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J Bisera

Publications and source records attributed to J Bisera.

At least 19 recordsLinked to original sources
PubMed1997

Phased chest and abdominal compression-decompression. A new option for cardiopulmonary resuscitation.

BACKGROUND: We describe a new manual method of phased chest and abdominal compression-decompression with a Lifestick resuscitator for cardiopulmonary resuscitation (CPR). METHODS AND RESULTS: Ventricular fibrillation (VF) was induced in 20 domestic pigs. After either 5 or 7 minutes of untreated VF, either phased chest and abdominal compression-decompression (Lifestick resuscitator) or precordial compression was initiated. Defibrillation was attempted at 2 minutes after the start of CPR. For the animals in which VF was untreated for 7 minutes, epinephrine was administered in doses of 20 micrograms/kg at 2 minutes after start of CPR. The coronary perfusion pressure generated by the Lifestick resuscitator was more than twofold greater (P < .01) than that generated by conventional precordial compression. Of 5 control animals, none were resuscitated after 5 minutes of VF. However, each of 5 animals treated with the Lifestick resuscitator was resuscitated (P < .01) and survived after 48 hours (P < .01). When untreated VF was prolonged to 7 minutes and epinephrine was administered, only 2 of the 5 control animals were resuscitated, and none of them survived for more than 4 hours. However, each of the Lifestick-treated animals was resuscitated and survived for more than 48 hours (P < .01). CONCLUSIONS: Phased chest and abdominal compression-decompression substantially increased hemodynamic efficacy of CPR and outcome in terms of successful resuscitation, 48-hour survival, and cerebral recovery.

Abdomen↗
PubMed1997

Esophageal PCO2 as a monitor of perfusion failure during hemorrhagic shock.

Measurement of gastric wall PCO2 (PgCO2) by tonometric method has emerged as an attractive option for estimating visceral perfusion during circulatory shock. However, gastric acid secretion obfuscates the tonometric measurement. We, therefore, investigated the option of measuring PCO2 in the esophagus to minimize these restraints. Hemorrhagic shock was induced in five Sprague-Dawley rats, and five rats served as sham controls. PgCO2 was measured with an ion-sensitive field effect transistor that was surgically implanted into the gastric wall. Esophageal luminal PCO2 (PeCO2) was measured by a second ion-sensitive field effect transistor sensor. During hemorrhagic shock, mean aortic pressure declined from 150 to 50 mmHg. Gastric blood flow decreased from 58 to 12 ml.min-1.100 g-1 (21% of preshock) and esophageal blood flow from 44 to 7 ml.min-1.100 g-1 (16% of preshock). PgCO2 simultaneously increased from 47 to 116 Torr and PeCO2 from 47 to 127 Torr. The increases in PgCO2 were highly correlated with increases in PeCO2 (r = 0.90). Esophageal tonometry may, therefore, serve as a practical alternative to gastric tonometry.

Animals↗
PubMed1996

Adrenergic vasopressor agents and mechanical ventilation for the treatment of experimental septic shock.

OBJECTIVE: Vasopressor agents and mechanical ventilation are routine interventions for the treatment of sepsis complicated by hypotension. It was our hypothesis that such treatment singly or in combination increases the duration of survival. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Thirty male Sprague-Dawley rats anesthetized with intraperitoneal injection of pentobarbital. INTERVENTIONS: Peritonitis was induced by cecal ligation and spillage of cecal contents into the abdominal cavity. The first phase of this study was performed on 15 spontaneously breathing Sprague-Dawley rats that were randomized to three groups of five animals each. One group received treatment with dopamine. The second group received norepinephrine. The third group received only the diluent as a placebo. Concentrations of the vasopressor agents were increased such that mean arterial pressure was maintained at approximately 80% of baseline values; the volumes infused were kept constant. For the second phase of this study, the grouping of animals and the techniques of study were identical, except that rats were mechanically ventilated. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure was best maintained with norepinephrine. However, no statistically significant differences in duration of survival, cardiac index, arterial blood lactate concentration, or arterial and venous PCO2 and PO2 values were identified between groups. With mechanical ventilation, survival was prolonged (p < .01). Survival was increased from an average of 291 mins to 342 mins with dopamine, from 257 mins to 352 mins in placebo controls, and from 280 mins to 329 mins with norepinephrine. Again, no significant differences in hemodynamic and blood gas measurements, or in the duration of survival between vasopressor-treated and control animals were documented. CONCLUSIONS: No benefit or detriment was demonstrated when vasopressor agents were administered to sustain arterial pressure in the course of experimental peritonitis in this murine model of septic shock. This finding contrasted with highly significant prolongation of survival when animals were mechanically ventilated. There was no evidence that routine vasopressor therapy, under these controlled experimental conditions in rats, improved duration of survival.

Adrenergic alpha-Agonists↗
PubMed1996

Myocardial dysfunction after successful resuscitation from cardiac arrest.

OBJECTIVE: To investigate the functional and metabolic changes in the myocardium after successful resuscitation from cardiac arrest. DESIGN: Prospective, randomized, sham-controlled study. SETTING: Animal laboratory at a university center. SUBJECTS: Domestic pigs. INTERVENTIONS: Electric induction of ventricular fibrillation by alternating current delivered to the right ventricular endocardium through a pacing electrode. Electric defibrillation was attempted after an interval of 12 mins of ventricular fibrillation, which included 4 mins of untreated ventricular fibrillation and 8 mins of precordial compression in 13 animals, seven of which were successfully resuscitated. Seven additional animals were randomized to serve as "sham" controls, in which cardiac arrest was not induced. MEASUREMENTS AND MAIN RESULTS: Left ventricular pressure-volume relationships utilizing the conductance method were obtained in conjunction with conventional hemodynamic and metabolic measurements at baseline and during a 6-hr interval after successful cardiac resuscitation. Progressive and striking increases in left ventricular volumes were observed after successful cardiac resuscitation. The end-diastolic volume increased from a prearrest level of 89 +/- 21 mL to a maximum of 154 +/- 53 mL (p<.05) at 360 mins after successful resuscitation. The time-coincident end-systolic volume increased from 54 +/- 21 to 126 +/- 54 mL (p<.05), such that the ejection fraction was reduced from 0.41 +/- 0.10 to 0.20 +/- 0.07 ( p<.05). Ventricular dilation was associated with marked reductions in stroke volume and ventricular work. However, compensatory increases in heart rate maintained cardiac output at levels that sustained adequate systemic oxygen delivery. The slope of the end-systolic pressure-volume relationships progressively decreased from 5.04 +/- 1.88 to 2.00 +/- 0.57 mm Hg/mL (p<.05) at 360 mins after successful resuscitation. The volume intercept at left ventricular pressure of 100 mm Hg increased from 43 +/- 19 to 94 +/- 51 mL (p=.03). Both the decrease in the slope and the increase in the volume intercept were characteristic of progressive impairment in contractile function. The rate of left ventricular pressure decrease was unchanged. Accordingly, no substantial changes in lusitropic properties were identified. Despite large increases in end-diastolic volume, the end-diastolic pressure remained unchanged. CONCLUSION: Postresuscitation myocardial dysfunction in this animal model was characterized by impaired contractile function, decreased work capability, and ventricular dilation.

Animals↗
PubMed1995

Hepatic, renal, and cerebral tissue hypercarbia during sepsis and shock in rats.

Earlier observations had indicated profound increases in the carbon dioxide tension of the myocardium, gastric wall, liver parenchyma, and renal cortex in the setting of extreme low-flow states of cardiac arrest and resuscitation, hemorrhagic shock, and anaphylactic shock. In venous blood draining the intestines, kidneys, and pelvic viscera, significant increases in PCO2 have also been observed during septic shock. In the present study, we investigated hepatic, renal, and cerebral cortical tissue carbon dioxide tension during intra-abdominal sepsis and shock in Sprague-Dawley rats. Peritonitis was induced by cecal ligation and fecal spillage. Over an interval of 320 +/- 60 minutes, we measured progressive reduction in mean aortic pressure from 152 +/- 11 mm Hg to 25 +/- 8 mm Hg and a decline in cardiac index from 492 +/- 75 ml/kg/min to 169 +/- 57 ml/kg/min. These hemodynamic deficits were accompanied by increases in liver tissue PCO2, from 58 +/- 4 mm Hg to 110 +/- 27 mm Hg (p = 0.006), in renal tissue PCO2, from 38 +/- 7 mm Hg to 115 +/- 24 mm Hg (p < 0.001), and in cerebral cortical tissue CO2, from 59 +/- 6 mm Hg to 108 +/- 16 mm Hg (p = 0.001). Arterial blood lactate content increased from 0.8 to 5.26 +/- 0.2 mmol/L (p = 0.001). Increases in blood lactate content preceded the changes in tissue PCO2 in each of these organs. These studies demonstrate that tissue hypercarbia is a more general phenomenon of low flow states, including that of circulatory shock associated with septic peritonitis.

Animals↗
PubMed1994

Gastric intramural PCO2 as monitor of perfusion failure during hemorrhagic and anaphylactic shock.

Indirect measurement of gastric intramural pH (pHG) utilizing a luminal tonometer in the stomach has been proposed for monitoring the severity and progression of perfusion failure. In the present study, we investigated gastric PCO2 and pHG as indicators and quantitators of the severity of perfusion failure in the experimental rodent model of both hemorrhagic and anaphylactic shock. Gastric intramural PCO2 (PGCO2) and pHG were directly measured with miniaturized sensors inserted into the anterior wall of the stomach. In hemorrhagic shock, animals were bled into a reservoir maintained at a pressure of 35 mmHg. pHG decreased from 7.39 +/- 0.08 to 6.67 +/- 0.11 (P < 0.01), and PGCO2 increased from 53 +/- 4 to 136 +/- 3 Torr (P < 0.01). Anaphylactic shock was induced in animals that had been sensitized 21 days before with crystallized ovalbumin. Antigen challenge produced an immediate reduction in mean aortic pressure from 144 to 60 mmHg. pHG decreased from 7.40 +/- 0.05 to 6.99 +/- 0.07 (P < 0.01), and PGCO2 increased from 48 +/- 5 to 133 +/- 9 Torr (P < 0.01). The increases in PGCO2 were highly correlated with decreases in gastric blood flow in both hemorrhagic (r = 0.96) and anaphylactic shock (r = 0.92). The correlations with pHG were more moderate. These experiments demonstrated prominent increases in PGCO2 and H+ during both hemorrhagic and anaphylactic shock. We further noted that the estimation of pHG based on the assumption that HCO3-concentrations of the stomach wall and arterial blood are the same was not fully sustained.

Anaphylaxis↗
PubMed1994

Spontaneous gasping during cardiopulmonary resuscitation without mechanical ventilation.

Spontaneous gasping is frequently observed during cardiac arrest, especially when mechanical ventilation is withheld during precordial compression. We related spontaneous gasping to pulmonary gas exchange and cardiac resuscitability in a rodent model of cardiac arrest. Ventricular fibrillation was electrically induced in 15 Sprague-Dawley rats. After 4 min untreated ventricular fibrillation, precordial compression was initiated. Coronary perfusion pressure was maintained between 25 and 30 mm Hg. Oxygen was supplied at the tracheal tube port coincident with start of precordial compression in 10 animals. Five additional control animals were identically treated except they were mechanically ventilated coincident with start of precordial compression. After 6 min precordial compression, defibrillation was attempted and five of 10 nonventilated animals, and all control animals, were resuscitated by direct current countershock. In the successfully resuscitated, nonventilated animals, the frequency of spontaneous gasping during precordial compression progressively increased to an average of 19 gasps/min but it was < 6 gasps/min in nonresuscitated animals. More frequent gasping was associated with correspondingly greater arterial PO2 (110 versus 51 mm Hg, p < 0.01) and lesser PCO2 (55 versus 91 mm Hg, p < 0.01). In control animals, no spontaneous gasping was observed during precordial compression. Arterial PO2 and PCO2 of mechanically ventilated animals was more like that of spontaneously gasping rats. According, the frequency of spontaneous gasping in absence of mechanical ventilation is predictive of cardiac resuscitation success and associated with improved arterial oxygenation and CO2 removal.

Analysis of Variance↗
PubMed1994

Cardiopulmonary resuscitation by precordial compression but without mechanical ventilation.

It is widely held that mechanical ventilation is essential for cardiopulmonary resuscitation (CPR). However, cardiac output and therefore pulmonary blood flow is reduced to less than one-third of normal during CPR. We therefore reasoned that ventilatory requirements are correspondingly reduced and postulated that gas exchange may be maintained during precordial compression with oxygen passively delivered to the airway in the absence of mechanical ventilation. After tracheal intubation, Sprague-Dawley rats were randomized. Fifteen animals were maintained on positive-pressure ventilation with room air and an additional 15 animals breathed spontaneously. Cardiac arrest was induced by electrical fibrillation. The inspired gas concentration of oxygen was then increased to 100% in both groups. Precordial compression was begun after 4 min of untreated ventricular fibrillation. After an additional 6 min of precordial compression, resuscitation was attempted by DC countershock. During cardiac resuscitation, there were no significant differences in coronary perfusion pressure between mechanically ventilated and spontaneously breathing animals, but arterial PO2 was significantly lower and arterial PCO2 was significantly higher in the absence of positive-pressure ventilation. However, neither resuscitability nor 24-h survival were affected. Postresuscitation myocardial contractility, reflected in the maximally generated dP/dt40, was also not adversely affected. In the unventilated group, only resuscitated animals developed spontaneous gaspings at an average frequency of 17 +/- 2/min-1. The current emphasis on mechanical ventilation as the highest priority for cardiopulmonary resuscitation is therefore not fully supported under the experimental conditions of this study.

Animals↗
PubMed1994

Cardiac resuscitation by retroaortic infusion of blood.

Current methods of closed-chest cardiac resuscitation generate coronary perfusion pressures that rarely exceed one fourth of normal, and this decreases with prolongation of cardiac arrest. The resuscitation effort is therefore almost uniformly unsuccessful when precordial compression is initiated after 8 minutes of untreated cardiac arrest. This report introduces a new option for cardiac resuscitation by infusion of oxygenated blood into the ascending aorta such as to transiently increase the pressure gradient for coronary perfusion. Thirty-six anesthetized, mechanically ventilated normovolemic rats were investigated. Cardiac arrest was induced with an alternating current delivered through an electrode catheter advanced into the right ventricle. Ventricular fibrillation was untreated for 4, 6, or 8 minutes, after which resuscitation was attempted without blood infusion, with infusion of oxygenated blood, or with infusion of oxygenated blood containing 30 mg/kg epinephrine. The boluses of blood were delivered through a catheter advanced from the right carotid artery into the ascending aorta. Except for mechanical ventilation and direct current precordial countershock for electrical defibrillation, no other mechanical resuscitation intervention, and specifically no precordial compression, was administered. None of six control animals that received either no retroaortic infusion or right atrial infusion was resuscitated after 4 minutes of untreated ventricular fibrillation. Each of five animals was successfully resuscitated by retroaortic infusion after 4 minutes of untreated cardiac arrest; one was resuscitated after 6 minutes, and none was resuscitated after 8 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Myocardial hypercarbic acidosis reduces cardiac resuscitability.

BACKGROUND: The severity of spontaneous myocardial hypercarbic acidosis during cardiac arrest previously has been predictive of the likelihood of restoring spontaneous circulation. The present study investigated whether hypercarbia itself impairs cardiac resuscitation. Since coronary perfusion pressure is the overriding determinant of cardiac resuscitability, we used a porcine model of cardiac arrest in which coronary perfusion pressure was controlled. METHODS: In 31 domestic pigs anesthetized with pentobarbital, the lungs were mechanically ventilate. Myocardial carbon dioxide tension and hydrogen ion concentration were measured by sensors advanced into the myocardium. After 15 min of untreated ventricular fibrillation, venoarterial extracorporeal circulation was initiated. Animals were randomized to receive a carbon dioxide gas fraction in the extracorporeal perfusate of 0.00, 0.10, 0.30, or 0.50 with oxygen concentration maintained constant at 0.50. Extracorporeal flow was adjusted to maintain a coronary perfusion pressure in the range of 60-80 mmHg, a level of predictive resuscitability. RESULTS: The proportion of animals successfully resuscitated and the proportion of animals maintaining spontaneous circulation for 60 min or longer decreased with increasing perfusate PCO2 and concurrent increases in myocardial CO2 tension in the absence of altered oxygen utilization (P < .01). CONCLUSIONS: Hypercarbia, in this experimental setting, was therefore a quantitative determinant of both myocardial resuscitability and the restoration of spontaneous circulation.

Acidosis↗
PubMed1993

Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation.

OBJECTIVE: To define changes in intramyocardial pH and PCO2 during cardiac arrest and resuscitation. DESIGN: Prospective and observational trial. SETTING: Mammalian research laboratory utilizing a porcine model of cardiac arrest. SUBJECTS: Sixteen domestic pigs. INTERVENTIONS: Ventricular fibrillation was induced by an alternating current delivered to the epicardium. Precordial compression was begun after 3 mins of untreated cardiac arrest and was initially adjusted to produce a coronary perfusion pressure of 10 mm Hg. Electrical defibrillation was attempted after an additional 8 mins of precordial compression. MEASUREMENTS AND MAIN RESULTS: A rapid-response, ion-selective field effect transistor sensor was adapted for measurement of intramyocardial PCO2. Intramyocardial PCO2 progressively increased from 54 to 346 torr (7.2 to 46.1 kPa) during the 11-min interval of cardiac arrest. Intramyocardial hydrogen ion concentrations were simultaneously measured with a glass electrode. The intramyocardial hydrogen ion value increased from 65 nmol/L (pH 7.20) to 441 nmol/L (pH 6.38) over the same interval. The increases in myocardial PCO2 were inversely correlated with coronary perfusion pressure and with the likelihood of successful resuscitation. Within 30 mins after successful cardiac resuscitation, myocardial PCO2 had almost completely returned to prearrest levels. CONCLUSIONS: Striking increases in myocardial PCO2 and hydrogen ion values accompany the global myocardial ischemia of cardiac arrest. The increases in myocardial PCO2, rather than decreases in pH, reflected more precisely the hemodynamic efficacy of the resuscitation effort, correlated inversely with coronary perfusion pressure, and predicted the likelihood of successful resuscitation.

Acidosis, Respiratory↗
PubMed1993

Progressive myocardial dysfunction after cardiac resuscitation.

OBJECTIVE: To investigate left ventricular function by the Langendorff method after successful cardiac resuscitation in rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Adult, male Sprague-Dawley rats. INTERVENTIONS: Myocardial function was investigated in three subsets of isolated, perfused rat hearts that were harvested either before inducing ventricular fibrillation (controls) or at defined intervals after successful resuscitation from ventricular fibrillation. Ventricular fibrillation was induced with an electrode catheter advanced into the right ventricle of 15 mature, mechanically ventilated Sprague-Dawley rats. After an interval of 4 mins of untreated ventricular fibrillation and an additional 5 mins of precordial compression, spontaneous circulation was restored by a direct current, transthoracic countershock. The heart of each animal was then harvested at either 2 or 20 mins after successful cardiac resuscitation. The same model was utilized for harvesting the controls. Animals were randomized to each of the three subsets immediately before induction of cardiac arrest. MEASUREMENTS AND MAIN RESULTS: There was a progressive decrease in myocardial contractility of the isolated, perfused hearts. Mean left ventricular systolic pressure was 128 +/- 8 mm Hg in control animals. In hearts harvested at 2 mins after successful resuscitation, the maximal generated pressure was reduced to 106 +/- 9 mm Hg. When harvested at 20 mins after successful resuscitation, it was reduced to 81 +/- 11 mm Hg. There were corresponding decreases in the mean maximal rate of left ventricular pressure increase (dP/dtmax) from 2880 +/- 110 to 2470 +/- 120 mm Hg/sec at 2 mins and to 1810 +/- 135 mm Hg/sec at 20 mins. These decreases in contractility were associated with striking decreases in myocardial relaxation and compliance. CONCLUSION: These studies, therefore, document progressive systolic and diastolic myocardial dysfunction immediately after successful cardiac resuscitation with restoration of spontaneous circulation.

Animals↗
PubMed1993

Augmented efficacy of external CPR by intermittent occlusion of the ascending aorta.

BACKGROUND: After prolonged cardiac arrest, conventional methods of closed-chest cardiac compression are ineffective. This is primarily because of failure to generate minimal threshold levels of coronary perfusion pressure for cardiac resuscitation. This report introduces a new option for cardiac resuscitation by use of a combination of intermittent ascending aortic balloon occlusion, aortic infusion, and precordial compression to increase the pressure gradient for coronary perfusion. METHODS AND RESULTS: Twenty anesthetized, mechanically ventilated, normovolemic domestic pigs were investigated. A 10F balloon catheter was advanced from the left femoral artery into the ascending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. Precordial compression was initiated after 7 minutes of untreated ventricular fibrillation. The animals were randomized to one of four groups: (1) balloon occlusion with proximal infusion of oxygenated saline, (2) balloon occlusion alone, (3) proximal aortic infusion together with epinephrine without balloon occlusion, and (4) injection of epinephrine without balloon occlusion or proximal infusion. For balloon occlusion, the balloon was inflated for 30 seconds during each minute of cardiopulmonary resuscitation. In the subsets of animals that received infusions, oxygenated saline (30 mL) was injected into the proximal aorta immediately after balloon occlusion. Epinephrine was used in two subsets: It was injected as a bolus in amounts of 30 micrograms/kg into the right atrium at 30 seconds after start of precordial compression and repeated as required to maintain coronary perfusion pressure within the range of 25 to 30 mm Hg. Defibrillation was attempted at 1 minute after start of precordial compression and at 1-minute intervals thereafter. Resuscitation attempts were continued until there was return of spontaneous circulation or for a total of 30 minutes after start of precordial compression. Coronary perfusion pressure generated by precordial compression was significantly increased after balloon occlusion. Each of 10 animals was successfully resuscitated and survived for 48 hours after balloon occlusion whether or not it was combined with infusion. Three of five animals were resuscitated by a combination of infusion and epinephrine in the absence of aortic occlusion, but none survived for 48 hours (P = .02). Only one epinephrine-treated animal was successfully resuscitated and survived for 48 hours in the absence of balloon occlusion or infusion (P < .05). CONCLUSIONS: Ascending aortic balloon occlusion with or without proximal aortic infusion strikingly increased resuscitability and 48-hour survival after cardiac arrest under conditions when conventional methods failed.

Animals↗
PubMed1993

Gastric intramural PCO2 during peritonitis and shock.

OBJECTIVE: To define whether increases in gastric intramural tissue CO2 and H+ increase during experimentally induced peritonitis with circulatory shock as they do under conditions of hemorrhagic shock and cardiac arrest. DESIGN AND SETTING: Peritonitis was induced in Sprague-Dawley rats by cecal ligation and fecal spillage. MEASUREMENTS AND RESULTS: Over an interval of 260 +/- 20 min in 5 animals, there was a progressive reduction in mean aortic pressure from 153 +/- 12 to 40 +/- 20 mm Hg and a decline in cardiac index from 429 +/- 135 to 178 +/- 7 ml/min. This was associated with increases in gastric intramural [H+] from 34 +/- 5 to 217 +/- 93 mmol/L (p = 0.001). Arterial blood lactate content concurrently increased from 0.9 +/- 0.1 to 4.6 +/- 0.7 mmol/L (p = 0.001). Only a late increase in gastric intramural PCO2 from 45 +/- 5 to 128 +/- 38 mm Hg (p = 0.01) was observed. CONCLUSION: In contrast to the gastric acid base changes that accompany hemorrhagic shock, in which there is an early and prominent increase in both PCO2 and [H+] in close relationship to decreases in cardiac output and arterial pressure, there was a prominent increase in gastric [H+] but only a delayed rise in gastric intramural PCO2. Arterial blood lactate and central venous oxygen saturation were earlier indicators of perfusion failure. Since the bicarbonate concentration in the stomach wall was substantially greater than that of simultaneously measured arterial blood, this has bearing on the current clinical method of gastric tonometry which assumes that arterial blood bicarbonate is equivalent to gastric wall bicarbonate.

Animals↗
PubMed1992

Cardiac anaphylaxis in the Sprague-Dawley rat.

Anaphylactic shock was induced in pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats that had been sensitized 21 days earlier to crystallized ovalbumin. The sensitization was confirmed by passive cutaneous anaphylaxis test. Antigen challenge produced an immediate reduction in mean aortic pressure from 168 to 67 mm Hg within 1 minute after intravenous injection of ovalbumin. Plasma histamine increased from 4.5 to 128 ng/ml within 5 minutes after injection of antigen. There were no changes in airway or esophageal pressures after antigen challenge. Left ventricular diastolic pressure was increased, and contractility, as measured by the rate of change of left ventricular pressure (dP/dt), was decreased over an interval exceeding 90 minutes. When isolated, constant flow--perfused hearts from sensitized Sprague-Dawley rats were challenged with antigen, decreases in left ventricular function were observed associated with decreased positive and negative maximum rate of change of left ventricular pressure (dP/dtmax). This experimental model in the rat therefore demonstrated selective myocardial impairment with reduced inotropism and lusitropism after anaphylaxis.

Anaphylaxis↗
PubMed1991

Reversible impairment of myocardial contractility due to hypercarbic acidosis in the isolated perfused rat heart.

BACKGROUND AND METHODS: Striking increases in PCO2 of the myocardium have recently been documented during cardiac arrest. The purpose of the present study was to investigate selective effects of hypercarbia as distinct from acidosis on left ventricular contractile function and oxygen utilization. An isolated, spontaneously beating rat heart preparation was utilized. The perfusate was equilibrated with gases containing 5%, 10%, 20%, and 30% CO2. In a subset of experiments, the [H+] was adjusted independently of PCO2 by decreasing the concentration of HCO3-. RESULTS: When the PCO2 of the perfusate was progressively increased from 36 to 146 torr (4.8 to 29.5 kPa), the left ventricular systolic pressure (LVSP) generated by the isolated heart and the maximum rate of pressure change in the left ventricle (dP/dt) were decreased to 20% of their control values. However, comparable acidosis in the absence of hypercarbia produced only minimal decreases in the LVSP or dP/dt such that contractility remained at greater than or equal to 88%. Increases in the perfusate PCO2 but not in the perfusate H+ were highly correlated with decreases in both myocardial contractility and oxygen consumption (r2 = .88). CONCLUSION: Hypercarbia rather than acidosis accounts for decreased contractility and oxygen utilization in the isolated perfused rat heart.

Acidosis↗
PubMed1991

Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation.

BACKGROUND: Epinephrine has been shown to impair pulmonary excretion of CO2 during resuscitation. This phenomenon was investigated in a rodent model of cardiac arrest and conventional resuscitation. METHODS AND RESULTS: The effects of racemic epinephrine were compared with the selective alpha 1-agonist methoxamine and with saline placebo during cardiac resuscitation in 15 Sprague-Dawley rats mechanically ventilated with gas containing 70% oxygen. Epinephrine and methoxamine but not saline placebo significantly increased coronary perfusion pressure from approximately 32 to 55 mm Hg. Following epinephrine, end-tidal PCO2 decreased from approximately 10 to 5 mm Hg. This was associated with a time-coincident decrease in PaO2 from approximately 130 to 74 mm Hg and an increase in PaCO2 from approximately 26 to 40 mm Hg. These changes indicated increases in alveolar dead space ventilation concomitant with increases in pulmonary arteriovenous admixture. No such effects were observed after administration of either methoxamine or saline placebo. Each of the 15 rats was successfully resuscitated. However, a significantly larger number of transthoracic countershocks were required after epinephrine compared with methoxamine or placebo before return of spontaneous circulation. CONCLUSIONS: Epinephrine induced ventilation/perfusion during cardiopulmonary resuscitation as a result of redistribution of pulmonary blood flow.

Animals↗