BACKGROUND: The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension. METHODS AND RESULTS: MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias. CONCLUSIONS: The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.
BACKGROUND: The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension. METHODS AND RESULTS: MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias. CONCLUSIONS: The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.
Authors: A Hagendorff; E Klemm; M Bangard; C Dettmers; C Wolpert; B Schumacher; H J Biersack; F Grünwald; B Lüderitz; D Pfeiffer Journal: J Interv Card Electrophysiol Date: 2001-12 Impact factor: 1.900
Authors: T J Doering; H J Trappe; B Panning; H G Fieguth; B Steuernagel; B Schneider; S Piepenbrock; G C Fischer Journal: Med Klin (Munich) Date: 1998-05-15
Authors: A Hagendorff; C Dettmers; P Danos; S Wetter; M Lassau; L Pizzulli; H Omran; T Bauer; A Hartmann; B Lüderitz Journal: Clin Investig Date: 1994-10