Volatile anesthetics protect the ischemic rabbit myocardium from infarction.

BACKGROUND: The influence of anesthetic agents on the infarction process in the ischemic myocardium is unclear. This study evaluated the effects of three intravenous and three inhalational anesthetic agents on myocardial infarction within a quantified ischemic risk zone in rabbit hearts subjected to a standardized regional ischemia-reperfusion insult. METHODS: Both in vitro and in situ rabbit models were used to investigate the effects of anesthetic agents on infarct size. In all rabbits the heart was exposed and a coronary artery surrounded with a suture to form a snare for subsequent occlusion. In in situ preparations, both intravenous and inhalational agents were tested, whereas only the latter were used in isolated hearts. Infarct size was determined by triphenyltetrazolium chloride staining. To determine whether an adenosine-mediated protective mechanism was involved, 8-(p-sulfophenyl)theophylline, an adenosine receptor blocker, was added to halothane-treated isolated hearts. Adenosine concentration in the coronary effluent was also measured in isolated hearts exposed to halothane. In other protocols, chelerythrine, a highly selective protein kinase C inhibitor, was administered to both halothane-treated and untreated isolated hearts. RESULTS: Infarcts in the three in situ groups anesthetized with halothane, enflurane, and isoflurane were about one half as large as infarcts in rabbits that underwent anesthesia with pentobarbital, ketamine-xylazine, or propofol. Volatile anesthetics also protected isolated hearts by a similar amount. Both adenosine receptor blockade and chelerythrine abolished cardioprotection from halothane in isolated hearts. Halothane treatment did not increase adenosine release. CONCLUSIONS: The volatile anesthetics tested protected the ischemic rabbit heart from infarction, in contrast to the three intravenous agents tested. Protection was independent of the hypotensive effect of the inhalational agents because halothane also protected isolated hearts, in which changing vascular tone is not an issue and coronary perfusion pressure is constant. Cardioprotection by volatile anesthetics depended on both adenosine receptors and protein kinase C, and thus is similar to the mechanism of protection seen with ischemic preconditioning.

An Expansion for Quasi-Reversible Linear Potential Sweep Voltammetry and the Use of Euler's Transformation of Series.

An expansion for the current-voltage curves occurring in quasi-reversible linear potential sweep voltammetry is obtained in the form of an exponential (double) series. Euler's transformation of series is used for practical evaluation. Numerical precision problems limiting past applications of Euler's transformation can be overcome by the use of arbitrary precision arithmetic, now commonly available in mathematical software. Sample calculations are given, and the relation of the solution to previous work in the area is described.

Pulmonary capillary pressure: a review.

OBJECTIVES: To demonstrate the importance of a) measuring effective pulmonary capillary pressure and b) evaluating the longitudinal distribution of pulmonary vascular resistance relative to pre- and postcapillary resistances. To review the development of methods used to determine pulmonary capillary pressure in experimental animal and clinical studies. DATA SOURCES: Human, animal, and modeling studies published since 1966 identified through MEDLINE and a review of bibliographies of relevant articles. STUDY SELECTION AND DATA EXTRACTION: All studies identified were reviewed with an emphasis on recent studies and those studies identifying various methodologies used to determine capillary pressure. Experimental studies were selected for their historical value and applicability to the clinical setting. DATA SYNTHESIS: Different models of the pulmonary circulation have been proposed. The electrical circuit model, which incorporated capacitance elements and two or four resistive elements, has been the basis for the determination of pulmonary capillary pressure in isolated lungs and in situ lungs in animals and patients. Methods used to determine pulmonary capillary pressure from a pulmonary arterial pressure tracing after balloon occlusion are: a) division of waveform into two components and logarithmic extrapolation of the slow component to occlusion time; b) visual determination of the pressure inflection point of the pulmonary arterial pressure tracing; and c) computer processing of the total arterial pressure transient. Both ease of calculations and difficulties can arise when each method is used. CONCLUSIONS: Pulmonary capillary hydrostatic pressure is an important determinant of pulmonary edema especially in the setting of pulmonary hypertension and adult respiratory distress syndrome. Hypoxia, sepsis, cardiac valvular disease, and inflammatory mediators produce variable changes in the longitudinal distribution of pulmonary vascular resistance so that an increased capillary pressure cannot be predicted by the pulmonary arterial or occlusion pressure. For proper therapy aimed at decreasing pulmonary vascular resistance, it is important to determine whether or not the particular therapy increases capillary pressure. Pulmonary capillary pressure is the most important determinant of lung fluid balance and is the major physiologic parameter that should be measured when various forms of plasma volume expansion and pulmonary vasodilators are used in the critically ill patient.

Pulmonary capillary pressures during hypoxia and hypoxemia: experimental and clinical studies.

Unlike the systemic circulation, the pulmonary vasculature constricts in response to hypoxia to divert blood flow to better-ventilated segments. The site of this response, the hypoxic pulmonary vasoconstriction, has been reported as precapillary in numerous experimental models of isolated animal lungs. In the present study, the response of intact chest dog and human lungs to hypoxia and hypoxemia, respectively, was also precapillary vasoconstriction. In dogs, hypoxia in the ipsilateral lung attenuated the normal vertical blood flow gradient. Contralateral hypoxia did not alter pulmonary regional blood flow, precapillary (Ra), postcapillary, or total pulmonary vascular resistance. In patients, an elevated alveolar-arterial oxygen pressure gradient of 50 to 150 torr resulted in significantly increased Ra. Further hypoxemia did not increase this response. In addition, the effective pulmonary capillary pressure did not bear a constant relationship to the pulmonary artery occlusion or wedge pressure (WP). Therefore, in patients in respiratory failure, WP does not reliably estimate hydrostatic pressure at the pulmonary capillaries.

Changes in the pulmonary capillary pressure after cardiac surgery.

The changes in the pulmonary circulation in 37 cardiac surgery patients undergoing coronary artery bypass (CABG), n=16; aortic valve replacement (AVR), n=13; and mitral valve replacement (MVR), n=8 were studied. The visual technique for the determination of pulmonary capillary pressure (Pc) was used in the preoperative and postoperative periods. The ratio of Pc to the pulmonary artery wedge pressure (Pw) was calculated to determine whether Pc and Pw varied independently. In addition, total pulmonary vascular resistance (PVR) was divided into precapillary (ra) and postcapillary (rv) components. Results from the CABG patients showed that the relationship between Pc and Pw remained constant despite an increased cardiac output. This differs from the data obtained from AVR and MVR patients in whom the Pc/Pw ratio was significantly higher after surgery. Therefore, Pw would underestimate Pc in this group of patients. In addition, MVR patients showed a significant postoperative increase in PVR and rv as compared with their preoperative values. This was also significantly higher than the rv in either AVR or CABG patients. The etiology of this change is unknown.

Measurement of effective pulmonary capillary pressure using the pressure profile after pulmonary artery occlusion.

Pulmonary artery catheters are frequently used to measure pulmonary vascular pressures, particularly the pulmonary wedge pressure (Pw), which reflects pulmonary venous and ideally left atrial pressures. However, the pulmonary capillary pressure (Pc) is the major force in the formation of pulmonary edema. Unfortunately, Pw has been interpreted as being identical to Pc. In this study we used 7-Fr pulmonary artery catheters to measure effective Pc in closed-chest animals and patients. The decreasing pressure profile after pulmonary artery occlusion was separated into fast and slow components, with the inflection point between them representing Pc. Pc was also estimated by mathematically analyzing the curves in terms of a precapillary resistance, a large pulmonary capillary capacitor, and a postcapillary resistance. In dogs, Pc was determined after pulmonary vascular resistance had been increased by infusing serotonin and histamine. While Pw remained unchanged, serotonin increased pulmonary artery pressure (Ppa) 52% and Pc 16%, whereas histamine increased Ppa only 25%, but increased Pc by 35%. This is consistent with studies showing that serotonin primarily elevates precapillary resistance, and histamine increases postcapillary resistance. In thoracic surgery patients, Pc was not consistently related to Pw. This measurement was simple, reproducible, and provided a more precise capillary filtration pressure than Pw. It should be clinically useful in monitoring patients with pulmonary hypertension and adult respiratory distress syndrome, especially those with pulmonary artery catheters.