Redistribution of peripheral blood flow during acute left ventricular failure in the dog.

Acute left ventricular failure was induced in anaesthetized dogs by repeated embolization of the left coronary artery with 57 micron microspheres. Tissue blood flow was measured with isotope-labelled microspheres in two stages of heart failure. With increasing doses of embolizing solution there was a progressive decline in systemic blood pressure and cardiac output.

Difference between beta-1-selective and non-selective beta-blockade during continuous and intermittent exercise.

Limiting factors of maximal exercise performance are not clearly defined. In order to differentiate between various factors, maximal exercise was studied during continuous (n = 12) and intermittent (n = 9) exercise. The non-selective beta-blocker timolol (10 mg b.

Tolerability of enalapril in congestive heart failure.

In a double-blind, randomized trial, 253 patients with heart failure (New York Heart Association functional class IV) received either enalapril (n = 127) or placebo (n = 126) in addition to their conventional therapeutic regimens (digitalis, diuretics and vasodilators other than angiotensin-converting enzyme inhibitors). Enalapril was administered in a dose of 2.5 to 40 mg/day.

Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

To evaluate the influence of the angiotensin-converting enzyme inhibitor, enalapril (2.5 to 40 mg/day), on the prognosis of severe congestive heart failure, defined as New York Heart Association functional class IV, a double-blind study was undertaken in which 253 patients were randomized to receive either placebo (n = 126) or enalapril (n = 127) in addition to conventional treatment, including vasodilators. Follow-up averaged 188 days (range 1 day to 20 months).

According to MIAMI and ISIS-I trials, can a general recommendation be given for beta blockers in acute myocardial infarction?

The goal of early intervention of acute coronary occlusion by beta blockers is to reduce ultimate infarct size and to consequently reduce morbidity and mortality. Until 1986 small early intervention trials suggested that infarct size may be reduced by 25% if treatment was started within 6 to 10 hours after the onset of symptoms. At this time, an average of 80% of the infarct is fully developed.

The effects of naloxone and timolol on plasma catecholamine levels during short-term dynamic exercise.

In order to study the role of opioid- and betareceptors on exercise-induced catecholamine responses, the effects of acute intravenous administration of 1 and 4 mg naloxone and of the non-selective betablocker timolol 2 mg of on circulating concentrations of adrenalin, noradrenaline and dopamine during exercise to exhaustion were examined in eight normal, healthy young men, using a double-blind, randomized, placebo-controlled design. During maximal exercise, adrenalin levels increased from 71 +/- 17 to 821 +/- 235 pg/ml (p less than 0.05), noradrenaline from 355 +/- 58 to 4235 +/- 1031 pg/ml (p less than 0.

Quantitative and temporal relation between the release of myoglobin and creatine kinase and the evolution of vectorcardiographic changes during acute myocardial infarction in man.

The relation in time and magnitude between QRS vector changes (QRS-VD), ST vectors (ST-VM), and the cumulated release of myoglobin, total creatine kinase, and creatine kinase isoenzyme MB was studied. Seventy four patients with a first myocardial infarction and a history of symptoms of up to 5 h were included. Blood samples for enzyme analysis were taken every 4-6 h for 72 h and cumulated enzyme release was calculated from a monocompartmental first order model.

Temporal pattern of enzyme changes in cerebrospinal fluid in patients with neurologic complications after open heart surgery.

We serially measured creatine kinase (CK), lactate dehydrogenase, aspartate aminotransferase (AST) and lactate from the lumbar cerebrospinal fluid in 14 patients with neurologic complications after open heart surgery with cardiopulmonary bypass (CPB). These analyses revealed a correlation between worsening neurologic deficit and the peak CK (r = .87, p less than .

Haemodynamics during repeated exercise tests with special reference to the 'warm-up' phenomenon in patients with angina pectoris.

The haemodynamic effect of two successive supine exercise tests 20 min apart was examined in 12 patients with angina pectoris. All the patients had coronary artery disease verified by angiography and were accepted for coronary bypass surgery. They exercised 20-40 W and all of them had angina during the first exercise test.

Fever after acute myocardial infarction in patients treated with intravenous timolol or placebo.

Body temperature was studied in 65 patients admitted to hospital within four hours of the onset of symptoms of acute myocardial infarction. Thirty three patients had been randomly assigned to intravenous timolol treatment and 32 to placebo treatment. Infarct evolution was assessed by continuous vectorcardiography and creatine kinase release.

Nitrates in acute myocardial infarction.

Nitrates relieve symptoms and improve left ventricular haemodynamics during acute myocardial ischaemia. The ability to increase cardiac output appears to be greatest in those patients with the most severe left ventricular failure. In humans and in animal experiments it has been demonstrated that indices of infarct evolution are reduced by early (less than 6 hours) administration of nitrate.

Effect of ACE-inhibition on tissue blood flow during acute left ventricular failure in the dog.

Anesthetized dogs in acute left ventricular failure were treated with the ACE-inhibitor enalaprilat (MK-422). ACE-inhibition produced a fall in the mean blood pressure and a redistribution of cardiac output to the brain, right ventricle, upper gastrointestinal tract, and the inner and middle part of the renal cortex. The flow to the spleen, adrenals, skin, muscle, fat, lower gastrointestinal tract, and outer renal cortex did not change significantly.

A comparison of cumulated CK release with three vectorcardiographic methods of estimating myocardial infarct size.

Infarct size estimated by three vectoracardiographic methods was compared with cumulated CK release in 66 patients admitted to hospital within five hours after onset of myocardial infarction. Infarctional changes in the QRS complex were sequentially computed from a continuous 24-hour recording of Frank lead VCG by: (I)-the integrals of QRS vector differences (QRS-VD) relative to the first recording obtained after hospitalization, (II)-the integral of spatial magnitude during the period of initial abnormal depolarization (IAD), (III)-The sum of R-wave amplitude in leads X and Y and Q-wave amplitude in lead Z (sigma R). From the time-trend curves of cumulated CK release, QRS-VD, IAD and sigma R terminal plateau levels were visually determined representing estimated infarct size (ISCK, ISQRS-VD, ISIAD and IS sigma R).

Effect of timolol on mortality and reinfarction after acute myocardial infarction: prognostic importance of heart rate at rest.

Long-term timolol treatment after acute myocardial infarction is associated with a significant reduction in mortality and nonfatal reinfarction. To evaluate whether the reduction in mortality and morbidity is exclusively or partly dependent on a reduction in heart rate (HR), cardiac events in the Norwegian Timolol Multicenter Study were analyzed according to resting HR at baseline and at 1 month of follow-up Resting HR at baseline was a significant predictor of total death and all events (total death plus nonfatal reinfarction) both in placebo- and in timolol-treated patients. In the placebo group the median resting HR was unchanged from baseline to 1 month control (72 beats/min), but was reduced from 72 beats/min to 56 beats/min in the timolol group.

Importance of heart rate in determining beta-blocker efficacy in acute and long-term acute myocardial infarction intervention trials.

Heart rate after an acute myocardial infarction (AMI) is an index of late mortality. The hypothesis--that the potential beneficial effect of beta-blocking drugs after an AMI is quantitatively dependent on the reduction of heart rate obtained by such treatment--was examined by reviewing available data from acute and long-term intervention trials. Only properly randomized and double-blind trials were considered.

Evolution of vectorcardiographic QRS changes during myocardial infarction in dogs and their relation to infarct size.

The ability of vectorcardiographic QRS changes to quantify myocardial ischaemia and necrosis in dogs was studied. Myocardial infarction was produced in 21 anaesthetised dogs by inflating a balloon inserted into the right, left anterior descending, or left circumflex coronary artery. A Frank vectorcardiogram was recorded before and every 15-30 minutes for 10 hours after the occlusion.

Coronary blood flow and myocardial segment dimensions during simulated dives in seals.

Three harbor seals Phoca vitulina richardsi and five spotted seals Phoca vitulina largha were used in studies of acute episodes of local myocardial ischemia in open-chest, anesthetized animals and of coronary blood flow and regional function as indicated by left ventricular segment dimensions during experimentally simulated dives of conscious, instrumented animals. We observed that seal myocardium, in which there are few coronary anastomoses, responded to brief local occlusion with prompt local dysfunction and systolic bulging; coronary flow in the nondiving seal oscillated irregularly and declined with spontaneous apnea and related falling heart rate; flow continued to oscillate but was much reduced during dives, frequently ceasing entirely for periods as long as 45 s; ventricular segment dimension shortening was reduced intermittently during dives; and elevated heart rate induced during dives by cardiac pacing or by administration of atropine diminished or eliminated the reductions in coronary blood flow. Responses of seal heart reflect the reduction in cardiac metabolic demand during diving and the seal's myocardial adaptation for enhanced anaerobic glycolysis.

Timolol maleate and HDL cholesterol after myocardial infarction.

The influence of long-term timolol treatment on plasma lipids was analysed in cohorts of the Norwegian timolol multicentre study. The prognostic importance of high-density lipoprotein (HDL) cholesterol concentration after myocardial infarction was also examined. One year timolol treatment was related to a significant reduction in HDL cholesterol levels, from 1.

Course of chest pain and its relation to CK release and ST/QRS vector changes in patients with acute myocardial infarction randomized to treatment with intravenous timolol or placebo.

Assessments of hourly pain scores (0 to 4) were made in 135 patients during the initial 24 hours after admission to the hospital. The duration of chest pain and the cumulative pain score obtained by adding the pain scores hour by hour were compared to ST and QRS vector changes and CK release. The cumulative pain score over a 24-hour period after admission correlated to the maximal QRS vector difference (r = 0.