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While physiological responses to hemorrhage are well-studied, hemorrhage is often accompanied by trauma, and it remains unclear how injury affects these responses. This study examined effects of extremity trauma on cardiorespiratory responses and survival to moderate (37%; H-37) or severe (50%; H-50) hemorrhage in rats. Transmitter and carotid catheter implantation, and extremity trauma (fibular fracture and muscle injury) were conducted 2 weeks, 24 hrs, and 90 min, respectively, prior to conscious hemorrhage. Mean arterial pressure (MAP) and heart rate (HR) (via telemetry), and respiration rate (RR), minute volume (MV), and tidal volume (TV) (via plethysmography) were measured throughout the 25 min hemorrhage and remainder of the 4 h observation period. There were four groups: 1) H-37, no trauma (NT; n=17); 2) H-37, extremity trauma (T, n=18); H-50, NT (n=20); and 4) H-50, T (n=20). For H-37, during and post-hemorrhage, T increased HR (P≤0.031) and MV (P ≤ 0.048) compared with NT-rats. During H-50, T increased HR (0.041) and MV (P=0.043). Post-hemorrhage, T increased MV (P=0.008), but decreased HR (P=0.007) and MAP (P=0.039). All cardiorespiratory differences between T and NT groups were intermittent. Importantly, both survival time (159.8 ± 78.2 min vs 211.9 ± 60.3 min; P = 0.022; mean ± SD) and percent survival (45% vs 80%; P = 0.048) were less in T vs NT-rats after H-50. Trauma interacts with physiological systems in a complex manner and no single cardiorespiratory measure was sufficiently altered to indicate that it alone could account for increased mortality after H-50.
While physiological responses to hemorrhage are well-studied, hemorrhage is often accompanied by trauma, and it remains unclear how injury affects these responses. This study examined effects of extremity trauma on cardiorespiratory responses and survival to moderate (37%; H-37) or severe (50%; H-50) hemorrhage in rats. Transmitter and carotid catheter implantation, and extremity trauma (fibular fracture and muscle injury) were conducted 2 weeks, 24 hrs, and 90 min, respectively, prior to conscious hemorrhage. Mean arterial pressure (MAP) and heart rate (HR) (via telemetry), and respiration rate (RR), minute volume (MV), and tidal volume (TV) (via plethysmography) were measured throughout the 25 min hemorrhage and remainder of the 4 h observation period. There were four groups: 1) H-37, no trauma (NT; n=17); 2) H-37, extremity trauma (T, n=18); H-50, NT (n=20); and 4) H-50, T (n=20). For H-37, during and post-hemorrhage, T increased HR (P≤0.031) and MV (P ≤ 0.048) compared with NT-rats. During H-50, T increased HR (0.041) and MV (P=0.043). Post-hemorrhage, T increased MV (P=0.008), but decreased HR (P=0.007) and MAP (P=0.039). All cardiorespiratory differences between T and NT groups were intermittent. Importantly, both survival time (159.8 ± 78.2 min vs 211.9 ± 60.3 min; P = 0.022; mean ± SD) and percent survival (45% vs 80%; P = 0.048) were less in T vs NT-rats after H-50. Trauma interacts with physiological systems in a complex manner and no single cardiorespiratory measure was sufficiently altered to indicate that it alone could account for increased mortality after H-50.
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