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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date there has been no description of the hemodynamic dose-response relationship between enflurane and sodium nitroprusside (SNP), although these drugs are often used together to induce deliberate hypotension. Utilizing aortic root cannulation and thermistor-tipped pulmonary artery catheters, this relationship was studied in six beagles during 1 and 2% enflurane anesthesia and compared with the hemodynamic response induced by SNP in the awake state and during anesthesia with intravenous morphine (6 mg/kg). Each animal received a standard infusion of 100 microgram/kg of SNP administered at three different flow rates (5, 10, and 20 microgram/kg/min). SNP infusion resulted in dose-related reductions in mean arterial pressure, systemic vascular resistance and left ventricular stroke work, whereas cardiac output increased. Enflurane potentiated the hypotensive effects of SNP in a dose-related fashion. During morphine anesthesia, however, the hemodynamic effects of SNP were virtually indistinguishable from those observed in the awake state.
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PMID:Sodium nitroprusside: hemodynamic dose-response during enflurane and morphine anesthesia. 57 54

Activity of Carnigen on the cardiovascular system, following intraduodenal and intravenous application, was investigated in normotone and hypotone dogs anaesthetized with sodium pentobarbital, 35-40 mg/kg intraperitoneally. Intraduodenal application of 1 and 3 mg Carnigen/kg caused an increase in blood pressure and tachycardia. The total peripheral resistance was lessened, in normotone as well as hypotone dogs, whereas the cardiac output and stroke volume were augmented. A rise in myocardial inotrophy and cardiac work in combination with a moderate increase in left ventricular O2 consumption also occurred as result of the action of Carnigen. An increase in the central and peripheral venous pressure was registered during continuous infusion of Carnigen. Coronary flow was also raised, in a dose dependent manner within the range of 0.1 to 1 mg Carnigen/kg i.v. The rise in arterial blood pressure is due to an increase in cardiac output, resulting from the positive inotropic action of this compound on the myocardium. The reduction in arterial resistance can be explained on the basis of a possible interaction between the inosine, released from Carnigen, and the adenosine already present in the system.
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PMID:Cardiovascular activity of Carnigen in normotone and in experimentally hypotone dogs. 59 55

The hemodynamic effects of dihydralazine and prazosin (0.1 and 1.0 mg/kg i.v.) on the circulatory system and left ventricular dynamics and contractility has been performed in 10 purebred beagle dogs (15.5 +- 1.4 kg) under pentobarbital sodium (35-40 mg/kg i.p.) anaesthesia by means of thermodilution and catheter technics. The changes of cardiovascular values were: 1. Either dihydralazine and prazosin decreased mean arterial blood pressure in the dose of 0.1 mg/kg i.v. Following application of 1.0 mg/kg intravenously, the arterial pressure abruptly decreased after prazosin. 2. Both pharmaca caused tachycardia. Being slowly introduced but continued by dihydralazine, the increase of pulse rate after prazosin was only initial. 3. The cardiac dynamics were differently influenced by dihydralazine and prazosin. In the estimated dose range prazosin led to an increase of cardiac output directly after application while dihydralazine induced a gradual enhancing of cardiac output. 4. The stroke volume was decreased by prazosin and slightly increased by dihydralazine. 5. While distinctly decreasing initially after prazosin, peripheral total resistance was slowly reduced by dihydralazine. 6. The contractility of the left ventricle, estimated as dp/dtmax and VCE, showed a distinct increase of the myocardial inotropy after both compounds. The maximal effect after prazosin, however, was to be seen immediately post applicationem. Dihydralazine led to a deferred enhancing of the measured contractility parameter.
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PMID:[Dihydralazin versus prazosin. The hemodynamic effect of the modul substances (author's transl)]. 60 53

Angiotensin antagonists have proved useful in elucidating the clinical role of the renin-angiotensin system; and their diagnostic and therapeutic efficacy in hypertension has been the subject of many reports but the hemodynamic effects remain unknown. Therefore, saralasin was infused intravenously (1.3 mg/min for 30 min) in 26 sodium-depleted patients with hypertension. Systemic hemodynamic alterations were determined before, during, and after infusion. On the basis of mean arterial pressure (MAP) changes, patients were classified as responders, nonresponders, or pressorresponders (MAP changes greater than or equal to 10 mm Hg). MAP fall in responders was achieved through reduced cardiac output and/or total peripheral resistance, with minimal or absent reflexive heart rate increase. In nonresponders, despite no change in MAP, output fell in parallel with stroke index and left ventricular ejection rate, In pressorresponders, saralasin increased vascular resistance. Thus, in addition to variable effects on vascular receptors, saralasin produced inhibitory cardiac effects either through altered venous return or inhibition of contractility.
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PMID:Hemodynamic correlates of saralasin-induced arterial pressure changes. 61 29

The haemodynamic effects of oxytocin (Syntocinon) and methyl ergometrin (Methergin) were studied in 9 healthy females in the first trimester of pregnancy. The patients were anaesthetized with sodium thiomebumal, pethidine and pancuronium bromide and ventilated on a Manley respirator. 10 i.u. oxytocin given as an i.v. bolus brought about a fall in femoral arterial pressure of 40%, systemic resistance 59% and pulmonary resistance 44% 30 sec after injection. However, the heart rate increased 31% and stroke volume 17%, so that the cardiac output increased by 54%. The pulmonary arterial pressure and wedge pressure were increased by 33% and 35%, respectively 150 sec after injection. No changes were seen in the haemodynamic parameters during infusion of 80 mU oxytocin for 10 min. 0.2 mg Methergin brought about an increase in the femoral arterial pressure of 11%, pulmonary arterial pressure 27% and wedge pressure 31%, with no changes in the other measured parameters. The use of oxytocic drugs in patients with compromised circulation is discussed.
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PMID:Haemodynamic effects of oxytocin (syntocinon) and methyl ergometrine (methergin) on the systemic and pulmonary circulations of pregnant anaesthetized women. 63 63

Seven chronically prepared dogs (electromagnetic flow transducers around the pulmonary and left renal artery, left atrial catheter) maintained on a controlled sodium and water intake were studied. About 20 h after the last intake of food and water, the effects of i.v. methohexitone (initial dose: 6.10 +/- 0.84 mg/kg bw; sustaining infusion: 0.34 +/- 0.10 mg/min.kg bw) on renal excretion of sodium, potassium, urea and water as well as on several haemodynamic values were investigated over a period of 60 min (MP) after a control period (CP) of 60 min in the unanaesthetized state. In 18 of 19 experiments water diuresis (U/Posm less than 1) was observed between 20 and 40 min after starting the administration of methohexitone. Urine volume increased from 44 +/- 21 microliter/min.kg bw (CP) to 104 +/- 62 microliter/min.kg bw (MP).I.v. administration of arginine-vasopressin (ADH) completely abolished water diuresis. During MP, there was a decrease in cardiac output (-11%), stroke volume (-36%) and left atrial pressure (-27%), heart rate increased (+ 43%). Mean arterial blood pressure and renal blood flow did not change. It is assumed-as plasma osmolality did not change-that the central release of antidiuretic hormone is suppressed by methohexitone.
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PMID:[Water diuresis during methohexitone anaesthesia. Studies in chronically instrumented dogs (author's transl)]. 65 67

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

Since 1969, we have investigated epidemiological studies of cerebro-cardiovascular diseases in the suburbs of Iwamizawa city in Hokkaido, the northernmost island of Japan. Cross-sectional surveys of 1,092 persons, equivalent to 90.3% of inhabitants over 40 years of age, revealed that the prevalence of hypertension amounted to 34%, and that the prevalence of abnormal ECG, CTR, fundi, albuminuria, glucosuria and overweight in the hypertensive group were significantly higher than in the normotensive group. After a 5-year cohort follow-up study concerning the incidence of strokes and heart attacks, age was found to be the highest risk factor in both incidents and hypertension was the second highest in cerebrovascular accidents, but not so high in heart attacks. In addition, we measured plasma renin activity (PRA) as a risk factor. On the basis of our observations, it is evident that the casual PRA of the rural Japanese population in Hokkaido, who usually excrete sodium more than 200 mEq per day, is valuable for our study. PRA was inversely proportional to systolic blood pressure in the normotensives and total group, but no correlation was found in the hypertensives alone. Observing 13 renin-determined accidents (8 strokes & 5 heart attacks) prospectively, incidence of strokes and heart attacks occurred more frequently in the high- and low-renin subgroups than in the normal-renin subgroup. Based on multivariate analysis, the following conclusion was drawn: systolic pressure, high renin, diastolic pressure and low renin, in this sequence, contribute largely toward the discrimination of cerebro-cardiovascular accident from no cerebro-cardiovascular accident. Thus it was suggested that the casual PRA was useful to predict the occurrence of vascular complications, in addition to the existence of hypertension. It has been said that the mortality rate of CVA in Hokkaido is less than the average of the rest of northern parts in Japan. By the vital statistics and our survey, it was clear that seasonal variation of the death rate from CVA and heart attack, which increases in the winter season, is weaker in Hokkaido than in Honshu. It is of interest to speculate that it is due to better-equipped heating in houses in Hokkaido than in other northern parts of Honshu.
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PMID:[Epidemiological survey of cerebro-cardiovascular diseases at Iwamizawa in Hokkaido (author's transl)]. 66 61

Thirteen patients with severe cardiac failure underwent a single crossover study of dopamine and dobutamine in order to compare the systemic and regional hemodynamic effects of the two drugs. The dose-response data demonstrated that dobutamine (2.5--10 microgram/kg/min) progressively and predictably increases cardiac output by increasing stroke volume, while simultaneously decreasing systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure. There was no change in heart rate or premature ventricular contractions (PVCs)/min at this dose range. Dopamine (2--8 microgram/kg/min) increased the stroke volume and cardiac output at 4 microgram/kg/min. Dopamine at less than 4 microgram/kg/min provided little additional increase in cardiac output and increased the pulmonary wedge pressure and the number of PVCs/min. At greater than 6 microgram/kg/min, dopamine increased heart rate. During the 24-hour maintenance-dose infusion of each drug (dopamine 3.7--4, dobutamine 7.3--7.7 microgram/kg/min), only dobutamine maintained a significant increase of stroke volume, cardiac output, urine flow, urine sodium concentration, creatinine clearance and peripheral blood flow. Renal and hepatic blood flow were not signfiicantly altered by the maintenance dose of either drug. Systemic and regional hemodynamic data suggest that dobutamine has many advantages over dopamine when infused in patients with cardiac failure.
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PMID:Comparative systemic and regional hemodynamic effects of dopamine and dobutamine in patients with cardiomyopathic heart failure. 67 37


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