Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aggregate anaphylaxis was induced in eight ovalbumin-sensitized monkeys (Macaca irus). Hemodynamics, blood flow distribution and myocardial performance were studied. Following challenge, severe circulatory shock developed. Systemic arterial and left atrial pressures decreased and pulmonary arterial and right atrial pressures increased. There was a tenfold increase in pulmonary vascular resistance, and cardiac output was markedly reduced (-75%). A redistribution of the blood flow to vital organs (brain, heart and liver) occurred, at the expense of flow to other regions (muscles, kidneys, pancreas and spleen). There was also a redistribution of the blood flow within the myocardium, resulting in an unchanged right ventricular blood flow, despite a decrease in total myocardial blood flow. Right ventricular stroke work was reduced in spite of high filling pressures, whereas the decrease in left ventricular stroke work coincided with low filling pressures. It is concluded that the initial main cause of the low outflow state was an increased resistance in the pulmonary circulation followed by acute right heart failure.
 ...
PMID:Anaphylaxis in the monkey: hemodynamics and blood flow distribution. 11 76

The integrated response to severe exercise involves fourfold to fivefold increases in cardiac output, which are due primarily to increases in cardiac rate and to a lesser extent to augmentation of stroke volume. The increase in stroke volume is partly due to an increase in end-diastolic cardiac size (Frank-Starling mechanism) and secondarily due to a reduction in end-systolic cardiac size. The full role of the Frank-Starling mechanism is masked by the concomitant tachycardia. The reduction in end-systolic dimensions can be related to increased contractility, mediated by beta adrenergic stimulation. Beta adrenergic blockade prevents the inotropic response, the decrease in end-systolic dimensions, and approximately 50% of the tachycardia of exercise. The enhanced cardiac output is distributed preferentially to the exercising muscles including the heart. Blood flow to the heart increases fourfold to fivefold as well, mainly reflecting the augmented metabolic requirements of the myocardium due to near maximal increases in cardiac rate and contractility. Blood flow to the inactive viscera (e.g., kidney and gastrointestinal tract) is maintained during severe exercise in the normal dog. It is suggested that local autoregulatory mechanisms are responsible for maintained visceral flow in the face of neural and hormonal autonomic drive, which acts to constrict renal and mesenteric vessels and to reduce blood flow. However, in the presence of circulatory impairment, where oxygen delivery to the exercising muscles is impaired as occurs to complete heart block where normal heart rate increases during exercise are prevented, or in congestive right heart failure, where normal stroke volume increases during exercise are impaired, or in the presence of severe anemia, where oxygen-carrying capacity of the blood is limited, visceral blood flows are reduced drastically and blood is diverted to the exercising musculature. Thus,, visceral flow is normally maintained during severe exercise as long as all other compensatory mechanisms remain intact. However, when any other compensatory mechanism is disrupted (even the elimination of splenic reserve in the dog), reduction and diversion of visceral flow occur.
 ...
PMID:Cardiovascular adjustments to exercise: hemodynamics and mechanisms. 79 Apr 60

Red cell mass and plasma volume were simultaneously measured by Cr51 and J125-albumine, respectively, in 36 patients with chronic obstructive lung disease and cor pulmonale. Additionally, pulmonary function tests and arterial blood gas analyses as well as pulmonary circulatory and right ventricular hemodynamic measurements were performed the same day. Patients were divided into 3 clinical subgroups: 1. a predominantely emphysematous A-type (n =12), 2. a predominantly bronchial B-type (n = 12), and 3. an intermediate type (n = 12) with about equal scores for A and B. With regard to the cardiac state, A-patients were clinically characterized by small ptotic hearts on chest x-ray and the absence of overt cardiac failure during the whole course of illness whereas B-patients generally showed radiological evidence of heart dilatation associated with recurrent episodes of manifest right ventricular failure. Patients of the intermediate type mostly had recovered from cardiac failure. The following results were obtained: 1. Red cell volume, plasma volume, and total blood volume were within normal limits in A-patients and in patients of the intermediate type. A marked hypervolemia in B-patients was almost entirely due to an increased red cell volume. 2. Close correlations of the red cell volume and total blood volume, respectively, to the arterial PO2 as well as to the arterial PCO2 could be established. 3. Total blood volume was significantly correlated to certain hemodynamic parameters, including cardiac output, stroke volume, pulmonary artery pressure, and right ventricular enddiastolic pressure. 4. The quotient body hematocrit/venous hematocrit was lowered to a significant degree as compared to normal subjects. As a consequence, indirect determination of red cell volume and total blood volume from plasma volume and venous hematocrit leads to a consistent overestimation of both parameters, amounting to 28% in the mean for the red cell mass and to 12% for the total blood volume in the present series.
 ...
PMID:[Red cell mass and plasma volume in chronic cor pulmonale (author's transl)]. 119 61

Left ventricular function and volume data from 17 control subjects and 27 young patients with secundum atrial septal defect (ASD) without overt left or right ventricular failure were compared. ASD patients were subdivided in low shunt (Qp/Qs less than 2.0) and high shunt (Qp/Qs larger than or equal to 2.0) groups. Mean left ventricular (LV) stroke volume was significantly less in ASD patients (46 +/- 16 ml/m2 in the low shunt and 44 +/- 9 ml/m2 in high shunt group) compared with control patients (51 +/- 13 ml/m2, P less than 0.01 and P less than 0.02, respectively). There was no significant difference in mean left ventricular end-diastolic volume (LVEDV) between any group of patients (control subjects 67 +/- 17 ml/m2; low shunt ASD 66 +/- 17 Ml/m2, and high shunt ASD 62 +/- 12 ml/m2). High shunt ASD had a significantly lower cardiac index compared with control patients (5.0 liters/min/m2 vs. 5.9 liters/min/m2, P less than 0.02). Both low shunt and high shunt ASD showed significantly lower stroke work indices than control subjects (42 +/- 13 GmM/m2 and 37 +/- 8 GmM/m2 compared with 51 +/- 14 GmM/M2 , P less than 0.05 and P less than 0.001, respectively) but only the high shunt group had a significantly lower peak systolic pressure (94 +/- 12 mm Hg vs. 109 +/- 11 mm Hg for control patients, P less than 0.01). There was no significant difference between the control and ASD groups in LV end-diastolic, mean right atrial, right ventricular end-diastolic, and pulmonary pressures. External systolic time intervals were compared in 5 control and 12 ASD patients. There was no significant difference between the two groups of patients in absolute values or indices for pre-ejection period, ejection time, or electromechanical systole. However, the ratio of the pre-ejection period index to left ventricular ejection time index (PEPI/LVETI) was significantly higher in ASD patients (P less than 0.05). In young subjects with large shunt ASD, certain indicators of left ventricular function are depressed. Evaluation of PEPI/LVETI may allow noninvasive determination of LV function.
 ...
PMID:Assessment of left ventricular function in secundum atrial septal defect: evaluation by determination of volume, pressure, and external systolic time indices. 119 7

The clinical features, hemodynamic parameters, Wilson's lead and head-chest (H-C) lead ECG of 23 cases with acute right ventricular infarction (ARVI) were analyzed. Results showed that 13 cases revealed clinical right heart failure, but 10 of them had clear lung fields. 11 cases showed hypotension. 20 cases had mean right atrial pressure (MRAP) > or = 10 mmHg. The remaining 3 cases had MRAP between 8 mmHg and 10 mmHg, but it was > or = 10 mmHg after volume loading. The ratio of MRAP to pulmonary wedge pressure was > 0.65 and the right ventricular stroke work index < 5.0 g.m/m2 in all the 23 cases. ST elevation > or = 1 mm in V3R to V6R was found in 12 cases (52%), while ST elevation > or = 1 mm in HV3R to HV8R in 20 cases (87%). The results showed that the diagnostic accuracy for ARVI with H-C lead (right chest) ECG is higher than that with Wilson's lead. H-C ECG is better correlated with hemodynamics in patients with ARVI.
 ...
PMID:[Evaluation of head-chest lead ECG in the diagnosis of acute right ventricular infarction]. 142 99

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.
 ...
PMID:Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation. 830 1

We used a chronic instrumented ovine model to investigate right heart function following an endotoxin bolus. Primary aim of the experiments was to elucidate the influence of the right heart on the cardiopulmonary system. Furthermore, we tried a thromboxane synthetase inhibitor as a therapeutical approach. At least we investigated the IR-ANF release, as the endocrinal function of the right heart, in this model. Following the endotoxin administration we observed a massive increase of the pulmonary arterial pressure. As a result of the increased right ventricular afterload right ventricular ejection fraction decreased and end-systolic volume increased. Impaired right heart function could not be compensated sufficiently using Frank Starling mechanism. Consequently, decreased left ventricular preload, stroke volume and cardiac output followed. Pretreatment with OKY-046, a selective thromboxane synthase inhibitor, attenuated the increase in pulmonary arterial pressure and prevented the early right heart failure including the drop of cardiac output. Furthermore, OKY-046 changed the thromboxane-prostacyclin relationship. Therefore we consider the cardiopulmonary reactions following pretreatment with OKY-046 as a result of the attenuated right ventricular afterload as well as of the increased prostacyclin concentration. Endotoxin induced hypoxaemia could not be prevented by pretreatment with OKY-046 and might be caused by interstitial edema following endothelial leakage. IR-ANF release in our model, accompanied by polyuria and natriuresis, seemed to be independent of right heart dysfunction and increase of right atrial pressure. We suggest endotoxin or a endotoxin induced mediator as a trigger of IR-ANF release.
 ...
PMID:[Right heart function and endotoxemia in animals]. 183 87

Systolic ventricular interactions may be partially responsible for right ventricular failure that sometimes occurs during clinical use of prosthetic left ventricular assist devices. In this hypothesis, it is proposed that the left ventricular assist device reduces left ventricular pressure and its contribution to right ventricular performance, thus impairing right ventricular output. On the other hand, these effects may be small compared with other causes of right ventricular failure such as ischemia. To test the systolic interaction hypothesis in the normal and ischemic right ventricle, we used a left ventricular assist device to pressure unload the left ventricle of anesthetized pigs, and we compared its effect on right heart function before and after 2 minutes of acute right coronary artery occlusion as a model of right heart failure. Pigs were instrumented for measurements of septal to left ventricular and right ventricular free wall dimensions with ultrasonic crystals, ventricular chamber pressures, and cardiac output with a pulmonary artery blood flow probe. Without right ventricular ischemia, the left ventricular assist device produced an 80% +/- 6% reduction in left ventricular pressure-time integral while maintaining aortic pressure. This resulted in a leftward septal shift with an 11.6% +/- 1.8% decrease in left ventricular septal-to-free wall dimension and a 12.5% +/- 2.4% increase in right ventricular septal-to-free wall dimension, with no changes in right ventricular cardiac output or stroke work. In contrast, right coronary artery occlusion alone produced right heart failure, with a 50% +/- 6% reduction in right ventricular global stroke work and 26% +/- 6% and 27% +/- 3% reductions in cardiac output and right ventricular peak systolic pressure, respectively. This right heart failure persisted during left ventricular unloading with the left ventricular assist device, which resulted in further leftward septal shifting and unchanged but still depressed stroke work and flow output. These findings support the hypothesis that a preexisting pathologic condition is the dominant factor in determining right ventricular function during prosthetic left ventricular support and that direct anatomic interactions play a minor role.
 ...
PMID:Effects of acute right ventricular ischemia on ventricular interactions during prosthetic left ventricular support. 192 35

The technique of surgically induced acute progressive right ventricular failure in experimental animals is described. It sumultates the hemodynamic situation of right ventricular failure in some patients after termination of extracorporeal circulation applied for carrying out procedures on the left ventricle. The described technique consists of rightsided longitudinal ventriculotomy, destruction of the tricuspid valve, and ligation of the right coronary artery. Nine control dogs died within two hours after induction of failure due to low stroke volume caused by low pulmonary and left atrial pressure. The use of rightsided support appliance draining blood from the right atrium in systole and pumping it into the trunk of the pulmonary artery in diastole by means of a membrane pump resulted in further 12 dogs in the restoration of left ventricular diastolic pressure, significant increase of aortal pressure (p less than 0.003) and stroke volume (p less than 0.003) and in a decrease of right atrial pressure (p less than 0.003). The study demonstrated that by using the described mechanical support the circulation can be adequately assisted so that the failing right side of the heart can get restored. (Tab.1,Fig.5,Ref.25.).
 ...
PMID:[Right-sided mechanical circulatory support in acute right ventricular failure in the dog]. 204 62

A right ventricular assist device (VAD) based on the principle of counterpulsation has been developed at our institution. The device is a valveless, pneumatically actuated, 40 cc, sac-type pump, with a single inlet-outlet port. For right ventricular support, the "Uniport" pump is anastamosed end-to-side to the pulmonary artery. In previous experimental trials, the device has been shown to impart minimal trauma to blood components. In this study, biventricular failure was induced in eight Holstein calves by normothermic ischemia during cardiopulmonary bypass. A Pierce-Donachy left VAD (LVAD) was used for left ventricular support following the ischemic insult. Hemodynamic measurements were obtained throughout the study, and each animal served as its own control. A significant increase in post injury cardiac output (33.5 +/- 11.4%) was obtained with use of the Uniport and LVAD, as compared to use of the LVAD alone (p less than or equal to 0.005). Other hemodynamic parameters of right heart failure, including right atrial pressure (RAP), pulmonary artery pressure (PAP), and left atrial pressure (LAP) were not significantly affected. These data suggest that the Uniport right ventricular assist device significantly improves cardiac output in this model of moderate right ventricular failure. Additional studies are required, however, to optimize pump stroke volume, and to further define the performance envelope of the device.
 ...
PMID:Hemodynamic effects of a new right ventricular assist device. 225 37


1 2 3 4 5 6 7 8 9 10 Next >>