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PubMed1986

[Comparative evaluation of prostaglandins E1 and E2 in patients with hypertension].

Changes in ABP, ECG, cerebral and peripheral hemodynamics were examined in 29 patients with second-stage essential hypertension before and within 1 or 2 days after PGE1 and PGE2 infusions administered during follow-up or in the presence of a hypotensive therapy. PGE were shown to be active vasodilators increasing cerebral and peripheral circulation. Vascular PG effects persisted for 1 or 2 days after the administration. Hypertensive patients demonstrated two patterns of hemodynamic response to PGE. The patients with higher total peripheral resistance (TPR) and low stroke and cardiac indices (SI and CI) during follow-up or hypotensive treatment were more sensitive to PGE, their ABP falling because of declining TPR. The patients with high SI and normal or slightly elevated TPR were less sensitive to PGE, their ABP falling mostly at the expense of declining SI. Most patients showed changed end portion of the ventricular complex immediately after PGE administration that vanished within one or two days. In coronary patients, angina of effort occurred less frequently after PGE infusion.

Adult↗

PubMed1985

Sodium acetate, an arterial vasodilator: haemodynamic characterisation in normal dogs.

Sodium acetate (SA) has been implicated in hypotensive episodes of haemodialysis because of its vasodilatory effects. The haemodynamic correlates of the changes in blood pressure, cardiac output (CO) and total peripheral resistance (TPR) are well known but the site of action of SA (i.e. arteriolar, venular or both) is not yet clarified. We thus studied the changes in CO, TPR and mean arterial pressure (MAP) induced by four graded doses of SA (0.034 to 0.300 mEq/kg/min) in seven normal dogs. To evaluate the site of vasodilation we also measured the changes in cardiopulmonary volume (CPV), mean pulmonary artery pressure (MPAP) and mean transit time (MTT). From control to the highest infusion rate, CO increased from 1.63 +/- 0.20 to 3.59 +/- 0.38L/min (p less than 0.001), TPR decreased from 78.2 +/- 11.3 to 36.4 +/- 4.8A.U. (p less than 0.001). MAP rose significantly from 107.2 +/- 4.0 to 116.5 +/- 8.5 mmHg (p less than 0.05) and stroke volume was maintained (17.2 +/- 2.3 to 19.6 +/- 2.1 ml, NS) in spite of the marked tachycardia observed (heart rate from 106.1 +/- 7.6 to 194.8 +/- 9.1bpm, p less than 0.001). This was associated with increases in MPAP (from 13.3 +/- 0.7 to 19.6 +/- 2.1mmHg, p less than 0.01) and CPV (from 195.0 +/- 21.3 to 224.4 +/- 24.3ml, p less than 0.01) and marked decrease in MTT (from 7.74 +/- 0.73 to 3.78 +/- 0.22 sec, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed1979

Ventilation:perfusion maldistribution secondary to the hyperdynamic cardiovascular state as the major cause of increased pulmonary shunting in human sepsis.

Cardiovascular and respiratory parameters were obtained in 374 studies from 151 patients (64 septic or septic shock and 87 with nonseptic cardiogenic syndromes). Cardiac output and related measures, respiratory parameters, pulmonary blood volume (DV/m2), cardiac ejection fraction (EFx), left ventricular end-diastolic volume (LVEDV), peripheral resistance (TPR), pulmonary shunt (QS/QT), physiologic dead space (VD/VT) and mean ventilation perfusion ratios (VA/QT) were calculated. Both physiologic evaluation and multivariable statistical analyses of the data were performed. For a given level of (A-aO2 gradient/PaO2) septic patients have a higher QS/QT than cardiogenic patients. Hyperdynamic septic patients have a larger QS/QT, a greater VD/VT, and a lower VA/QT and TPR than cardiogenics. The decrease in VA/QT and the rise in VD/VT are strong functions of the increased EFx, which raises cardiac index (CI) and reduces LVEDV and the mean dispersion of pulmonary blood volume, thus causing hemodynamic redistribution of flow. QS/QT is mainly a direct function of the increase in CI which also tends to reverse the EFx-mediated rise in VD/VT. The role of the septic mediated decrease in TPR as a contributing pathologic feature and the use of volume infusion to raise LVEDV and VA/QT in high-CI septics with large QS/QT is discussed.

Blood Circulation↗

PubMed1981

[Hemodynamic effects of some beta-adrenergic blocking agents in conscious spontaneously hypertensive rats (author's transl)].

The hemodynamic effects of propranolol, pindolol and practolol were investigated i conscious spontaneously hypertensive rats (SHR). Mean blood pressure (MBP), heart rate (HR) ard cardiac output (CO) were measured and total peripheral resistance (TPR) was calculated. CO was determined by the modified dye dilution method using an arterio-venous shunt between the left carotid artery and the right jugular vein. Intraperitoneal administration of propranolol (5 mg/kg), pindolol (0.1 mg/kg) or practolol (50 mg/kg) caused a sustained antihypertensive effect of a similar degree. The antihypertensive effect of propranolol (20-30 mmHg, 0.5-8 hr) was attributed to an early decrease of CO (0.5-4 hr) followed by a reduction of TPR (6-8 hr), while that of pindolol or practolol (30-50 mmHg, 0.5-8 hr, 30 mmHg, 2-8 hr) was apparently related to a reduction of TPR with a CO increment. HR decreased with propranolol but increased with pindolol, while only slight changes were observed with practolol. Antihypertensive effects of propranolol, pindolol or practolol were associated with characteristic hemodynamic changes.

Adrenergic beta-Antagonists↗

PubMed1984

Beta-adrenoceptor blockade and vasodilatation in essential hypertension. Hemodynamic studies at rest and during exposure to stress.

The purpose of this study was to evaluate the acute and long-term effects on blood pressure and hemodynamics both at rest and during acute exposure to loud noise of drugs with beta-adrenoceptor blocking and vasodilating properties. Prizidilol and carvedilol both act as nonselective beta-blocking and precapillary vasodilating compounds. Prizidilol (200 mg X 2) was compared to propranolol (80 mg X 2) plus hydralazine (25 mg X 2) and showed similar antihypertensive effect in a long-term double-blind randomized trial. Carvedilol was evaluated acutely with invasive (dye-dilution) and noninvasive (plethysmography) technique and showed an acute antihypertensive effect without causing a rise in TPR and with a decrease in regional resistance in the fore-arm. Acutely, carvedilol (25 mg and 50 mg) decreased blood pressure and regional resistance (50 mg) in contrast to propranolol (80 mg) which did not lower blood pressure acutely and caused an increase in regional resistance. In a long-term double-blind, randomized comparison, both propranolol (80 mg X 2) and carvedilol (25 mg X 2 and 50 mg X 2) showed a useful antihypertensive effect. After 29 days, however, it was still possible to demonstrate an acute decrease in resistance with carvedilol (50 mg) after tablet intake, indicating the vasodilating activity of this compound. When patients with essential hypertension were exposed to an even broad band noise (100 dBA), there was a rise in blood pressure due to an increase in TPR. Alpha 1-adrenoceptor blockade (prazosin 2 mg) prevented the rise in TPR but blood pressure increased in spite of this due to a rise in CO. Moreover, nonselective beta-adrenoceptor blockade and alpha 1-adrenoceptor blockade in combination (labetalol 200 mg) were unable to prevent the rise in blood pressure induced by noise. Finally, precapillary vasodilatation and beta-adrenoceptor blockade (prizidilol 400 mg) given as long-term treatment were also inefficient in preventing the noise-induced (105 dBA) rise in blood pressure. The absolute level of blood pressure obtained, however, was significantly lower than during placebo administration.

Adrenergic beta-Antagonists↗

PubMed1980

Differing haemodynamic stability due to differing sympathetic response: comparison of ultrafiltration, haemodialysis and haemofiltration.

In 12 RDT patients the volume removal related haemodynamic changes were correlated with concomitant changes in sympathetic activity during pure ultrafiltration (UF), post dilution haemofiltration (HF) and haemodialysis using either acetate (HDA) or bicarbonate (HDB) as buffer substitute. Total peripheral resistance (TPR) and plasma noradrenaline concentrations (PNA) increased during UF indicating a qualitatively adequate reaction of ESRD patients to volume removal. This physiological response is maintained during HF, resulting in intratreatment haemodynamic stability. In contrast no increase of PNA and insignificant changes of TPR were seen in HDA and HDB. As small molecule clearances were matched to those in HF, the behaviour of PNA indicates that not PNA removal but an impaired sympathetic response during HDA and HDB is responsible for the inadequate rise of TPR.

Adult↗

PubMed1978

Circulatory adaptation after aortic valve replacement. A clinical study peroperatively and in the early postoperative period.

The myocardial function and the central and peripheral circulation were studied after aortic valve replacement. All patients showed a similar postoperative pattern of response. During the operation, after termination of bypass, the mean arterial blood pressure (Pa,m) was low. The total peripheral vascular resistance (TPR) and pulmonary vascular resistance (PVR) were normal. Immediately after the operation Pa,m, TPR and PVR were higher than peroperatively. The cardiac index (CI) and stroke index (SI) were low, and the heart rate (HR) was high. At this stage the oesophageal temperature was increasing, but there was no shivering. Then followed a period in which Pa,m and TPR decreased, while CI and SI remained essentially unchanged. The oesophageal temperature reached its highest value 5 hours postoperatively. Peripheral warming began in the 3rd hour postoperatively and was completed in the 6th hour, when the peripheral temperature was 35 degrees C. The progressive peripheral warming, with peripheral cutaneous vasodilatation and slight reduction of the heart rate, took place without signs of increasing CI or SI. The left and right ventricular function, expressed as the relation between LVSWI and Pla,m, and RVSWI and Pra,m, respectively, varied postoperatively and showed no signs of improvement at the time of peripheral warming. Cardiac output and myocardial function seemed to be little affected by the obvious changes appearing during the systemic and peripheral vasodilatation in connection with central and peripheral warming.

Aged↗

PubMed1981

[Effect of the acid-base status on circulatory stability during acetate and bicarbonate hemodialysis].

In the preceding circulatory studies (Hampl et al. 1977, Hampl et al. 1978, Hampl et al. 1979, Hampl et al. 1980) we have proved in our patients that during the acetate dialysis (HDA) the circulatory insufficiency results from the inadequate response of the total peripheral vascular resistance (TPR) to the deprivation of the volume. Of these previously studied patients we selected six ones with frequency episodes of symptomatic hypotension during HDA, treated them with bicarbonate dialysis (HDB) and found a good tolerance to the treatment without symptomatic hypotension despite the same deprivation of the volume. We examined invasively the parameters of the circulation during HDB and found in all six patients a stability of the circulation due to the significant increase of the TPR. In addition to this we examined in the intraindividual comparison the arterial acid-base-status with simultaneous measurement of blood pressure and heart frequency in the six patients during five treatments each with HDA and HDB. Arterial PCO2, base excess and standard bicarbonate were significantly higher during HBL compared with HDA. On the other hand under HDB we did not find any significant PO2, O2-saturation and pH values lasting during the period of treatment. We concluded that the adequate adaptation of the vascular TPR to the deprivation of the volume during HDB is to be referred to a sufficient correlation of the metabolic acidosis; in particular to the normalisation of the arterial PCO2.

Acetates↗

PubMed1981

Hemodynamics, hypoglycemia, and hepato-pancreatic pathology during the course of endotoxin shock.

The interrelationships between hemodynamics and hypoglycemia during the course of endotoxin shock (ES) has not been fully defined. In the following study, ES (E. coli, 1 mg/kg; n = 7) was induced in a canine model and systemic hemodynamics, glucose metabolism, and hepatic and pancreatic function monitored for 5 hr and compared to time-matched controls (TMC, n = 7). Total peripheral resistance (TPR, dynes-sec-cm-5) increased from 3227 +/- 430 to 4050 +/- 750 at 30 min and then declined to 3050 +/- 1100 at 90 minutes. TPR progressively increased to 6225 +/- 749 by 5 hours. Plasma glucose did not significantly differ from control values (105 +/- 4 mg%) for the first 90 min but then declined to 68 +/- 6 mg% at 4.5 hours. (TMC = 103 +/- 17, P less than 0.05). Serum amylase during the 5 hr protocol was not elevated (TMC = 110.9 +/- 2.4; ES = 100 +/- 1.97%; P greater than 0.1), and light microscopy of the exocrine pancreas demonstrated normal acinar structure. Islet cell structure from the ES group is not significantly different from the TMC. Hepatic histology in the ES group demonstrated periportal and perilobular degranulation and hepatocyte disruption not seen in the TMC. It is hypothesized that ES results in a circle of positive feedback initiated by an increase in TPR and subsequent decrease in flow resulting in hepato-pancreatic ischemia. Ischemic damage is most apparent at the liver and leads to changes in hepatic metabolic activities which contribute to the developing hypoglycemia of the late phase of ES.

Animals↗

PubMed1995

Circadian variation in baroreflex sensitivity evaluated by beat-to-beat hemodynamic change in patients with essential hypertension.

The mechanisms underlying the higher incidence of cardiovascular events in the morning were investigated by studying the circadian variation in hemodynamics and baroreflex sensitivity (BRS) in 20 untreated inpatients with essential hypertension. Direct blood pressure (BP) and heart rate (HR) were recorded using telemetry. Cardiac output (CO) was measured by the dye dilution method. Beat-to-beat stroke volume (SV) and total peripheral vascular resistance (TPR) were obtained using the pulse contour method. The coefficient of regression between HR and systolic BP (SBP) change (delta HR/delta SBP = Ahr) was calculated for in 5 consecutive heart beats during which BP decreased spontaneously and linearly (r > 0.9). Similarly, the delta SV/delta SBP (= Asv) and delta TPR/delta SBP (= Atpr) were also measured, and the negative values of these coefficients (-Ahr, -Asv and -Atpr) were calculated. Comparisons between morning (6-11 a.m.) and evening (4-9 p.m.) values showed no significant difference in mean BP (122 vs 127 mmHg) and HR (72 vs 73 bpm). However, CO (3.7 vs 4.2 l/min), -Ahr (0.28 vs 0.43 bpm/mmHg) and -Asv (-1.5 vs 1.4 ml/mmHg) were lower in the morning than in the evening (p < 0.01). In contrast, TPR (40 vs 34 mmHg/l/min) and -Atpr (1.2 vs -1.4 min/l) were higher in the morning than in the evening (p < 0.01). These findings suggest that lower -Ahr and -Asv and higher TPR and -Atpr may cause stress to the cardiovascular system in the morning in patients with essential hypertension.

Adult↗

PubMed1993

[The use of oral and intravenous isosorbide mononitrate (5-MNi) in the acute phase of myocardial infarction].

OBJECTIVE: To evaluate the hemodynamic effects of 5-IMN in acute myocardial infarct. DESIGN: Open trial. SETTING: Medical ICU at a general hospital. PATIENTS: 19 sequential patients with the diagnosis of AMI and clinical suspicion of pulmonary stasis, with a pulmonary capillary wedge pressure > 12 mmHg and a systolic blood pressure > 90 mmHg. INTERVENTIONS: No vasoactive drugs other than 5-IMN were given during the trial. The following parameters were measured at admission: heart rate (HR), mean blood pressure (BP) (indwelling arterial catheter), right atrial pressure (RAP), pulmonary arterial pressures (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). The cardiac index (CI), systolic index (SI), total peripheral resistances (TPR) and pulmonary vascular resistances (PVP) were calculated. The patients were started on 5-IMN either intravenous or oral accordingly to PCWP. The hemodynamic parameters were registered again at 30 min, 1 hour, 2, 6, 8, 24 and 48 hours and 5-IMN was stopped in all the following conditions: Severe hypoxia not improving with 5-IMN or requiring mechanical ventilation. Systolic blood pressure decreasing below 90 mmHg despite an adequate left ventricular filling pressure. Any other clinical condition forcing the use of other vasoactive drugs. MEASUREMENTS AND RESULTS: We discuss the hemodynamic parameters registered on admission and compare them with those obtained 48 hours after treatment with 5-IMN. The patients were divided in two groups according to PCWP: a group of 11 patients with 12 mmHg < PCWP < or = 18 mmHg who were given oral 5-IMN, and a group of 8 patients with PCWP > 18 mmHg and left ventricular failure, who were given an intravenous perfusion of 5-IMN in a dose that could keep PCWP < or = 18 mmHg. The differences between both groups are discussed. In patients with no left ventricular failure, 5-IMN decreased significantly PCWP and TPR, while increasing CO. In patients with PCWP > 18 mmHg there was also a decrease in PCWP and TPR and significant increases in both cardiac and systolic indexes. The decrease in BP was not significant in both groups. CONCLUSIONS: 5-IMN proved to be a safe drug when used during the first 48 hours of myocardial infarct even in patients with PCWP < or = 18 mmHg. It improved hemodynamics in all patients especially in those with left ventricular failure.

Administration, Oral↗

PubMed1993

Characterization of a c-met proto-oncogene activated in human xeroderma pigmentosum cells after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

Human xeroderma pigmentosum (XP) fibroblasts were transformed with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The transformed cells, called ASKMN, were immortalized, grew in agar and were tumorigenic in nude mice. A trp-met oncogene was identified in ASKMN cells, after transfection of high molecular weight DNA on 3T3 mouse cells. The ASKMN cells and the 3T3 transformants expressed the 5-kb mRNA transcribed by the tpr-met oncogene and its p65tpr-met phosphorylated protein. Using the polymerase chain reaction (PCR) technique followed by hybridization with synthetic probes or direct sequencing, we showed that the sequence encompassing the 'rearranged breakpoint' was the same as that previously described in the tpr-met oncogene present in the MNNG-HOS cells. However, G to A transitions found in the tpr or met sequences of the ASKMN oncogene, probably the result of the specific mutagenic activity of MNNG, were absent in the MNNG-HOS gene. Apparently normal chromosomes 1 and 7 were identified in the ASKMN cell metaphases using several cytogenetic techniques.

Animals↗

PubMed1995

Haemodynamic changes induced by the correction of anaemia by erythropoietin: role of antiplatelet therapy.

BACKGROUND: In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. In order to ascertain the role of antiplatelet drugs in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied. METHODS: The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 patients). Cardiac index (CI) by echo-Doppler, total peripheral resistance (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo therapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialysis who had never received rHuEpo therapy served as the control group. RESULTS: One patient in the group without antiplatelet drugs discontinued the study due to the development of severe hypertension after 12 weeks on rHuEpo therapy. There were no significant differences in the haemodynamic parameters at baseline. At 10 weeks, MAP was higher in patients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg respectively, P = 0.0047), TPR was also higher in patients without antiplatelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm-5m2 respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was still higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (112.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respectively, P = 0.075), but at this stage TPR and Cl did not differ among the three groups. CONCLUSIONS: These data reinforce the previous observation that antiplatelet therapy may prevent the development of rHuEpo-induced hypertension.

Adult↗

PubMed1995

Cardiovascular effects of centrally administered endothelin-1 in rats.

The effect of centrally administered endothelin-1 (ET-1) or IRL 1620 (5, 15, and 45 ng) on systemic hemodynamics was studied in anesthetized rats using a radioactive microsphere technique. Administration of saline (5 microliters, i.c.v.) did not product any significant cardiovascular effects. The lower doses of ET-1 (5 and 15 ng) did not produce any significant effect on blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), and total peripheral resistance (TPR). However, the highest dose (45 ng) produced a transient rise followed by a sustained fall in BP. The CO and SV decreased significantly, whereas HR and TPR were not affected. Pretreatment with BQ-123 (10 micrograms, i.c.v.) 15 min before administration of ET-1, completely antagonized the systemic hemodynamic effects of ET-1. Centrally administered IRL 1620, a specific ETB receptor agonist, did not produce any effect on BP, HR, CO, SV, and TPR in rats. It is concluded that ETA but not ETB receptors are involved in the central cardiovascular actions of ET.

Amino Acid Sequence↗

PubMed1977

[Effect of the angiotensin antagonist saralasin on blood pressure and hemodynamics in patients with terminal renal insufficiency].

The angiotensin antagonist saralasin was infused both before and 10 hrs after dialysis in 10 hypertensive and 4 normotensive patients hemodialyzed for terminal renal failure. A significant increase in mean arterial pressure (MAP) and total peripheral resistance (TPR) without change in cardiac output measured by impedance cardiography were observed during the first few minutes of saralasin infusion. MAP and TPR decreased during the second half of the infusion in 4 hypertensive patients and remained at the preinfusion levels in 6 hypertensive and 4 normotensive patients. Plasma renin activity (PRA) was significantly higher in patients in whom MAP fell both before and after hemodialysis. There was a significant correlation between PRA before saralasin and the fall in MAP and TPR. The fall in MAP in 4 of 10 hypertensive patients demonstrates that inappropriately high renin and angiotensin levels are involved in the pathogenesis of hypertension in some patients with terminal renal failure. Volume factors are probably of primary importance in the other patients.

Adult↗

PubMed1996

Comparative cardiopulmonary effects of intramuscularly administered etorphine and carfentanil in goats.

OBJECTIVE: To determine comparative cardiopulmonary effects of IM administered etorphine and carfentanil in goats. ANIMALS: Seven clinically normal adult female goats. DESIGN: Each goat received at least 9 drug treatments (etorphine HCl, 5 [twice], 10, 20, and 40 and carfentanil citrate, 5, 10, 20 and 40 micrograms/kg of body weight), with a minimal 2-day interval between trials. Although drug dosages were randomized, etorphine and carfentanil treatments were alternated. To assess for drug tolerance, the first and last treatments always were etorphine (5 micrograms/kg). PROCEDURE: All goats were instrumented for long-term cardiopulmonary variable data collection. RESULTS: Both drugs induced rapid catatonic immobilization, characterized by limb and neck hyperextension, with occasional vocalization and bruxation. Etorphine elicited transient violent struggling and vocalization immediately. Time to immobilization appeared dose-dependent, and was more rapid with carfentanil (< or = 5 minutes) than etorphine (5 to 10 minutes) at all dosages. Recovery to standing occurred earlier for etorphine (1 to 2 hours) than carfentanil (> 2 hours) at all dosages. Both drugs at all dosages significantly (P < or = 0.05) increased systemic and left ventricular (LV) end-diastolic pressures, LV peak negative dP/dt, total peripheral resistance (TPR), hemoglobin concentration, and left atrial (LA) and pulmonary O2 contents. They also significantly decreased heart and respiration rates, and TPR. A significant increase was observed at some dosages for LV stroke volume and index, LV peak positive dP/dt, mean pulmonary artery pressure, PaO2, pulmonary artery oxygen partial pressure, PaCO2, pulmonary mixed venous carbon dioxide partial pressure, LA hemoglobin saturation, LA transport index, and body temperature. Pulmonary and systemic mixed venous carbon dioxide and oxygen contents were significantly decreased at some dosages. CONCLUSIONS: Intramuscularly administered etorphine and carfentanil induce hypertension, bradycardia, and bradypnea in goats. The hypertension appears attributable to an increase in TPR. CLINICAL RELEVANCE: Although the cardiopulmonary effects of carfentanil occurred more rapidly, these effects were similar in magnitude for etorphine and carfentanil over the evaluated dosage range.

Analgesics↗

PubMed1996

Differential systemic and pulmonary hemodynamic effects of L-arginine in patients with coronary artery disease or primary pulmonary hypertension.

The endothelial EDRF/NO-mediated relaxing mechanism is impaired in atherosclerotic and in hypertensive arteries. Recently, it was suggested that primary pulmonary hypertension might be another disease in which the endothelial EDRF/NO pathway is disturbed. We tested the hypothesis that intravenous administration of L-arginine (L-ARG), the physiological precursor of EDRF/NO, stimulates the production of NO, subsequently increasing plasma cGMP levels and reducing systemic and/or pulmonary blood pressure, in patients with coronary artery disease (CAD, n = 16) or with primary pulmonary hypertension (PPH, n = 5). L-ARG (30 g, 150 ml, 15 min) or placebo (150 ml NaCl) was infused in CAD patients, and L-ARG was infused in PPH patients during cardiac catheterization. Mean aortic (Pao) and pulmonary (PAPmean) arterial pressures were continuously monitored. Cardiac output (CO, by thermodilution), total peripheral resistance (TPR), and pulmonary vascular resistance (PVR) were measured before and during the infusions. In CAD patients Pao decreased from 87.2 +/- 4.9 to 81.8 +/- 5.1 mmHg during L-ARG (p < 0.05), whereas PAPmean and PVR were unchanged. TPR decreased from 1008.9 +/- 87.9 to 845.0 +/- 81.7 dyne x sec x cm-5 during L-ARG administration (p < 0.01). CO significantly increased during L-ARG (from 7.3 +/- 2.8 to 8.1 +/- 0.9 l/min, p < 0.05). Placebo did not significantly influence any of the hemodynamic parameters. Plasma cGMP (determined by RIA) slightly increased by 12.2 +/- 9.6% during L-ARG, but slightly decreased during placebo (-12.3 +/- 9.2%) (p < 0.05 for L-ARG vs. placebo). In PPH patients, L-ARG induced no significant change in Pao, TPR, and CO, PAPmean was 59.4 +/- 8.5 mmHg at the beginning of the study and was not significantly reduced by L-ARG nor was PVR (basal: 1042.4 +/- 211.4 dyne x sec x cm-5) changed by L-ARG. Plasma cGMP was not significantly affected by L-ARG in these patients. We conclude that L-ARG stimulates NO production and induces vasorelaxation in CAD patients but not in patients with primary pulmonary hypertension.

Adult↗

PubMed1997

Altered endometrial progesterone/oestrogen receptor ratio in luteal phase defect.

The total oestrogen and progesterone receptor levels (TER, TPR) were measured in endometrial biopsy samples of 10 infertile patients with luteal phase defect (LPD) and compared to those of controls. Serum levels of progesterone (P), obtained in the luteal phase, were also measured. Midluteal phase P values were significantly decreased in LPD cycles; however some overlap of values existed. LPD cycles had significantly lower endometrial TER and TPR concentrations than did control cycles. TPR/TER ratio was found to be a reliable test for diagnosis; having a sensitivity, and specificity of 90% and the odds ratio of 81. The TPR/TER ratio for inphase endometria ranged between 1.13 and 58.22, with 95% confidence. It seems that abnormal folliculogenesis, as a cause of LPD, results in wide ranges of endometrial TER and TPR concentrations, yet with well defined alteration in TPR/TER ratio. Summation of the results of the present study along with those previously reported, indicates that TPR/TER ratio may be of great value in characterisation of a well defined endometrial receptor imbalance in luteal phase defect, whatever the underlying aetiology.

Adult↗