Am. J. Respir. Crit. Care Med., Volume 156, Number 5, November 1997, 1473-1482

Structure-Function Relationships in the Septic Rat Heart

RICHARD D. PIPER, FU YAN LI, MARY LEE MYERS, and WILLIAM J. SIBBALD

A. C. Burton Vascular Biology Laboratory and Cardiovascular Surgery, Victoria Hospital, London, Ontario, Canada

Myocardial edema and histologic changes consistent with tissue injury are reported in association with sepsis-induced myocardial depression. The objective of the present study was to determine whether, in the absence of shock, such changes (assessed by studying microvascular albumin flux, tissue edema, and morphometry) are prerequisites for the development of contractile dysfunction in sepsis. Sprague-Dawley rats were randomized into groups for either cecal ligation and perforation (CLP) or sham study. Twenty-four hours after entry of animals into the study, their myocardial function was assessed with the Langendorff isolated heart technique. Left-ventricular developed pressure (preload: 5 mm Hg) was reduced in CLP animals (34.9 ± 3.3 mm Hg, n = 10) as compared with time-matched controls (46.4 ± 4.0 mm Hg, n = 8, p < 0.05, unpaired t test). This was associated with a significant reduction in the maximal rate of increase (+dP/dt_max) and decrease (dP/dt_max) in left ventricular pressure in the CLP group (sham versus CLP, unpaired t test, p < 0.05). Upon reperfusion, after 30 min of ischemia, left ventricular resting tension was decreased in CLP as compared with sham-treated animals (sham versus CLP, analysis of variance (ANOVA) with repeated measures, p < 0.05). At 24 h, sepsis was not associated with myocardial edema (wet:dry weight ratio, sham = 4.094 ± 0.098, n = 10; CLP = 4.185 ± 0.066, n = 7), and tissue albumin flux was reduced (sham = 194 ± 27 µl · h¹ · g dry wt¹, n = 10; CLP = 100 ± 14 µl · h¹ · g dry wt¹, n = 7). In tissue processed for electron microscopy, we found no evidence of tissue injury or edema at either 24 or 48 h after CLP. We conclude that polymicrobial normotensive sepsis causes myocardial contractile depression in the absence of changes in myocardial structure.

This article has been cited by other articles:

				A. D. Niederbichler, L. M. Hoesel, M. V. Westfall, H. Gao, K. R. Ipaktchi, L. Sun, F. S. Zetoune, G. L. Su, S. Arbabi, J. V. Sarma, et al. An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction J. Exp. Med., January 23, 2006; 203(1): 53 - 61. [Abstract] [Full Text] [PDF]

				A. W. Sielenkamper, P. Yu, O. Eichelbronner, T. MacDonald, C. M. Martin, I. H. Chin-Yee, and W. J. Sibbald Diaspirin cross-linked Hb and norepinephrine prevent the sepsis-induced increase in critical O2 delivery Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1922 - H1930. [Abstract] [Full Text] [PDF]

				R. D. Piper, F. Y. Li, M. L. Myers, and W. J. Sibbald Effects of isoproterenol on myocardial structure and function in septic rats J Appl Physiol, March 1, 1999; 86(3): 993 - 1001. [Abstract] [Full Text] [PDF]

				A. KOVACS, M. R. COURTOIS, B. BARZILAI, I. E. KARL, P. A. LUDBROOK, and R. S. HOTCHKISS Reversal of Hypocalcemia and Decreased Afterload in Sepsis . Effect on Myocardial Systolic and Diastolic Function Am. J. Respir. Crit. Care Med., December 1, 1998; 158(6): 1990 - 1998. [Abstract] [Full Text] [PDF]