removed and fixed in 10% neutral buffered formalin. 5-^m-thick hematoxylin and eosin-stained paraffin-embedded sections were examined on an Axio Cam MRcS digital video fixation microscope. Results. The administration of propranolol suppresses cardiac hemodynamics and causes respiratory depression in a dose-dependent manner. At the same time compensatory mechanisms are aimed at eliminating hemodynamic disorders and hypoxia. To increase the dose of propranolol results in rapid circulatory decompensation, as suggested by the changes in heart rate, BP, TPVR, CVP, and CO. With smaller propranol doses (Group 2), BP is maintained by a less pronounced decrease in TPVR. Worse provision of O2 and oxidation substrates to tissues causes their metabolic disturbances and generalized cell damage — a change in the levels of carbohydrate metabolites, enzymes, and chemiluminescence values. Noradrenaline-induced stimulation of o^-adrenoceptors in the heart stabilizes hemodynamics and the analyzed biochemical parameters. Conclusion. When injected intraabdominally in a single dose of 1 and 2 mg/100 animal body weight, propranolol causes dose-dependent changes in systemic hemodynamics, respiration, carbohydrate metabolites, blood enzyme levels, and the activity of prooxidant and antioxidant systems. Noradrenaline-induced stimulation of 0^-adrenoceptors in the heart stabilized systemic hemodynamics, the values of plasma chemiluminescence, the activity of enzymes, and the level of carbohydrate metabolites. Key words: poisoning, experiment, propranolol, myocardium, systemic hemodynamics.

Erythrocyte sodium lithium countertransport in normal and hypertensive pregnancy: relation to haemodynamic changes.

To establish the changes in erythrocyte sodium lithium countertransport (SLC) with advancing normal pregnancy and to determine if these changes were different in pregnancy induced hypertension (PIH). The changes in both groups were assessed in relation to haemodynamic changes. SLC, mean arterial pressure (MAP), cardiac output (CO) and total peripheral vascular resistance (TPVR) were determined serially during normal pregnancy and cross-sectionally in PIH. Women were studied again 20 weeks after delivery where possible. Routine antenatal clinic and antenatal ward of a regional reference centre. Fifty-one normal primigravid women were studied serially and 41 primigravid women with PIH were studied at time of diagnosis. During normal pregnancy SLC (mmol Li/h/l cells) increased from a nonpregnant value of 0.24 +/- 0.02 (mean +/- SEM) to 0.32 +/- 0.02 at 14 weeks, and 0.37 +/- 0.02 at 20 weeks gestation. This was maintained until 38 weeks (0.40 +/- 0.02). The increase until 20 weeks occurred at the time of greatest change in CO (5.10 +/- 0.18 to 6.79 +/- 0.20 l/min) and TPVR (1327 +/- 58 to 969 +/- 33 dyn/s/cm-5). The decrease in TPVR with a rise in SLC is opposite to the relation reported in essential hypertension so that a functional relation is unlikely. However, the changes within pregnancy were positively correlated (r = 0.43, P < 0.01). In hypertensive pregnancies TPVR was elevated compared with normotensive pregnancies (1543 +/- 100 vs 1090 +/- 37) but the SLC was not different from that found in normotensive pregnancies (0.43 +/- 0.02 vs 0.40 +/- 0.02). The changes in SLC activity suggest dynamic effects on erythrocyte membrane function during pregnancy. However, no differences could be found between normal and hypertensive pregnancy and SLC is unlikely to be of value as a marker of hypertensive risk during pregnancy.

Effects of a Senso (Toad Venom) Containing Drug on Systemic Hemodynamics, Cardiac Function and Myocadial Oxygen Consumption in Anesthetized Dogs

Effects of a Senso (toad venom)-containing drug, KY, on cardiovascular system were examined in anesthetized open-chest dogs. KY increased aortic pressure, peak positive first derivative of left ventricular pressure, stroke work index, percent segment shortening in left ventricular myocardium and myocardial oxygen consumption, and decreased heart rate and total peripheral vascular resistance (TPR). Propranolol augmented the increase in aortic pressure with KY, inhibited the increase in aortic flow with KY and reversed KY-induced decrease in TPR to an increase. These results indicate that KY has positive inotropic and vasodilating actions possibly originating from both digitalis- and adrenaline-like action of a Senso.

Effects of doparaine D 1 and dopamine D 2 receptor agonists on coronary and peripheral tiemodynamics

This study evaluated the coronary dopamine receptors by using the dopamine D 1 receptor agonist fenoldopam, dopamine D 2 receptor agonist propylbutyldopamine, and their selective antagonists SCH23390 and domperidone. Left circumflex coronary flow (CF), coronary perfusion pressure at constam flow, left ventricular hemodynamics, and total peripheral vascular resistance (TPR) were measured in pentobarbital-anesthetized dogs at constant arterial pressures. At doses of 200, 500 and 5000 nM, both fenoldopam and propylbutyldopamine induced dose-related inotropic effects, as evidenced by maximal dp/dt and cardiac output, an increase in CF, decrease in coronary vascular resistance and a decrease in TPR. Fenoldopam was more potent in its cardiac and coronary effects while propylbutyldopamine was more potent peripherally. On the basis of dosage used, the positive inotropic effects of fenoldopam and propylbutyl-dopamine were much weaker than dopamine. After β-receptor blockade, the inotropic and coronary effects of fenoldopam and propylbutyldopamine were extremely attenuated. Domperidone could largely antagonize the proylbutyldopamine-induced inotropic and coronary effects while SCH23390 showed no significant effect. In addition, under our experimental conditions, the fenoldopam- and propylbutyldopamine-induced decreases in TPR were markedly reduced by SCH23390 and domperidone, respectively. The results indicate that the coronary effects of fenoldopam and propylbutyldopamine result not from a primary coronary vasodilating action, but from vasodilation secondary to positive inotropic effects. Both dopamine D 1, and dopamine D 2 receptors are involved in the peripheral vascular hemodynamics.

Systemic haemodynamics in renovascular hypertension: changes after revascularization with percutaneous transluminal angioplasty.

The systemic haemodynamic pattern and its changes after at least 6 months of successful percutaneous transluminal angioplasty (PTRA) was evaluated in a group of patients with renovascular hypertension (RVH). Fourteen patients, nine males and five females, aged 21 to 58 years, were studied; 12 had fibrodysplastic and two had atherosclerotic stenosing renal vascular lesions. Seven were cured and seven improved. Hypertension was characterized by increased plasma volume (PV) and total peripheral vascular resistance (TPR). Mean peripheral plasma renin activity (PRA) and 24-h urine aldosterone (UA) were elevated. However, the vasoconstriction did not appear to be related to the increased activity of the renin-angiotensin system. After at least 6 months of a successful PTRA, the fall in blood pressure (BP) was associated with a decrease in TPR; PV appeared normal, and PRA and UA became normal.

Hemodynamic profile in acute myocardial infarction.

Hemodynamic and clinical evaluation of 50 patients with acute myocardial infarction were performed. A majority of patients had depressed left ventricular function, but the level of depression was not uniform and a wide spectrum existed. Left ventricular function curves appeared to demonstrate a peak or plateau with a pulmonary arterial end-diastolic pressure (PAEDP) from 17 to 19 mmHg. There was negative correlation between stroke volume index and total peripheral vascular resistance (TPRI). Mean arterial blood pressure (MABP), TPRI, PAEDP were decreased significantly and cardiac index (CI) was markedly increased after administration of nifedipine. Seventeen patients had congestive heart failure. These patients showed a marked increase in PAEDP and a wide degree of valiability in CI and left ventricular stroke work index (LVSWI). Sixteen of 17 patients with congestive heart failure showed a PAEDP greater than 18 mmHg. Six patients developed cardiogenic shock. In these patients CI and LVSWI were markedly reduced. Two patients showed normal PAEDP. Three patients with septic shock showed a marked increase in CI and a decrease in TPRI. Hemodynamic subsets established by a PAEDP of 18 mmHg and a mean right atrial pressure (MRAP) of 100 mmH2O was beneficial to evaluate the right ventricular function. Four patients with the findings of elevated MRAP out of proportion to PAEDP were diagnosed as right ventricular infarction. Three of them showed normal PAEDP. Two patients who showed hypotension and low CI died with shock. It is concluded that hemodynamic evaluation of patients with acute myocardial infarction is useful in understanding the extent of altered cardiac function, classifying the severity of the clinical state, measuring the response to various treatments and predicting the prognosis of the patient.