The end-systolic pressure-volume relationship is the state of the art in the measurement of myocardial contractility. This index is load-independent and relatively independent of heart rate. In this study the load-independent character of the end-systolic pressure-length (ESPL) relationship was evaluated in dogs under general anaesthesia. The results indicated that the ESPL is pre- and afterload-independent, since the comparative values of ESPL from afterloaded and reduced preload contractions did not differ significantly (N = 75; P = 0.5993). The application of the ESPL relationship as a means of describing the function of the heart as a muscle as well as a pump is discussed.

The interaction of various concentrations of N2O and a stable halothane-fentanyl-pancuronium anesthetic technique was examined in nine pigs. Segmental myocardial contractility was measured with the end-systolic pressure-length relationship (Ees), and the effective arterial elastance (Ea) was quantified based on the Windkessel model. The addition of 30, 50, and 70% N2O did not change myocardial contractility or the effective arterial elastance. During the 30 and 70% N2O challenge, however, arterial capacitance decreased significantly from a mean (+/- SEM) 0.86 +/- 0.15 to 0.71 +/- 0.0.11 mL/mm Hg with 30% N2O (P less than 0.05) and from 0.90 +/- 0.09 to 0.71 +/- 0.07 mL/mm Hg (P less than 0.05) with 70% N2O. A dose-response relationship for the effect on the arterial capacitance could not be demonstrated. We concluded that in the presence of halothane, fentanyl, and pancuronium, N2O does not depress the normal myocardium or change left ventricular afterload. The decrease in arterial capacitance that occurred when 30 and 70% N2O were given was not sufficient to change the effective afterload and appears to be of no importance to normal left ventricular function.

This study, in open-chested dogs, sought to explore the relationship between whole-body oxygen delivery and oxygen consumption during anaesthesia, using increasing concentrations of halothane, enflurane and isoflurane. Results indicate that the cardiac index and oxygen delivery became critical at less than 1 MAC (minimal alveolar concentration of anaesthetic) for the three commonly used vapours. Halothane caused the least depression of contractility, but the stroke volume was reduced by the well-maintained afterload at 1 MAC. Enflurane and isoflurane were associated with more depression of contractility, but the cardiac output was maintained by an increase in heart rate in the case of isoflurane and reduced mean arterial pressure during the use of enflurane.

The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.

Myocardial oxygen supply and demand in the normal dog were evaluated as the concentration of halothane, enflurane or isoflurane was increased. Although coronary blood flow decreased as the anaesthetic gas concentration increased, the O2 supply-to-demand ratio remained stable owing to a decrease in the myocardial O2 consumption.

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.

The correct measurement of various blood pressures in clinical practice is of obvious importance. A method by which the frequency response and damping of various transducers and catheters can be determined is discussed and reference is made to values obtained in the validation of certain catheters.

Myocardial contractility was measured using the end-systolic pressure-length (ESPL) relationship in dogs subjected to increasing concentrations of halothane (0,5-2 per cent), enflurane (0.77-2.6 per cent) or isoflurane (0.70-2.13 per cent), combined with an infusion 7 ¼g·kg-1 ·min-1 offentanyl, after induction of anaesthesia with 15 mg·kg-1; thiopentone. The relationship between the concentrations of the different drugs and contractility (ESPL) can best be described by ESPL = a + bi(MAC fraction) where “a” is a constant and “b” is the slope of the curve relating ESPL to MAC. At 1.0 MAC values, the ESPL for halothane (69.04 ± 25.83 mmHg· mm-1) did not differ from that of isoflurane (63.19 ± 17.36 mmHg·mm-1). However, the myocardial contractility during 1.0 MAC halothane and isoflurane anaesthesia was better preserved than that of enflurane (38.66 ± 9.73 mmHg·mm-1;:p < 0.01, p < 0.05 respectively).

The effect of corticosteroid therapy on the broncho-alveolar cell response, the changes in activity of some lysosomal enzymes and the protein and lipid biosynthesis rates in lung tissue of normal rabbits and of rabbits after induction of an acute inflammation by the intravenous injection of complete Freund's adjuvant (CFA) 0,2 ml/kg body weight was investigated. Three intramuscular injections of methylprednisolone acetate (Depo-Medrol) 1,2 mg/kg over a period of 8 days reduced the mean total broncho-alveolar free cell yields significantly. The percentages of lymphocytes and granulocytes were decreased. The increase in the macrophage percentage was associated with a significant increase in the acid phosphatase activity of the broncho-alveolar cells. The beta-glucuronidase activity, on the other hand, was lowered in alveolar cells and even significantly suppressed in lung tissue. Protein and lipid biosynthesis was significantly retarded in lung tissue 8 days after the start of therapy. Administration of a single dose of CFA 0,2 ml/kg evoked an acute lung inflammation and a significant increase in total alveolar free cell yields. The macrophage percentage was reduced and the lymphocyte numbers doubled, whereas the granulocyte percentage increased more than sevenfold. The change in the percentage distribution of granulocytes may be associated with the marked increase in beta-glucuronidase activity of the cells as well as of the lung tissue. In the inflammatory phase, protein biosynthesis was significantly increased but lipid synthesis was not affected. Corticosteroid therapy in animals treated with adjuvant reversed all the effects of CFA. It has very pronounced anti-inflammatory action and a catabolic effect on protein and lipid metabolism.