Reduction In Systemic Arterial Pressure Research Articles

Surgical treatment of a giant unruptured left sinus of Valsava aneurysm requiring coronary artery bypass grafting

The present article describes a case involving a 74-year-old woman who presented with atypical chest pain and was found to have a giant aneurysm of the left sinus of Valsalva. Computed tomography coronary angiography performed before surgery showed a left main stem arising from the superior aspect of the left coronary sinus (stretched superiorly over, but not within, the aneurysm sac). The patient underwent surgery and an aortic valve replacement and root graft were performed. Intraoperatively, there was a progressive reduction in systemic arterial pressure and cardiac output disappeared, culminating in ventricular fibrillation, which was believed to be due to ischemia induced by the stretching of the native coronary arteries over the roof of the aneurysm sac. Therefore, the patient underwent coronary artery bypass grafting with revascularization of the left-sided system. The authors suggest that preoperative assessment, including noninvasive assessment of myocardial ischaemia, should be part of the work-up.

English

Medical paradox of induced hypotension has arisen because bleeding during operative interventions has become a problem of increasing importance during the past few years. Certain surgical procedures are now so vastly extensive and that other operations have penetrated so deeply into the vital structure of the body. A number of workers, both on this continent and abroad, have suggested that one effective method of controlling either gross hemorrhage or excessive vascular ooze may be by the reduction of systemic arterial pressure. When such a deliberate hypotension is combined with proper posturing of the patient so that the operative site is superior, permitting gravitational venous drainage away from the wound to the dependent portions of the body, the technique has been called “controlled hypotension,” and has been employed to achieve a relatively ischemic operative field.

Physical Training as Non-Pharmacological Treatment of Neurocardiogenic Syncope

BackgroundCharacterized as a sudden and temporary loss of consciousness and postural tone, with quick and spontaneous recovery, syncope is caused by an acute reduction of systemic arterial pressure and, therefore, of cerebral blood flow. Unsatisfactory results with the use of drugs allowed the nonpharmacological treatment of neurocardiogenic syncope was contemplated as the first therapeutic option. ObjectivesTo compare, in patients with neurocardiogenic syncope, the impact of a moderate intensity aerobic physical training (AFT) and a control intervention on the positivity of head-up tilting test (HUT) and orthostatic tolerance time. MethodsWere studied 21 patients with a history of recurrent neurocardiogenic syncope and HUT. The patients were randomized into: trained group (TG), n = 11, and control group (CG), n = 10. The TG was submitted to 12 weeks of AFT supervised, in cycle ergometer, and the CG to a control procedure that consisted in 15 minutes of stretching and 15 minutes of light walk. ResultsThe TG had a positive effect to physical training, with a significant increase in peak oxygen consumption. The CG did not show any statistically significant change before and after the intervention. After the intervention period, 72.7% of the TG sample had negative results to the HUT, not having syncope in the revaluation. ConclusionThe program of supervised aerobic physical training for 12 weeks was able to reduce the number of positive HUT, as it was able to increase tolerance time in orthostatic position during the HUT after the intervention period.

Lack of NO formation is involved in the vasodilative response to contrast media

Intravascular injection of angiographic contrast media results in peripheral vasodilation and hypotension. The mechanisms underlying these hemodynamic changes are not entirely clear. We hypothesized that increased formation of nitric oxide (NO) could be involved in the vasodilatory response to contrast media. To address this assumption we have investigated whether N(G)-monomethyl-L-arginine (L-NMMA, 200 mg/kg) and N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg), two specific NO formation inhibitors, can abolish the hypotensive response to intravascular injection of isopaque amin (1 g/kg), a contrast medium, as well as bradykinin (10 µg/kg), a NO-dependent vasodilator, in anaesthetized normotensive rats. In rats before pretreatment with L-NMMA and L-NAME, the absolute values of the average fall in mean arterial pressure (MAP) induced by intravascular injection of isopaque amin and bradykinin were 21.3 +/- 2.1 and 37.2 +/- 4.4 mmHg, respectively. Pretreatment with L-NMMA and L-NAME failed to affect the hypotensive response to isopaque amin; by administering isopaque amin in rats pretreated with L-NMMA and L-NAME the absolute values of the average fall in MAP were 25.6 +/- 4.9 and 23.4 +/- 3.9 mmHg, respectively, similar to the average fall in MAP before treatment with NO formation inhibitors. In contrast, the hypotensive response to bradykinin was significantly inhibited; by administering bradykinin in rats pretreated by L-NMMA and L-NAME, the absolute values of the average fall in MAP were 10.2 +/- 2.8 and 7.2 +/- 2.2 mmHg, respectively, much less than the average fall in MAP before treatment with NO formation inhibitors. We conclude that intravascular injection of isopaque amin causes reduction in systemic arterial pressure. However, this vasodilative effect seems unrelated majorly to augmented endothelium-derived NO formation.

Combined Use of PDE5 Inhibitors and Nitrates in the Treatment of Pulmonary Arterial Hypertension in Patients With Heart Failure

Background Phosphodiesterase-5 (PDE5) inhibitors, which induce relaxation of smooth muscle with some selectivity for the pulmonary vasculature, are used in the treatment of pulmonary hypertension. In some patients, the use of PDE5 inhibitors does not result in the desired magnitude of pulmonary vasodilation. The use of additional vasodilators to further reduce pulmonary vascular resistance is often accompanied by unacceptable reductions in systemic arterial pressure. Methods and Results In 3 patients with heart failure, pulmonary hypertension and low systemic arterial pressures treated with sildenafil, systemic nitrates were added to reduce pulmonary hypertension further. Hemodynamic measurements were made before and after addition of nitrates. Addition of systemic nitrates to sildenafil led to a reduction in mean pulmonary arterial pressure of 11 mm Hg, from 37 mm Hg to 26 mm Hg ( P = .06), whereas mean systemic arterial pressure decreased by only 4 mm Hg, from 77 mm Hg to 73 mm Hg ( P = .53). The ratio of pulmonary vascular resistance to systemic vascular resistance was reduced by 45% ( P = .1). Treatment with sildenafil and nitrates was continued for two to eight months, with no episodes of marked systemic hypotension, syncope, or lightheadedness. Conclusions These results suggest that addition of systemic nitrates to sildenafil results in a potentiation of vasodilation that is relatively selective for the pulmonary vasculature, and that this combination may be safe and effective in the treatment of pulmonary hypertension in patients with low systemic arterial pressures.

Effects of Estrogen and Progrestin on Hypothalamic Blood Flow Autoregulation

The consequences of female sex hormone deficiency and the effects of hormone replacement therapy are controversial because individual hormones and their derivates can result in partially antagonistic activities. This intricate system involving cerebral autoregulatory mechanisms caused by ovariectomy and female sex hormone replacement was studied in rats. The lower limit of cerebral blood flow autoregulation was determined by stepwise reduction of systemic arterial pressure while simultaneously measuring the changes of the hypothalamic blood flow (HBF) using the hydrogen gas-clearance method. In ovariectomized rats resting HBF decreased substantially and the threshold of cerebrovascular autoregulation decreased to 40 mm Hg. Estrogen replacement prevents the former change and shifts the latter upwards. Similarly, progestin replacement restores autoregulation to the physiological levels found in control animals, whereas it has no influence on the ovariectomy-induced reduction of resting blood flow. Steady-state HBF and compensatory changes of regional cerebral vascular autoregulation are altered significantly following ovariectomy. Estrogen or progestin replacement has an opposite effect on these cerebral circulatory parameters. Our observations highlight the essential role of female sex hormones in hypothalamic autoregulation during hypotensive stress.

Melatonin reduces pancreatic prostaglandins production and protects against caerulein‐induced pancreatitis in rats

Melatonin has been used to treat experimental pancreatitis, although not all the drug's therapeutic mechanisms of melatonin have been defined. Prostaglandins (PGs) are proinflammatory mediators that exert their effects mainly locally during inflammatory diseases. The present study was undertaken to examine whether treatment with melatonin influences local PG production. An acute pancreatitis model in male Sprague-Dawley rats (225-275 g) was established by continuously infusing caerulein (15 mg/kg/hr). Mean arterial pressure and pancreatic perfusion were monitored continuously. Melatonin was delivered via the intraperitoneal route at doses of either 2 or 10 mg/kg, 30 min after caerulein injection. Malondialdehyde and glutathione levels of the pancreas and liver and the trypsinogen activation peptide levels in the serum were measured at the end of the experiment (8 hr after infusion of caerulein). Intraperitoneal injection of melatonin (2 and 10 mg/kg) reduced the reduction in systemic arterial pressure and decreased pancreatic perfusion in the rat model of caerulein pancreatitis. Moreover, melatonin treatment changed local PG production toward control level. Higher dose of melatonin was somewhat more effective in preventing the caerulein-induced alterations than was the lower dose.

Lack of NO formation is involved in the vasodilative response to contrast media

Intravascular injection of angiographic contrast media results in peripheral vasodilation and hypotension. The mechanisms underlying these hemodynamic changes are not entirely clear. We hypothesized that increased formation of nitric oxide (NO) could be involved in the vasodilatory response to contrast media. To address this assumption we have investigated whether NG-monomethyl-L-arginine (L-NMMA, 200 mg/kg) and NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg), two specific NO formation inhibitors, can abolish the hypotensive response to intravascular injection of isopaque amin (1 g/kg), a contrast medium, as well as bradykinin (10 μg/kg), a NO-dependent vasodilator, in anaesthetized normotensive rats. In rats before pretreatment with L-NMMA and L-NAME, the absolute values of the average fall in mean arterial pressure (MAP) induced by intravascular injection of isopaque amin and bradykinin were 21.3 ± 2.1 and 37.2 ± 4.4 mmHg, respectively. Pretreatment with L-NMMA and L-NAME failed to affect the hypotensive response to isopaque amin; by administering isopaque amin in rats pretreated with L-NMMA and L-NAME the absolute values of the average fall in MAP were 25.6 ± 4.9 and 23.4 ± 3.9 mmHg, respectively, similar to the average fall in MAP before treatment with NO formation inhibitors. In contrast, the hypotensive response to bradykinin was significantly inhibited; by administering bradykinin in rats pretreated by L-NMMA and L-NAME, the absolute values of the average fall in MAP were 10.2 ± 2.8 and 7.2 ± 2.2 mmHg, respectively, much less than the average fall in MAP before treatment with NO formation inhibitors. We conclude that intravascular injection of isopaque amin causes reduction in systemic arterial pressure. However, this vasodilative effect seems unrelated majorly to augmented endothelium-derived NO formation.

Lack of NO Formation Is Involved in the Vasodilative Response to Contrast Media

Intravascular injection of angiographic contrast media results in peripheral vasodilation and hypotension. The mechanisms underlying these hemodynamic changes are not entirely clear. We hypothesized that increased formation of nitric oxide (NO) could be involved in the vasodilatory response to contrast media. To address this assumption we have investigated whether NG-monomethyl-L-arginine (L-NMMA, 200 mg/kg) and NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg), two specific NO formation inhibitors, can abolish the hypotensive response to intravascular injection of isopaque amin (1 g/kg), a contrast medium, as well as bradykinin (10 μg/kg), a NO-dependent vasodilator, in anaesthetized normotensive rats. In rats before pretreatment with L-NMMA and L-NAME, the absolute values of the average fall in mean arterial pressure (MAP) induced by intravascular injection of isopaque amin and bradykinin were 21.3 ± 2.1 and 37.2 ± 4.4 mmHg, respectively. Pretreatment with L-NMMA and L-NAME failed to affect the hypotensive response to isopaque amin; by administering isopaque amin in rats pretreated with L-NMMA and L-NAME the absolute values of the average fall in MAP were 25.6 ± 4.9 and 23.4 ± 3.9 mmHg, respectively, similar to the average fall in MAP before treatment with NO formation inhibitors. In contrast, the hypotensive response to bradykinin was significantly inhibited; by administering bradykinin in rats pretreated by L-NMMA and L-NAME, the absolute values of the average fall in MAP were 10.2 ± 2.8 and 7.2 ± 2.2 mmHg, respectively, much less than the average fall in MAP before treatment with NO formation inhibitors. We conclude that intravascular injection of isopaque amin causes reduction in systemic arterial pressure. However, this vasodilative effect seems unrelated majorly to augmented endothelium-derived NO formation.

MK-591 acutely restores glomerular size selectivity and reduces proteinuria in human glomerulonephritis

Leukotrienes are 5-lipoxygenated (5-LO) metabolites of arachidonic acid that mediate some of the glomerular hemodynamic and structural changes in experimental and human glomerulonephritis. We conducted an open-label, pilot study of the short-term effects of leukotriene biosynthesis inhibition using an orally active 5-LO activating protein (FLAP) antagonist (MK-591) on glomerular function in patients with glomerulonephritis. Eleven adult patients (seven women, median age 38 years) with glomerulonephritis (5 lupus nephritis, 2 IgA nephropathy, 1 membranoproliferative, 1 membranous, 1 C1q-deficiency, and 1 idiopathic crescentic) and moderate renal insufficiency [glomerular filtration rate (GFR) 62 +/- 9 ml/min/1.73 m2] were given MK-591 at a dose of 100 mg orally twice a day for four days. MK-591 reduced proteinuria (albumin and IgG excretion rates) from 3233 +/- 1074 to 1702 +/- 555 microg/min and from 196 +/- 78 to 148 +/- 55 microg/min for albumin and IgG, respectively (P < 0.05 for both). This was not accompanied by a reduction in systemic arterial pressure, GFR, or renal plasma flow. By analysis of the fractional clearance of polydisperse dextrans, baseline proteinuria resulted from a loss of size selectivity with enhanced passage of large (>52 A) dextrans as compared with healthy controls. Treatment with MK-591 caused a selective improvement in the enhanced passage of large (>58 A) dextrans without affecting the handling of smaller dextrans, indicating an improvement in glomerular size selectivity. MK-591 was well tolerated, and no adverse effects were observed. Short-term therapy with MK-591 reduces proteinuria by restoring glomerular size selectivity and thus reduces transglomerular protein trafficking. These benefits may result from glomerular leukotriene biosynthesis inhibition, but other MK-591-specific actions cannot be excluded.

Effect of Speed of Injection on Vital Signs, Dose Requirement and Induction Time for Induction of Anesthesia using Propofol

Background : Induction of anesthesia with propofol commonly associated with reduction in systemic arterial pressure, especially in elderly and high risk patients. This reduction is influenced by the dose and rate of propofol injection. The aim of this study was to examine the effect of different injection rate of propofol on vital signs, dose requirement and induction time during induction period. Methods : Unpremedicated one hundred and twenty ASA physical status I and II patients aged 20∼60 years scheduled for elective surgery were randomly allocated into one of four(150, 300, 600, 1200 ml/hr) groups according to speed of injection of propofol during induction period. Loss of verbal contact was taken as the end-point of induction. Vital signs, SpO2, dose requirement of propofol and induction time were checked. Results : As the injection rate of propofol became slower, there were significant reduction in induction dose and increase in induction time(P<0.05). For example, induction dose and time were 1.82 mg/kg, 223±58 sec in 150 ml/hr group and 3.14 mg/kg, 50±11 sec in 1200 ml/hr group, respectively. Also, decrease in systolic and diastolic pressure were less marked at lower injection rates. Conclusions : Slower injection of propofol produces less vital sign changes and dose requirement for the induction of anesthesia. (Korean J Anesthesiol 1997; 33: 262∼266)

Tonic inhibition of renin secretion by the 12 lipoxygenase pathway: augmentation by high salt intake.

Recent evidence suggests that lipoxygenase (LO) metabolites inhibit renin production in vitro. However, the physiological significance of this effect has not been determined. This study examined the role of the LO pathway in the regulation of plasma renin concentration (PRC) in vivo. The acute administration of two structurally unrelated LO inhibitors, phenidone (30 and 60 mg/kg) and esculetin (60 mg/kg), resulted in suppression of platelet 12 hydroxyeicosatetraenoic acid (12HETE) production, reduction in systemic arterial pressure and a 2- to 3-fold increase in PRC. To determine whether the esculetin-induced increase in PRC was secondary to hypotension, esculetin was also administered to rats preinfused with a pressor dose of norepinephrine. In these acutely hypertensive rats, esculetin still induced a 2.5-fold increase in PRC, whereas blood pressure remained over 40 mm Hg above basal levels. Further, esculetin (10(-6)M) increased renin release in renal slices from 150 +/- 10 to 310 +/- 20 ng/ml.h (P < 0.05) and this rise was entirely blocked in the presence of 12HETE (10(-7)M; 130 +/- 40 ng/ml.h). In rats placed on high salt intake, 12HETE concentration in renal slices from the outer cortex was considerably higher than in renal slices from salt-restricted rats (116.5 +/- 15.7 vs. 65 +/- 12 pg/mg protein; P < 0.05). Chronic administration of the LO inhibitor phenidone also resulted in an increase of PRC, which was independent of changes in blood pressure. On either high salt (3.15%0 or low salt (0.05%) diet phenidone-treated rats had higher PRC levels than the respective control groups [high salt 9.7 +/- 3.5 vs. 1.9 +/- 1.4 ng/ml.h; P < 0.05; low salt 33.2 +/- 5.3 vs. 19.4 +/- 3.10 ng/ml.h; P < 0.05]. The finding that LO blockers are potent stimulators of PRC in vivo suggests the existence of a physiological tonic inhibition of renin secretion by LO products that is operative under a wide range of salt intake. High salt intake enhances this inhibitory tone by increasing renal cortical 12 LO activity and, in fact, normal suppression of PRC during high salt diet does not occur in LO-blocked animals. Thus, the LO pathway exerts a tonic inhibitory effect on renin release, which appears particularly important for renin suppression during high salt intake.

Effects of zaprinast and dissolved nitric oxide on the pulmonary circulation of fetal sheep.

This study was designed to determine indirectly if the changes in ovine fetal pulmonary vascular tone caused by i.v. injections of nitric oxide-containing solutions are mediated by cGMP. We first characterized the dose-response relationship of bolus intrapulmonary injections of zaprinast (a cGMP-selective phosphodiesterase inhibitor) and nitric oxide solutions. Injections of nitric oxide solutions as well as zaprinast solutions resulted in dose-dependent decreases in pulmonary arterial pressure that were greater than reductions in systemic arterial pressure. We also evaluated the effects of simultaneous infusions of zaprinast and U46619 (a thromboxane mimetic) on the response to bolus injections of 1.0 micrograms of acetylcholine, 100 ng of endothelin-1, and 10.0 microL of ethanol saturated with nitric oxide. Zaprinast was infused at a rate of 1.5 mg/min, and the concentration of U46619 was titrated to raise mean left pulmonary arterial pressure (LPAP) to the steady state level that was present before infusing zaprinast. All bolus injections reduced left pulmonary arterial pressure more than they reduced mean systemic arterial pressure. However, neither the response magnitudes nor the response durations were affected by simultaneous infusions of zaprinast and U46619. We therefore suggest that modulation of fetal pulmonary vascular tone by endogenously produced nitric oxide may involve mechanisms other than raising smooth muscle cytoplasmic cGMP concentrations.

Differing effects of antihypertensive agents on urinary albumin excretion.

Increased urinary albumin excretion is a good predictor of future progression of renal disease in patients with both insulin-dependent and non-insulin-dependent diabetes mellitus. In addition, it is an independent predictor of cardiovascular morbidity and mortality in patients with essential hypertension. Whether urinary albumin excretion represents a prognostic indicator for progressive renal dysfunction in patients with normal blood pressure, or essential hypertension and normal renal function, remains to be determined. In patients with diabetic renal disease, urinary albumin excretion is a good predictor for the future development of renal injury, and an effort has thus been made to study the success of antiproteinuric therapies in delaying progression of renal injury. Some antihypertensive agents have demonstrated abilities to reduce urinary albumin excretion either with or without a reduction in systemic arterial pressure. Whether the abilities of these drugs to protect renal function is related to their antihypertensive effects or antiproteinuric effects, or both, is unknown. This review will explore the influence of different antihypertensive agents on urinary albumin excretion in patients with and without essential hypertension, as well as in patients with nondiabetic and diabetic renal disease.

The Role of Arterial Baroreceptors in the Undivided Circulation of Anuran Amphibians

Baroreceptors with afferent fibers in branches of the glossopharyngeal nerve or the vagus have been identified in all three arterial arches in anuran amphibians. Baroreceptors in the pulmocutaneous arch (PCA) appear to provide the principal feedback of arterial blood pressure to the cardiovascular centers of the medulla. An additional contribution arises from receptors within the aortic arch. The receptors are slowly adapting mechanoreceptors and, at least in the case of the PCA baroreceptors, transmit baroreceptive information via nonmyelinated afferents. Pressure thresholds coincide with the range of systolic arterial pressures associated with undisturbed toads. Therefore, increases in systolic pressure above resting result in both increases in firing frequency and the recruitment of previously inactive receptors. Denervation experiments demonstrate that feedback from PCA baroreceptors tonically inhibits the cardiovascular system even at rest. Experimental elevation of PCA pressure above resting values causes bradycardia and reduces systemic vascular resistance, resulting in a compensatory reduction in systemic arterialpressure. In addition, PCA resistance increases, which probably reflects a constriction of the extrinsic pulmonary artery. This response opposes the negative feedback regulation of arterial pressure but may protect the pulmonary microvasculature by increasing upstream resistance, thereby reducing intravascular pressures in pulmonary vessels. This is consistent with the view that the primary role of anuran PCA baroreceptors is to protect the delicate vasculature of the gas-exchange organ against high central driving pressures transmitted by the incompletely divided anuran circulation. Future studies should be directed toward an investigation of the central pathways involved in the PCA baroreflex.

Angiotensin II receptor blockade improves nerve function, modulates nerve blood flow and stimulates endoneurial angiogenesis in streptozotocin-diabetic rats and nerve function.

We examined the effect of the angiotensin II receptor blocker, ZD 8731, on nerve function, capillary density, and blood flow in streptozotocin-diabetic rats. Deficits in sciatic motor and saphenous sensory nerve conduction velocity of 21% and 15%, respectively, were observed after 1 month of diabetes mellitus (p < 0.001). These were completely ameliorated by a further month of ZD 8731 treatment (p < 0.001). Treatment of non-diabetic rats for 1 month with ZD 8731 had no effect on motor or sensory conduction velocity. Sciatic nerve capillary density was not significantly affected by 1- or 2-month untreated diabetes, however, there was a 15% increase in density with ZD 8731 treatment (p < 0.001). Treatment of non-diabetic rats for 1 month had no effect on capillary density. Diabetes prolonged the time taken for 80% conduction failure by 19% (p < 0.05) and 49% (p < 0.001) for 1 and 2 months of diabetes, respectively, when sciatic nerve was exposed to hypoxia in vitro. ZD 8731 treatment during the second month of diabetes limited the prolongation to 22%, not significantly different from 1 month of untreated diabetes but less than for the 2-month diabetic group (p < 0.001). Concentrations of sciatic nerve polyol pathway metabolites were elevated six-fold and myo-inositol was reduced 40% by diabetes; ZD 8731 treatment was without effect. Acute experiments examined the effect of ZD 8731 on sciatic nerve blood flow using laser-Doppler flowmetry. In non-diabetic rats, blood flow changes followed the dose-dependent reductions in systemic arterial pressure and there were no significant variations in sciatic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic and angiographic comparison of intravenous nitroglycerin and nicardipine mainly in subjects without coronary artery disease

Twenty patients were studied during cardiac catheterization to compare hemodynamic and quantitative angiographic effects of intravenous nicardipine and nitroglycerin. After baseline measurements, nicardipine or nitroglycerin was administered by randomized continuous infusion beginning at 10 μg/min titrated to achieve a 10 to 12% reduction in systemic arterial pressure. Hemodynamic measurements and angiography were then repeated. Nicardipine did not change heart rate, and a small decrease (82 ± 4 vs 75 ± 4 beats/min) was observed with nitroglycerin, whereas mean arterial pressure decreased similarly (−11%) in both groups. Nicardipine increased (+13%) and nitroglycerin decreased (−21%) cardiac output. Although both drugs were associated with significant reductions in pulmonary artery wedge and pulmonary artery pressures, changes were greater with nitroglycerin for pulmonary artery wedge (−49% vs −26%) and pulmonary artery (−39% vs −13%) pressures, whereas only nitroglycerin reduced right atrial pressure significantly. Neither drug altered left ventricular ejection fraction or pulmonary vascular resistance, and only nicardipine decreased systemic vascular resistance significantly. Quantitative coronary angiography (videodensitometry) showed dilation of the left main, proximal, mid and distal anterior descending and circumflex segments by both nitroglycerin and nicardipine. Nicardipine dilated small (<2 mm 2) and large (>2) arterial segments equally, whereas nitroglycerin showed a proportionately greater effect on small vessels.

Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation

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.

The Effect of Prostaglandin E1 on Acute Pulmonary Artery Hypertension during Oleic Acid-Induced Respiratory Dysfunction

This study examined the general effect of intravenous PGE1 on RV Ees and effective PA elastance (EA) during acute pulmonary hypertension associated with oleic acid infusion. In eight pigs, RV end-systolic elastance was quantified with the Ees and Ea was defined with reference to the Windkessel model. Oleic acid infusion increased mean PAP and Ea. Prostaglandin E1 reduced PAP and decreased Ea. Ees did not change throughout the study. Mean arterial pressure was reduced and the pulmonary shunt was increased after PGE1 infusion. The PaO2 was reduced. Data from this study suggest that although PGE1 is effective in reducing PAP, it is not as effective in reducing RV afterload. Furthermore, PGE1 does have significant side effects such as reduction of systemic arterial pressure and an increase in pulmonary shunt.

The Effect of an Increase in Systemic Arterial Pressure in the Newborn with Right Ventricular Hypertension

To evaluate the effect of an elevation in systemic arterial pressure upon pulmonary blood flow and arterial oxygenation during right ventricular hypertension (RVH), we acutely studied 13 1-d-old piglets. Catheters were positioned in the pulmonary artery, both atria, and the aorta for hemodynamic measurements. An electromagnetic probe was positioned in the main pulmonary artery for pulmonary blood flow measurement. Systemic and regional blood flow were measured with the radiolabeled microsphere technique. A balloon-mounted catheter was advanced in the aorta and maintained at the lower thoracic level. After induction of RVH (pulmonary artery banding), a significant decrease in arterial O2 pressure from 54.4 +/- 1.6 to 10.6 +/- 0.4 kPa (p less than 0.01), a 30% reduction in systemic arterial pressure, and a 44% decrease in pulmonary blood flow were observed. During RVH, partial inflation of the aortic balloon to restore the systemic arterial pressure to its initial value led to an increase in arterial O2 pressure to 23.5 +/- 3.1 kPa (p less than 0.01). Full inflation of the balloon further increased the arterial O2 pressure to 32.6 +/- 2.9 kPa (p less than 0.01). Aortic balloon inflation increased pulmonary blood flow in 11 and systemic O2 delivery in nine of the 13 animals. RVH was associated with a significant increase in cerebral and right ventricular myocardial free-wall blood flow and a decrease in renal and bowel blood flow and O2 delivery (p less than 0.01). Aortic balloon inflation during RVH did not change either the cerebral or myocardial free-wall blood flow, but further significantly decreased renal and bowel blood flow and O2 delivery.(ABSTRACT TRUNCATED AT 250 WORDS)