Influence of dobutamine on the variables of systemic haemodynamics, metabolism, and intestinal perfusion after cardiopulmonary resuscitation in the rat
ABSTRACT Global left ventricular dysfunction after successful resuscitation from cardiac arrest may be treated successfully with dobutamine but the effects on intestinal perfusion are unknown.
In 24 male Sprague-Dawley rats ventricular fibrillation was induced. After 4 min of untreated cardiac arrest, precordial chest compression was performed for 4 min; adrenaline (epinephrine) (90 microg kg(-1)) was injected, followed by defibrillation. Return of spontaneous circulation was achieved in 18 animals, which were allocated to receive saline 0.9% (control group, n = 6), dobutamine at 5 microg kg(-1) min(-1) (n = 6) or dobutamine at 10 microg kg(-1) min(-1) (n = 6). Measurements of haemodynamic variables and intestinal tonometer P(CO2) were made before induction of ventricular fibrillation and 15, 30, 60, and 120 min postresuscitation.
At 120 min postresuscitation, mean aortic pressure was 82 +/- 20, 104 +/- 19, and 113 +/- 15 mmHg for the control group, the dobutamine (5 microg kg(-1) min(-1)) group and the dobutamine (10 microg kg(-1) min(-1)) group (P < 0.05 for comparison of the dobutamine (10 microg kg(-1) min(-1)) group versus the control group). Respective abdominal aortic blood flow was 107 +/- 16, 133 +/- 49, and 145 +/- 18 ml min(-1) kg(-1) (P < 0.05 for comparison of the dobutamine (10 microg kg(-1) min(-1)) group versus the control group), and superior mesenteric artery blood flow was 25 +/- 9, 28 +/- 8, and 33 +/- 8 ml min(-1) kg(-1). Arterial lactate was significantly higher (P < 0.05) in the control group (2.3 +/- 0.6 mmol l(-1)) than in the dobutamine (5 microg kg(-1) min(-1)) group (1.6 +/- 0.3 mmol l(-1)) and dobutamine (10 microg kg(-1) min(-1)) group (1.5 +/- 0.3 mmol l(-1)). Tonometrically derived P(CO2) gap was highly elevated at 15 min of postresuscitation and returned to prearrest level at 120 min postresuscitation in all groups.
Dobutamine enhances the recovery of global haemodynamic and metabolic variables early after cardiac arrest.
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ABSTRACT: One of the main challenges in Wireless Sensor and Actuator Networks (WSAN) is the delay caused by shared and nondeterministic behavior of wireless communication medium. The Retry-Limit parameter of IEEE 802.11 standard can be used to control packet reliability, whereas other parameters mostly effect on the packet delay. In this paper, at first the delay-reliability trade-off in WSANs based on MIMO-Enabled IEEE 802.11 standard, utilizing Enhanced Distributed Channel Access (EDCA) at Medium Access Control (MAC) layer and Maximum Likelihood Spatial Multiplexing at PHYsical (PHY) Layer is studied. Then two simple adaptive schemes have been proposed to minimize packet delay while satisfying the required reliability at noisy factory environment.Procedia Computer Science 12/2011; 5:945-950. DOI:10.1016/j.procs.2011.07.133
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ABSTRACT: We demonstrate the usefulness of left ventricular pressure–volume (PV) loops generated by the use of conductance catheter measurements and investigate the influence of the type of general anesthesia on postresuscitation myocardial dysfunction in a rat model of cardiac arrest (CA) and subsequent cardiopulmonary resuscitation. A total of 42 Wistar-Han rats were randomized to receive general anesthesia with sevoflurane and resuscitation after CA, general anesthesia with pentobarbital intraperitoneally and resuscitation after CA, or general anesthesia with pentobarbital without CA (sham group). Myocardial function, assessed by analysis of PV loops, was measured continuously and in real-time by using a PV–conductance catheter. Rats were monitored for 3 h after restoration of spontaneous circulation (ROSC). The use of PV–conductance catheters supported objective and reliable evaluation of myocardial function and proved feasible in this rat model of CA. End-diastolic volume increased in rats anesthetized with pentobarbital after ROSC (before CA, 237 ± 45 μL; after ROSC, 402 ± 64 μL). Preloadadjusted maximal power before CA was the same in all groups but decreased in both resuscitated groups. The decrease was less pronounced in rats anesthetized with sevoflurane compared with pentobarbital (11.8 ± 4.9 mW/μL2 compared with 4.8 ± 1.9 mW/μL2 at 3 h after ROSC). This finding indicates that the type of general anesthesia influences postresuscitation myocardial dysfunction in this rat model of experimentally induced CA and cardiopulmonary resuscitation. Rats that were anesthetized with sevoflurane exhibited less postresuscitation myocardial dysfunction than did those anesthetized with pentobarbital.Journal of the American Association for Laboratory Animal Science: JAALAS 01/2014; 53(4). · 0.73 Impact Factor
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ABSTRACT: Cardiopulmonary arrest remains one of the leading causes of death and disability in Western countries. Although ventricular fibrillation (VF) models in rodents mimic the "square wave" type of insult (rapid loss of pulse and pressure) commonly observed in adult humans at the onset of cardiac arrest (CA), they are not popular because of the complicated animal procedure, poor animal survival and thermal injury. Here we present a modified, simple, reliable, ventricular fibrillation-induced rat model of CA that will be useful in studying mechanisms of CA-induced delayed neuronal death as well as the efficacy of neuroprotective drugs. CA was induced in male Sprague Dawley rats using a modified method of von Planta et al. In brief, VF was induced in anesthetized, paralyzed, mechanically ventilated rats by an alternating current delivered to the entrance of the superior vena cava into the heart. Resuscitation was initiated by administering a bolus injection of epinephrine and sodium bicarbonate followed by mechanical ventilation and manual chest compressions and countershock with a 10-J DC current. Neurologic deficit score was higher in the CA group compared to the sham group during early reperfusion periods, suggesting brain damage. Significant damage in CA1 hippocampus (21% normal neurons compared to control animals) was observed following histopathological assessment at seven days of reperfusion. We propose that this method of VF-induced CA in rat provides a tool to study the mechanism of CA-induced neuronal death without compromising heart functions.10/2013; 4(5). DOI:10.1007/s12975-013-0267-0