A review of daycase GA services for Special Care patients at University Hospital, Bristol.

This paper describes and discusses a review of adult special care dentistry day cases in a UK hospital over a two year period and makes recommendations for other such reviews and for practice. Dental public health competencies illustrated: oral health needs assessment and evaluation of dental health services.

Association of B lymphocyte antigen receptor polypeptides with multiple chaperone proteins.

The B cell antigen receptor (BCR) is comprised of four different polypeptides, immunoglobulin (Ig) heavy chain, Ig light chain, and the two signaling subunits of this receptor, Ig-alpha and Ig-beta. These four chains must assemble correctly in the endoplasmic reticulum (ER) before the BCR can be transported to the cell surface. The roles of the different chaperone proteins in mediating the assembly of mIg with the Ig-alpha/beta are not fully understood. To gain insights into the roles of chaperone proteins in BCR assembly, we have generated transfected non-lymphoid cell lines that express various intermediate assembled forms of the BCR and used them to examine the interactions of chaperone proteins with subunits of the BCR. We examined the interactions of BiP (GRP78), GRP94 and calnexin with the mu heavy chain, lambda light chain, Ig-alpha and Ig-beta. We report for the first time that Ig-alpha associates with GRP94 and that this interaction increases dramatically when other BCR chains are co-expressed. In contrast, the mu heavy chain interacts strongly with BiP (GRP78) when expressed by itself but this interaction is reduced when the lambda light chain is expressed, with the resulting mu(lambda) complexes interacting with GRP94 and calnexin. Thus, our data are consistent with the idea that there is an ordered association of BCR components with different protein chaperones during BCR assembly.

Coffee and coronary heart disease.

BACKGROUND: The role of coffee consumption in the onset of myocardial infarction remains uncertain. A review of published reports showed that although cohort data suggest very little excess risk of coronary heart disease among habitual coffee drinkers, case-control data suggest an excess risk of the order of 60% for people drinking five or more cups per day. METHODS: We obtained as much information as possible on the lifestyle and habits, including coffee consumption, of people admitted with chest pain to the Coronary Care Unit at the Royal Perth Hospital, Australia. A questionnaire was given to them by the attending nursing staff. Details were recorded by the patient, often with help from the nursing staff. A similar questionnaire was completed by patients attending the Cardiology Outpatient Clinic. RESULTS: One of the outstanding differences between the 182 patients with myocardial infarction or unstable angina and 185 patients with chronic stable coronary heart disease who filled in forms while waiting in the Cardiology Outpatient Clinic was that more people with acute coronary syndromes were drinking in excess of five cups of coffee per day (18 vs 7.5%; P = 0.003). In logistic regression analysis adjusted for age, smoking status (past and current), hypertension, dyslipidaemia and diabetes, the odds ratio was 2.51 (95% CI 1.43,4.43; P = 0.021). CONCLUSION: The present case-control study provides evidence for an increased risk of myocardial infarction or unstable angina among individuals drinking more than five cups of coffee per day.

Men's experiences of their partner's primary and recurrent breast cancer.

The reaction and support from the partner of the woman with breast cancer is viewed by health professionals as an important factor in her adjustment to disease. However, there is little theory and research that focuses on the individual concerns and experiences of the man living with a woman who has breast cancer. Literature concerning the experience of breast cancer recurrence for both the partner and the patient is particularly sparse. The aim of this literature review is to explore the experiences of male partners of women with breast cancer. The role of the male partner supporting the woman with breast cancer, and the potential concerns he may have, will be explored. It will also focus on the partners' experience of living with a woman with primary breast cancer. Finally, the partners' experience of living with a woman with a recurrence of metastatic breast cancer will be considered. Relevant literature is reviewed and critiqued to place current knowledge in context, including identifying areas for further research.

Hypereosinophilic syndrome with Hodgkin's-like lymphoma in a ferret.

Hodgkin's-like lymphoma involving the lung, mediastinum, liver, kidneys and mesenteric lymph nodes was diagnosed in a ferret. The diagnosis was based on the presence of an admixture of CD3+ small lymphocytes with smaller numbers of macrophages, eosinophils, and large, pleomorphic, frequently multinucleated, Reed-Sternberg-like cells which were immunoreactive to BLA.36 monoclonal antibody. In addition, the liver, pancreas, small intestine and lungs were infiltrated with moderate to large numbers of eosinophils, forming eosinophilic granulomas with occasional deposition of Splendore-Hoeppli material, supporting a diagnosis of hypereosinophilic syndrome. The concurrent diagnosis of hypereosinophilic syndrome and Hodgkin's-like lymphoma in this ferret provides further support to the concept that, in animals, multisystemic eosinophilic infiltrates may be caused by the abnormal proliferation of T lymphocytes, as has been demonstrated in man.

Hemodynamic comparison of dopexamine and nitroprusside at high and low doses in patients with coronary artery disease and impaired left ventricular function.

Pure vasodilator drugs are currently the preferred agents for treatment of acute and chronic heart failure of all grades of severity. In contrast, the role of drugs that combine vasodilation with inotropic action remains highly controversial despite their several advantageous physiological actions and long therapeutic history in heart failure. We hypothesize that this uncertainty might be due first to subtle unfavorable hemodynamic effects not detectable by the relatively crude hemodynamic methods by which these agents are usually analyzed, particularly with regard to the quantification of afterload, and secondly to the narrow therapeutic range of these drugs, such that the dose administered is critical. We tested this hypothesis by comparing several refined hemodynamic measurements of dopexamine, an inotropic vasodilator, with a pure arteriovenous dilator (sodium nitroprusside, SNP) on left ventricular (LV) systolic and diastolic function, large arterial behavior, and coupling of the left ventricle to the arterial system at two dose levels in 35 patients with ischemic heart disease. The study protocol was a fixed order of 15-min infusions of saline, dopexamine 1 microg/kg/min, and dopexamine 3 + ++microg/kg/min, or saline, SNP 1 microg/kg/min, and SNP 3 microg/kg/min. Detailed hemodynamic observations were made at the end of each 15-min infusion period. Both drugs produced equivalent arterial vasodilation, as measured by the decrease in systemic vascular resistance index (SVRI), but dopexamine resulted in a significantly greater increase in cardiac index (CI). Myocardial contractility, assessed by several load-independent indexes, increased with dopexamine, as anticipated with an inotropic drug, but did not alter with SNP. Arterial compliance, a measure of the distensibility of large conduit arteries, was increased by SNP but not by dopexamine. Arterial wave reflection was increased by dopexamine, especially at high doses, but reduced by SNP. Increased arterial compliance and reduced wave reflection reduce LV afterload. SNP reduced preload, whereas dopexamine had no effect on this aspect of ventricular function. Vasodilator drugs and those which combine vasodilator and inotropy increase cardiac output (CO) and reduce SVR. Therapy with inotropic vasodilators has no effect on preload and does not reduce the dynamic components of ventricular afterload, although it does reduce its static components. These effects are dose dependent; there is less perturbation of afterload at lower doses. In contrast, vasodilator therapy reduces preload and both static and dynamic parts of afterload.

Signal transduction by the B-cell antigen receptor.

The antigen receptor of B lymphocytes (BCR) plays important roles in recognition of foreign antigens and self-components to allow the immune system to make appropriate antibody responses. The BCR is a complex between membrane immunoglobulin and the Ig-alpha and Ig-beta heterodimer. Site-directed mutagenesis experiments have shown that the mu heavy chain transmembrane domain plays a key role in the association of mIgM with Ig-alpha/Ig-beta. In the absence of complex formation, mIgM is retained in the endoplasmic reticulum, and this function is also specified by the mu chain transmembrane domain. The ability of various mutant mIgM molecules to associate with Ig-alpha/Ig-beta correlates well with their ability to induce signal transduction reactions such as protein tyrosine phosphorylation and phosphoinositide breakdown. Thus, the signaling ability of the BCR appears to reside in the Ig-alpha/Ig-beta heterodimer. The cytoplasmic domains of Ig-alpha and Ig-beta each contain an ITAM sequence, which is defined by its limited homology with subunits of the T-cell antigen receptor and of Fc receptors. Moreover, chimeric proteins containing these ITAMs and surrounding sequences from the cytoplasmic domains of Ig-alpha or Ig-beta exhibit signaling function characteristics of the intact BCR. The Ig-alpha and Ig-beta chimeras are each capable of inducing all of the BCR signaling events tested and thus represent redundant functions. Cross-linking these chimeras leads to their phosphorylation and to binding of the intracellular tyrosine kinases Lyn and Syk. The BCR expressed in the nonlymphoid AtT20 cells, which express the Src-family tyrosine kinase Fyn but not Syk, was not able to trigger vigorous signaling reactions. Introduction of the active form of Syk into these cells restored some signaling events. These results are consistent with a model in which the ITAMs act to initiate the BCR signaling reactions by binding and activating tyrosine kinases.

Neurohormonal changes after acute myocardial infarction. Relationships with haemodynamic indices and effects of ACE inhibition.

To determine the neurohormonal response to angiotensin-converting enzyme (ACE) inhibition after acute myocardial infarction, 36 patients presenting within 6 h of the onset of chest pain were studied in a single regional cardiology service. In this double-blind study, 13 patients were randomized to receive captopril, 12 patients received enalapril, and 11 patients received placebo, for 12 months. In patients receiving placebo, acute myocardial infarction was associated with activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, and stimulation of plasma brain natriuretic peptide and atrial natriuretic peptide levels. ACE inhibition did not significantly alter circulating levels of norepinephrine, brain natriuretic peptide or atrial natriuretic peptide. Compared with placebo, enalapril induced a steep decline in plasma ACE activity, and plasma angiotensin II levels were reduced by both ACE inhibitors. Using grouped data, circulating levels of brain natriuretic peptide at the zero sampling time were significantly higher than atrial natriuretic peptide values. Brain natriuretic peptide levels at 72 h were significantly correlated with the radionuclide left ventricular ejection fraction measured 5 days and 3 months after infarction. Similar associations were observed for atrial natriuretic peptide and norepinephrine. We confirm activation of the renin-angiotensin-aldosterone and sympathetic nervous systems after acute myocardial infarction. The atrial natriuretic peptide and brain natriuretic peptide and sympathetic nervous system responses to acute myocardial infarction were not significantly modified by ACE inhibition. Brain natriuretic peptide and atrial natriuretic peptide levels were significantly correlated with the left ventricular ejection fraction measured 5 days and again 3 months after myocardial infarction, and may prove a useful prognostic index.

Comparison of enalapril versus captopril on left ventricular function and survival three months after acute myocardial infarction (the "PRACTICAL" study).

Left ventricular (LV) function and survival can be improved with captopril when initiated later than 24 hours after acute myocardial infarction. Animal studies suggest additional benefits may be obtained with earlier initiation of angiotensin-converting enzyme (ACE) inhibitors. The effects on LV function of captopril and enalapril initiated within 24 hours of myocardial infarction were studied. Two hundred twenty-five patients with acute myocardial infarction were enrolled within 24 hours of the onset of chest pain. They were randomized to receive either captopril 25 mg three times daily, enalapril 5 mg three times daily, or placebo. LV ejection fraction (EF) and volumes were measured by radionuclide ventriculography at baseline during treatment and at 3 months after a 3-day withdrawal from therapy. The ACE inhibitor group had a significant increase in EF (45 +/- 1 to 47 +/- 1%; p = 0.005) and significantly attenuated LV dilatation compared with results in the placebo group (175 +/- 6 to 189 +/- 7 ml in the placebo group vs 168 +/- 4 to 172 +/- 4 ml in the ACE inhibitor group; p = 0.051 for LV end-diastolic volume; and 99 +/- 6 to 108 +/- 7 ml in the placebo group vs 94 +/- 3 to 94 +/- 4 ml; p = 0.026 for LV end-systolic volume). The beneficial effects of ACE inhibitor therapy on LV function were observed irrespective of the degree of initial LV dysfunction and were comparable in both the captopril and enalapril groups.(ABSTRACT TRUNCATED AT 250 WORDS)

A mutation of the mu transmembrane that disrupts endoplasmic reticulum retention. Effects on association with accessory proteins and signal transduction.

The mu heavy chain has an unusually high content of hydroxyl-containing amino acids in its membrane-spanning region. We have examined the involvement of two of these hydrophilic residues in endoplasmic reticulum (ER) retention, interactions with Ig-alpha/Ig-beta, and transmembrane signaling. Neighboring tyrosine and serine residues were mutated to either phenylalanine and alanine (mutant YS/FA) or valine and valine (mutant YS/VV). Membrane Ig (mIgM) molecules containing these mutant mu chains were expressed on the surface of transfected B lymphoma cells. Anti-Ig-induced signaling by the YS/FA mutant mIgM was equivalent to wild-type (wt) mIgM, whereas signaling by the YS/VV mutant mIgM was notably diminished. Association between mutant YS/VV mIgM and Ig-alpha/Ig-beta was detectable but reduced in comparison to YS/FA or wt mIgM. Signaling by YS/VV mutant mIgM appeared to involve Ig-alpha/Ig-beta, because these proteins were tyrosine phosphorylated on receptor cross-linking. When YS/VV and wt mu chains were cotransfected with light chains into nonlymphoid cells, mutant mIgM was expressed at the cell surface in the absence of Ig-alpha/Ig-beta, whereas wt mIgM was not. These data suggest that the mutated residues contribute to ER retention and directly or indirectly to association with Ig-alpha/Ig-beta. Moreover, ER retention can be disrupted without preventing functional association with Ig-alpha/Ig-beta. In addition, these data indicate that the hydroxyl groups of the mutated residues are not required for functional association between mu and Ig-alpha/Ig-beta because their removal did not reduce the ability of the YS/FA mutant mIgM to associate with accessory proteins or to participate in signal transduction.

Plasma corticotrophin releasing hormone, vasopressin, ACTH and cortisol responses to acute myocardial infarction.

OBJECTIVES: We assessed the magnitude and duration of the response of hypothalamic-pituitary-adrenal hormones to the stress of myocardial infarction, in the presence and absence of angiotensin converting enzyme inhibitors. In particular, we wished to analyse the interrelationships between peripheral plasma levels of corticotrophin releasing hormone (CRH), vasopressin (AVP) and adrenocorticotrophin (ACTH), and also between ACTH and cortisol, during a prolonged medical stress. DESIGN: All hormones were measured within 6 hours of the onset of an acute myocardial infarction. Patients were randomly allocated to three different study groups according to a double blind procedure. PATIENTS: Group 1 (10 patients) received placebo treatment, Group 2 (13 patients) received a maintenance dose of captopril 25 mg three times daily, Group 3 (11 patients) received enalapril 5 mg three times daily. MEASUREMENTS: Peptide hormones were measured by radioimmunoassay, and cortisol by ELISA. Reference ranges for all hormones were obtained from 40 or more volunteers from the electoral roll. RESULTS: At the start of the study, mean +/- SEM plasma AVP (27.9 +/- 4.6 pmol/l) was significantly (P < 0.001) raised above the mean for the reference range (1.82 +/- 0.09 pmol/l), and 12 patients had values > 50 pmol/l. Mean plasma cortisol (960 +/- 89.6 nmol/l) was also raised above the reference range mean (554 +/- 28 nmol/l, P < 0.001), as was mean plasma CRH (4.97 +/- 0.5 pmol/l, reference mean 1.52 +/- 0.09 pmol/l, P < 0.001). By contrast, mean ACTH (3.88 +/- 0.66 pmol/l) was significantly less than the reference mean (10.7 +/- 0.7 pmol/l, P < 0.001). During the 72-hour observation period there was a highly significant fall (P < 0.001) in plasma CRH, AVP and cortisol. By contrast, plasma ACTH rose, and the change with time of ACTH was significantly different from the fall in plasma CRH, AVP or cortisol (P < 0.001 for each comparison). No significant differences in plasma CRH, AVP, ACTH or cortisol responses to placebo, captopril or enalapril were observed. CONCLUSIONS: Within 6 hours of a myocardial infarction, mean plasma CRH, AVP and cortisol values were very significantly raised above mean control values, while ACTH was very significantly reduced. During the 3 days following an acute myocardial infarction, plasma CRH, AVP and cortisol fell substantially, and this pattern was not influenced by angiotensin converting enzyme inhibitors. By contrast, plasma ACTH showed a significant increase with time. This suggests that the usual relationships between CRH, AVP and ACTH, and between ACTH and cortisol are disturbed in patients admitted to hospital with myocardial infarction. Maximum levels of AVP observed in 12 patients exceeded 50 pmol/l, which may be sufficiently high to interfere with tissue perfusion. It is postulated that V1 AVP receptor antagonists may have a therapeutic application in limiting infarct size.

Angiotensin converting enzyme inhibition in chronic stable angina: effects on myocardial ischaemia and comparison with nifedipine.

OBJECTIVES: To determine the anti-ischaemic effects of a new angiotensin converting enzyme inhibitor, benazepril, compared with nifedipine, alone and in combination, in chronic stable angina caused by coronary artery disease. DESIGN: Placebo controlled, double blind, latin square design. SETTING: Regional cardiology service for a mixed urban and rural population. SUBJECTS: 40 patients with stable exertional angina producing at least 1 mm ST segment depression on exercise test with the Bruce protocol. 34 patients completed all four phases of the trial. INTERVENTIONS: Each patient was treated with placebo, benazepril (10 mg twice daily), nifedipine retard (20 mg twice daily), and a combination of benazepril and nifedipine in the same doses, in random order for periods of two weeks. MAIN OUTCOME MEASURES AND RESULTS: Total duration of exercise was not increased by any treatment. Exercise time to the development of 1 mm ST segment depression was not significantly changed with benazepril alone or in combination with nifedipine but was increased with nifedipine from 4.18 (1.8) min to 4.99 (1.6) min (95% confidence interval (95% CI) 0.28 to 1.34; p < 0.05). There was a significant relation between increase in duration of exercise and resting renin concentration (r = 0.498; p < 0.01). Myocardial ischaemia during daily activity, as assessed by ambulatory electrocardiographic monitoring, was reduced by benazepril and by the benazepril and nifedipine combination. This was significant for total ischaemic burden (451(628) min v 231(408) min; 95% CI -398 to -41 min; p < 0.05) and maximal depth of ST segment depression (-2.47(1.2) mm v -2.16 mm; 95% CI 0.04 to 0.57; p < 0.05) for the combination and for maximal ST segment depth for benazepril monotherapy (-2.47 (1.2) mm v -1.96(1.2) mm; 95% CI 0.18 to 0.91; p < 0.05). Benazepril significantly altered the circadian rhythm of cardiac ischaemia, abolishing the peak ischaemic periods at 0700 to 1200 and 1700 to 2300 (p < 0.05). CONCLUSIONS: Benazepril, an angiotensin converting enzyme inhibitor, had a modest anti-ischaemic effect in effort angina, but this effect was not as pronounced as with nifedipine. The anti-ischaemic action was more noticeable in asymptomatic ischaemia during daily activity, whereas nifedipine had little effect on this aspect of myocardial ischaemia. The combination of benazepril and nifedipine reduced ischaemia of daily activity.

Mechanism of B cell antigen receptor function: transmembrane signaling and triggering of apoptosis.

The antigen receptor of B lymphocytes (BCR) plays important roles in virtually every stage in the development, inactivation, or activation of B cells. The BCR is a complex of membrane immunoglobulin (mIg) and a heterodimer of two transmembrane polypeptides called Ig-alpha and Ig-beta. Site directed mutation of the mu immunoglobulin heavy chain has demonstrated that the mu transmembrane domain plays a key role in the assembly of mIgM with Ig-alpha/Ig-beta. In addition, there is a strong correlation between the ability of various mutant mIgM molecules to associate with Ig-alpha/Ig-beta and their ability to induce signal transduction reactions such as protein tyrosine phosphorylation and phosphoinositide breakdown. The cytoplasmic domains of Ig-alpha and Ig-beta share a region of limited homology with each other and with components of the T cell antigen receptor and of the Fc receptor. The presence of regions of the cytoplasmic domains of Ig-alpha or Ig-beta including this conserved amino acid sequence motif is sufficient to confer signaling function on chimeric transmembrane proteins. Both Ig-alpha and Ig-beta chimeras are capable of inducing all of the BCR signaling events tested. Based on these and related observations, we propose that the motifs act to initiate the BCR signaling reactions by binding and activating tyrosine kinases. Among the important events mediated by BCR signaling is induced expression of a series of genes referred to as early response genes. In B cells these include transcription factors and at least one component that regulates signaling events. One of these genes, c-myc, appears to play an important role in mediating apoptosis in B cells stimulated via the BCR complex.

Electrophysiological effects of atrial natriuretic peptide on the cardiac conduction system in man.

We assessed the effect of atrial natriuretic peptide (ANP) on electrophysiological parameters in man. Electrophysiological parameters were measured before, at 15, and at 30 minutes after the commencement of ANP or placebo infusions (six patients in each group). ANP levels were normal prior to infusion and rose with ANP to 159 +/- 43 pmol/L, but were stable during placebo infusion. No change in heart rate or blood pressure occurred in either group. ANP infusion resulted in significant falls in intraatrial conduction time (60 +/- 15 to 49 +/- 15 msec), PR interval (170 +/- 21 to 155 +/- 16 msec), right atrial effective refractory period (232 +/- 33 to 218 +/- 33 msec), and ventriculoatrial refractory period (452 +/- 148 to 393 +/- 183 msec) while no change was seen with placebo. We conclude that ANP infusion appears to affect atrial refractoriness and velocity of conduction and atrioventricular nodal refractoriness. However, the mechanism of action and clinical significance of this observation remain to be determined.

Twenty-four hour profile of the anti-hypertensive action of isradipine in essential hypertension.

Isradipine, 2.5 mg twice daily and placebo were administered for 4 weeks to 11 untreated essential hypertensives in a double-blind, random order, crossover study. At the end of each phase patients were assessed by 36 h of continuous intra-arterial blood pressure monitoring, surface electrocardiography, and measurement of endogenous creatinine clearance, serum biochemistry and plasma renin activity. Arterial pressure was significantly reduced by isradipine, with mean reduction in systolic blood pressure of 11.0 mmHg and diastolic pressure of 13.2 mmHg over 24 h. There was no significant change in heart rate, endogenous creatinine clearance, serum biochemistry or plasma renin activity.

Tissue plasminogen activator using a rapid-infusion low-dose regimen for unstable angina.

The clinical effect of a low-dose rapid-infusion intravenous regimen was assessed using human recombinant tissue-type plasminogen activator (rt-PA) in unstable angina. Fifty patients with unstable angina pectoris were randomly assigned to blinded treatment with either placebo (24 patients) or low-dose (20 mg bolus, 30 mg infusion over 1 hour) intravenous rt-PA (26 patients). Before randomization, all patients were treated with aspirin, twice-daily subcutaneous heparin, and maximally tolerated antianginal therapy. Of the 50 patients assigned, 26 received rt-PA and the outcome was successful in 15 (58%) (angina settled, no myocardial infarction or urgent intervention) compared with 9 (38%) successful outcomes in the 24 who received placebo (0.5 greater than p greater than 0.1). Angina remained refractory in 8 (31%) of the rt-PA group and in 13 (54%) of the placebo group (0.1 greater than p greater than 0.05). Urgent interventions were required in 6 patients (23%) who received rt-PA and in 11 patients (46%) who received placebo. Three patients in each group sustained a myocardial infarction within 72 hours of entering the trial and there were 3 deaths (1 in the active treatment group, 2 in placebo group) within 2 weeks of the trial (p = not significant). Administration of intravenous rt-PA was not associated with any complications. Low-dose rt-PA administration in patients with unstable angina was associated with a tendency to stabilization of anginal symptoms and a reduction in the need for urgent intervention. However, these trends did not achieve statistical significance.

Acute haemodynamic effects of dopexamine in patients with coronary arterial disease.

We assessed the acute haemodynamic effects of dopexamine 1 microgram/kg/min and 3 micrograms/kg/min in 21 patients with coronary arterial disease following routine catheterisation. Patients were aged 38 to 72 years and left ventricular ejection fraction ranged from 23 to 79%. Dopexamine was well tolerated in all patients except one in whom transient ventricular arrhythmias occurred with 3 micrograms/kg/min. No patient developed angina. Dopexamine increased cardiac index (2.6 +/- 0.4 to 3.2 +/- 0.1 (P less than 0.001) and 4.0 +/- 1.0 1/min/m2 (P less than 0.001), control to 1 microgram/kg/min and 3 micrograms/kg/min, respectively) and decreased systemic vascular resistance index (3356 +/- 1506 to 2318 +/- 809 (P less than 0.001) and 2252 +/- 1973 dyne.sec.cm-5/m2 (P less than 0.001], but did not affect systemic arterial, pulmonary arterial or right atrial pressure. Maximum positive dP/dt was increased (1294 +/- 324 to 1597 +/- 505 (P less than 0.001) and 2199 +/- 819 mmHg/sec (P less than 0.001] as was left ventricular stroke work index (44 +/- 20 to 51 +/- 21 (P less than 0.05) and 56 +/- 27 g.m/m2 (P less than 0.001) control to 1 microgram/kg/min and 3 micrograms/kg/min, respectively). Left ventricular end diastolic pressure fell with 3 micrograms/kg/min from 19.8 +/- 6.9 to 12.4 +/- 4.6 mmHg (P less than 0.05) in patients with preserved left ventricular ejection fraction (greater than 50%, n = 6), but not in those with impaired left ventricular ejection fraction (less than 50%, n = 15), otherwise the effects in these two subgroups were similar. We conclude that dopexamine has both inotropic and vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)