Edaravone attenuates sustained pial arteriolar vasoconstriction independently of endothelial function after unclamping of the abdominal aorta in rabbits.

BACKGROUND: Cerebral blood flow (CBF) has direct effects on neuronal function and neurocognitive disorders. Oxidative stress from abdominal aortic surgery is important in the pathophysiology of CBF impairment. We investigated the effect of edaravone on the pial arteriolar diameter changes induced by abdominal aortic surgery and the involvement of the endothelium in the changes. METHODS: The closed cranial window technique was used in rabbits to measure changes in pial arteriolar diameter after the unclamping of abdominal aortic cross-clamping with an intravenous free radical scavenger, edaravone (control group [n = 6], edaravone 10 µg/kg/min [n = 6], 100 µg/kg/min [n = 6]). Pial vasodilatory responses to topical application of acetylcholine (ACh) into the cranial window were investigated before abdominal aortic cross-clamping and after unclamping with intravenous administration of edaravone (control group [n = 6], edaravone 100 µg/kg/min [n = 6]). RESULTS: Aortic unclamping-induced vasoconstriction was significantly attenuated by continuous infusion of edaravone at 100 µg/kg/min. Topical ACh after unclamping did not produce any changes in pial arteriolar responses in comparison to before aortic cross-clamping in the control or edaravone groups. The changes in the response to topical ACh after unclamping in the saline and edaravone groups did not differ significantly. CONCLUSIONS: Free radicals during abdominal aortic surgery might have contracted cerebral blood vessels independently of endothelial function in rabbits. Suppression of free radicals attenuated the sustained pial arteriolar vasoconstriction after aortic unclamping. Thus, the free radical scavenger might have some brain protective effect that maintains CBF independently of endothelial function.

The effects of transient cerebral ischemia on vasopressin-induced vasoconstriction in rabbit cerebral vessels.

BACKGROUND: Vasopressin is a drug of choice for use during cardiopulmonary resuscitation because several experimental studies have shown that it is better than epinephrine at increasing systemic perfusion pressure and improving cerebral perfusion pressure without increasing myocardial oxygen consumption. We used a pial window preparation to determine the effects of vasopressin when applied topically to pial vessels and whether any effects were altered after cerebral ischemia in rabbits (n = 27). METHODS: We first examined the effects of topical application of arginine-vasopressin (AVP) (10(-11) M, 10(-9) M, 10(-7) M, and 10(-5) M, sequentially). We then examined the effects of topical application of AVP (10(-9) M and 10(-7) M, sequentially) before and after a 5-min intervention consisting of cerebral ischemia produced by inflation of a neck tourniquet plus systemic hypotension or systemic hypotension alone. RESULTS: Pial arteriolar diameters were (a) dilated by 10(-11) M AVP [7% +/- 11% (P = 0.014 versus baseline)], but constricted by 10(-9) M, 10(-7) M, and 10(-5) M AVP [7% +/- 14%, 20% +/- 14%, and 16% +/- 16% (each P < 0.05), respectively], and (b) constricted before hypotension (7% +/- 10% at 10(-9) M, 20% +/- 15% at 10(-7) M) or ischemia (7% +/- 11% at 10(-9) M, 21% +/- 15% at 10(-7) M). However, after the 5-min of ischemia, the decrease in diameter induced by 10(-7) M AVP was significantly reduced but not by hypotension alone [hypotension control group: 7% +/- 10% at 10(-9) M, 19% +/- 14% at 10(-7) M; ischemia group: 5% +/- 11% at 10(-9) M, 10% +/- 13% at 10(-7) M (P = 0.35 versus hypotension control)]. CONCLUSIONS: Topical application of AVP (except at the lowest concentration used here) induced concentration-dependent vasoconstriction of pial arterioles in anesthetized rabbits. The vasoconstrictor effect of 10(-7) M AVP was reduced after transient (5-min) cerebral ischemia.

Effects of dexmedetomidine on cerebral circulation and systemic hemodynamics after cardiopulmonary resuscitation in dogs.

PURPOSE: Our purpose was to examine the effect of dexmedetomidine, when used with phenylephrine during cardiopulmonary resuscitation (CPR), on the cerebral and systemic circulations. METHODS: In pentobarbital-anesthetized, mechanically ventilated dogs, we evaluated pial vessel diameters, cerebral oxygen extraction, and systemic hemodynamics before and after cardiac arrest (5 min) and resuscitation, in the presence or absence of dexmedetomidine (n = 7 each; dexmedetomidine or control group). RESULTS: In both groups: (a) pial arterioles were dilated at 5 and 15 min after CPR, and had returned to baseline diameters at 30 min; (b) sagittal sinus pressure was significantly raised at 5 and 15 min after CPR; and (c) cerebral oxygen extraction was decreased at 5, 15, and 30 min after CPR, and had returned to baseline level at 60 min after CPR. We could find no differences between the two groups in the cerebral circulation after CPR. However, the number of defibrillation electric shocks required to restore spontaneous circulation (5.5 vs 3.6; P < 0.05), the dose of phenylephrine used for CPR (1193 microg vs 409 microg; P < 0.01), and the number of postresuscitation ventricular ectopic beats observed during the first 120 min after successful resuscitation (1606 vs 348; P < 0.05) were all significantly lower in the dexmedetomidine group. CONCLUSION: Although intravenous dexmedetomidine, as used for CPR, does not have a beneficial effect on either cerebral vessels or cerebral oxygen extraction, it may reduce the number of defibrillation shocks needed and the number of postresuscitation ventricular ectopic beats, and help to bring about stable systemic circulation after CPR.

Automated cardiac output measurement by transesophageal color Doppler echocardiography.

UNLABELLED: Automated cardiac output measurement (ACOM), which integrates digital color Doppler velocities in space and in time, has been validated using transthoracic echocardiography but has not been tested using transesophageal echocardiography (TEE). Therefore, we determined the feasibility of the ACOM method by TEE in 36 patients undergoing cardiovascular surgery. Regions of interest for ACOM were placed within a color sector across the main pulmonary artery (PA), the mitral annulus, and the left ventricular outflow tract. Cardiac output was determined from the PA flow, the mitral flow, and the left ventricular ejection flow at each view using the ACOM method. We compared measurements of cardiac output derived from the ACOM method with measurements simultaneously obtained by thermodilution (TD). In the mitral flow analysis, the values derived from ACOM correlated well with those from TD (R(2) = 0.85; mean difference = 0.01 +/- 0.58 L/min in the 2-chamber view; R(2) = 0.78; mean difference = -0.10 +/- 0.68 L/min in the 4-chamber view). In the PA flow analysis, the values derived from ACOM did not correlate with those from TD (R(2) = 0.30). In the left ventricular outflow tract analysis, it was very difficult to obtain the optimal view (44%) in which color Doppler flow signals adequately appeared. Using the ACOM method, we obtained good correlation and agreement for cardiac output measurements in the mitral flow analysis compared with TD. The ACOM method is a practical and rapid method to measure cardiac output by TEE analysis of mitral flow. IMPLICATIONS: Automated cardiac output measurement by transesophageal color Doppler echocardiography is a practical and rapid method to measure cardiac output. This technique is a promising new approach to echocardiographic quantification in the intraoperative setting.