NITRIC OXIDE SYNTHASE INHIBITION IMPROVES CORONARY PERFUSION PRESSURE AND OUTCOME DURING CARDIOPULMONARY RESUSCITATION (CPR) IN A PORCINE MODEL OF VENTRICULAR FIBRILLATION

1999 ◽  
Vol 27 (Supplement) ◽  
pp. A30
Author(s):  
Werner Lingnau ◽  
Anette C Krismer ◽  
Karl H Lindner ◽  
Volker Wenzel ◽  
Bernd Rainer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ventricular Fibrillation ◽  
Nitric Oxide Synthase ◽  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Oxide Synthase

Endobronchial Vasopressin Improves Survival during Cardiopulmonary Resuscitation in Pigs 

1997 ◽  
Vol 86 (6) ◽  
pp. 1375-1381 ◽  
Author(s):  
Volker Wenzel ◽  
Karl H. Lindner ◽  
Andreas W. Prengel ◽  
Keith G. Lurie ◽  
Hans U. Strohmenger
Keyword(s):  
Placebo Group ◽  
Cardiopulmonary Resuscitation ◽  
Drug Administration ◽  
Porcine Model ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Successful Resuscitation ◽  
Short Period

Background Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. This study evaluated the effect of endobronchial vasopressin during CPR. Methods After 4 min of untreated ventricular fibrillation and 3 min of CPR, 21 pigs were randomized to be treated with 0.8 U/kg intravenous vasopressin (n = 7), 0.8 U/kg endobronchial vasopressin (n = 9), or an endobronchial placebo of normal saline (n = 5). Defibrillation was performed 5 min after drug administration to attempt return of spontaneous circulation. Results All animals in the intravenous and endobronchial vasopressin group were resuscitated successfully, but only two of five animals in the placebo group were. At 2 and 5 min after drug administration, coronary perfusion pressure in the intravenous and endobronchial vasopressin group was significantly higher than in the placebo group (50 +/- 10, 34 +/- 5 vs. 16 +/- 6 mmHg, respectively; and 35 +/- 10, 39 +/- 10 vs. 19 +/- 5 mmHg, respectively; P < 0.05). Conclusions Endobronchial vasopressin is absorbed during CPR, coronary perfusion pressure is increased significantly within a short period, and the chance of successful resuscitation is increased in this porcine model of CPR. Endobronchial vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.

Nitroglycerin and Epinephrine Improve Coronary Perfusion Pressure in a Porcine Model of Ventricular Fibrillation Arrest: A Pilot Study

2009 ◽  
Vol 37 (4) ◽  
pp. 369-375 ◽  
Author(s):  
Vassiliki Kitsou ◽  
Theodoros Xanthos ◽  
Konstantinos Stroumpoulis ◽  
George Rokas ◽  
Dimitrios Papadimitriou ◽  
...  
Keyword(s):  
Pilot Study ◽  
Ventricular Fibrillation ◽  
Porcine Model ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

scholarly journals Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

AbstractPrimary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

Selective neuronal nitric oxide synthase inhibition blocks furosemide-stimulated renin secretion in vivo

1995 ◽  
Vol 269 (1) ◽  
pp. F134-F139 ◽  
Author(s):  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Neuronal Nos ◽  
Oxide Synthase

The macula densa is a regulatory site for renin. It contains exclusively the neuronal isoform of nitric oxide synthase (NOS), suggesting NO could stimulate renin secretion through the macula densa pathway. To test whether neuronal NOS mediates renin secretion, renin was stimulated by either the renal baroreceptor or the diuretic furosemide (acting through the macula densa pathway). Renin secretion rate (RSR) was measured in 12 Inactin-anesthetized rats at normal (104 +/- 3 mmHg) and reduced renal perfusion pressure (65 +/- 1 mmHg), before and after selective blockade of the neuronal NOS with 7-nitroindazole (7-NI, 50 mg/kg ip). 7-NI had no effect on basal blood pressure (102 +/- 2 mmHg) or renal blood flow (RBF). Decreasing renal perfusion pressure doubled RSR from 11.8 +/- 3.3 to 22.9 +/- 5.7 ng ANG I.h-1.min-1 (P < 0.01) (ANG I is angiotensin I). Similarly, in 7-NI-treated rats, reduced perfusion doubled RSR from 8.5 +/- 1.8 to 20.5 +/- 6.2 ng ANG I.h-1.min-1 (P < 0.01). Renal hemodynamics and RSR were measured in response to 5 mg/kg iv furosemide in 12 control rats and 11 rats treated with 7-NI. Blocking neuronal NOS did not alter blood pressure (102 +/- 2 mmHg), RBF (5.8 +/- 0.4 ml.min-1.g kidney wt-1), or renal vascular resistance (18.7 +/- 1.4 mmHg.ml-1.min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Perfusion Pressure During Cardiopulmonary Resuscitation After Spinal Anesthesia in Dogs

1996 ◽  
Vol 82 (1) ◽  
pp. 84-87
Author(s):  
Jack M. Rosenberg ◽  
Joyce A. Wahr ◽  
Ho Choon Sung ◽  
Young Suk Oh ◽  
Lori J. Gilligan
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Spinal Anesthesia ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion

scholarly journals Effects of selected endothelium-dependent vasodilators on fetoplacental vasculature: physiological implications

1999 ◽  
Vol 277 (2) ◽  
pp. H842-H847
Author(s):  
Saral Amarnani ◽  
Belinda Sangrat ◽  
Gautam Chaudhuri
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Receptor Antagonist ◽  
Perfusion Pressure ◽  
Ang Ii ◽  
Hoe 140 ◽  
Oxide Synthase

The endothelium-dependent vasodilators ACh, histamine, and bradykinin were studied in the isolated, perfused human placental cotyledon. Histamine caused a decrease in perfusion pressure that was attenuated by cimetidine. Bradykinin, at lower concentrations (10−20 to 10−14 M), produced a concentration-dependent decrease in perfusion pressure, whereas at higher concentrations it produced an increase in perfusion pressure. ACh was without any effect. The decrease in perfusion pressure observed with bradykinin was potentiated by captopril and was significantly attenuated in the presence of HOE-140, the B2-receptor antagonist, or by pretreatment with an inhibitor of nitric oxide synthase, but not by an inhibitor of cyclooxygenase. The decrease in perfusion pressure observed with bradykinin was potentiated by ANG I but not by ANG II. It is concluded that endothelium-dependent vasodilation can be demonstrated with histamine and bradykinin in the fetoplacental vessels, and at least for bradykinin, this is partly mediated by release of nitric oxide. The potentiation of the bradykinin response in the presence of ANG I may serve to buffer the vasoconstriction produced by ANG II in the fetoplacental circulation.

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