Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship.

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The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated with nitroglycerin infusion for greater than 24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest greater than 2 days after infarction. 4.4 +/- 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments (Th1-7) for 98 +/- 9 min. Heart rate decreased significantly from 70 +/- 3 to 64 +/- 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 +/- 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 +/- 0.3 the first day to 0.9 +/- 0.3 the fourth day (P less than 0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of the present investigation was to study the effect of high thoracic epidural anaesthesia (TEA) on the incidence of ventricular arrhythmias after ligation of the left coronary artery in chloralose-anaesthetized rats. Forty animals were randomly assigned to receive either 40-50 microliter of bupivacaine (5 mg/ml) or saline in implanted thoracic epidural catheters. TEA decreased mean arterial pressure (MAP) from 118 +/- 5 mmHg to 72 +/- 4 mmHg and heart rate (HR) from 450 +/- 9 to 387 +/- 8 beats/min, while epidural saline did not affect MAP and HR. In both groups coronary artery ligation induced a transient decrease in MAP within the first 5-10 min after ligation. In the control group HR increased, during the 30-min post-ligation period, from 453 +/- 9 to 474 +/- 10 beats/min (P less than 0.05) while no significant change was seen in the TEA group. In both groups the mortality rate was 10%. In the TEA group 30% and in the control group 0% had normal sinus rhythm during the recording period (P less than 0.001). The incidence of ventricular fibrillation and/or tachycardia was significantly lower (P less than 0.05) in the TEA group (20%) compared to the control group (53%). The incidence of ventricular extrasystoles did not differ between the two groups. We conclude that TEA-induced blockade of sympathetic afferents and efferents may offer protection against malignant ventricular arrhythmias in the early phase of acute myocardial infarction.

Cemented hemiarthroplasty in patients with femoral neck fracture causes a pronounced pulmonary vasoconstriction and an impairment of RV function accompanied by pulmonary ventilation/perfusion abnormalities.

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The study aimed to compare the effects of thoracic epidural anaesthesia (TEA) with those of the beta-adrenoceptor blocker, metoprolol, on central haemodynamics in conscious rats with acute myocardial infarction. During methohexital anaesthesia, appropriate vascular catheters were inserted, a thoracic epidural catheter was implanted and the left coronary artery was ligated. A recovery period of 1-2 h elapsed after termination of surgery and anaesthesia. Experiments were performed on four separate groups of animals (A-D). In Group A (n = 10) mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) were measured, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated before and 10-15 min after the induction of TEA (bupivacaine 5 mg.ml-1). In Group B (n = 6) left ventricular end-diastolic pressure (LVEDP) and maximal dP/dt were recorded as in Group A. In Group C (n = 10) central haemodynamics were measured 10 min after i.v. metoprolol (0.5 mg.kg-1) and again 10-15 min after the addition of TEA. In Group D (n = 6) LVEDP and max dP/dt were measured as in Group C. The reduction in CO, SV, HR and max dP/dt was of the same magnitude with TEA and metoprolol. TEA lowered MAP by 17%, while metoprolol did not change MAP. Metoprolol caused an increase in LVEDP from 20.8 +/- 1.8 to 27.5 +/- 2.7 mmHg (2.8 +/- 0.2 to 3.7 +/- 0.4 kPa) (P less than 0.01), while TEA induced a decrease in LVEDP from 24.2 +/- 1.4 to 17.8 +/- 1.6 mmHg (3.2 +/- 0.2 to 2.4 +/- 0.2 kPa) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)