Mean Pulmonary Blood Pressure Research Articles

Effects of Insulin on the Resuscitation by Epinephrine for Bupivacaine-Induced Cardiovascular Depression in Dogs

Background: Because of the difficulty of resuscitation caused by bupivacaine-induced cardiotoxicity, the choice of resuscitation medication is still unclear. We investigated whether insulin can improve outcomes of resuscitation by epinephrine from bupivacaine-induced cardiovascular collapse. Methods: Twenty-four mongrel dogs were randomly allocated to one of the two groups: an EPI group (n = 12), and an EPI + RI group (n = 12). Sixty minutes after induction of general anesthesia, baseline measurement of hemodynamic parameters and arterial blood gas tension was performed. Bupivacaine infusion was started at a rate of 0.5 mg/kg/min and kept until mean arterial blood pressure fell below 40 mmHg and heart rate 40 beats per minute. At this point, bupivacaine infusion was stopped and resuscitation was started, with epinephrine in EPI group and epinephrine combined with regular insulin in EPI + RI group. Results: Bupivacaine infusion caused significant decreases in mean arterial blood pressure, heart rate, cardiac output, and systemic vascular resistance and increases in mean pulmonary blood pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance, and central venous pressure. The recovery rate of EPI + RI group (8/12) was higher than that of EPI group (2/12). Conclusions: Combined administration of epinephrine and regular insulin improves outcomes of resuscitation of bupivacaine- induced cardiovascular collapse. Therefore, we believe that prompt administration of insulin should be strongly considered in case of bupivacaine-induced cardiotoxicity.

Effect of Hemoperfusion Using Polymyxin B-Immobilized Fiber on IL-6, HMGB-1, and IFN Gamma in a Neonatal Sepsis Model

To evaluate effects of polymyxin B direct hemoperfusion (PMX-DHP) on a neonatal sepsis cecal ligation and perforation (CLP) model, in 24 anesthetized and mechanically ventilated 3-d-old piglets, 16 were assigned to CLP and an arteriovenous extracorporeal circuit from 3 h until 6 h post-CLP, with a PMX-column in PMX-DHP-treated group (8 piglets) and 8 as sham. Plasma lipopolysaccharide (LPS) was measured at before CLP and at 3 and 9 h. Changes in mean systemic blood pressure (mSBP), mean pulmonary blood pressure, serum IL-6, tumor necrosis factor alpha, interferon gamma, and highly mobile group-1 box protein were measured before CLP and at 1, 3, 6, and 9 h. LPS was lower in the sham and PMX-DHP groups than in the control at 9 h. The mSBP was higher in the sham and PMX-DHP groups than in the control at both 6 h. IL-6 was lower in the sham and PMX-DHP groups than in the control at 6 h. HMGB-1 was lower in the PMX-DHP group than in the control at 6 h. IFN-gamma was only detected in the control group at 9 h. Survival times in the PMX-DHP group were longer than in the control. Thus, PMX-DHP improved septic shock in a neonatal septic model.

Atrial natriuretic peptide as a preload depressor in acute renal failure secondary to congestive heart failure

The present study was undertaken to verdy the hypothesis that infusion of atrial natriuretic peptide (ANP) might lower preload and be beneficial in the treatment of pulmonary congestion even without a diuresis in patients with acute renal failure (ARF) secondary to severe congestive heart failure (CHF). We studied 22 patients with ARF secondary to CHF. The mean age of the patients (14 men and 8 women) was 72 years (range 36 to 85 years). Seven of the patients had dilated cardiomyopathy, ten had ischemic heart disease, and five had valvular heart disease. ANP was infused intravenously and the following data before and 1 hour after the start of ANP infusion were recorded; urinary output, systemic blood pressure (SBP), pulmonary blood pressure (PBP), right atrial pressure (RAP), cardiac index (CI), heart rate (HR), and arterial blood oxygen pressure. Diastolic PBP were employed as plumonary capillary wedge pressure. Urinary output did not change. Mean SBP decreased from 92 to 85 mmHg (p < 0.05), and mean PBP decreased from 34 to 28 mmHg (p < 0.01). Mean RAP decreased from 11 to 9 mmHg (p < 0.01) and diastolic PBP decreased from 25 to 19 mmHg (p < 0.01). HR did not change significantly and CI increased 2.4 to 2.5 mi/min/m2 (p < 0.05). Arterial blood oxygen partial pressure increased significantly from 71 to 82 mmHg (p < 0.05). In conclusion, ANP decreased and improved arterial blood oxygen partial prissure, though diuretic response to ANP is attenuated in ARF secondary to CHE. Infusion of ANP will be very beneficial in cases in which dyspnea and pulmonary edema due to elevation of preload are the principal clinical problems.

Cardiorespiratory effects of induction and maintenance of anesthesia with ketamine-midazolam combination, with and without prior administration of butorphanol or oxymorphone

Summary Cardiorespiratory effects of an iv administered bolus of ketamine (7.5 mg/kg of body weight) and midazolam (0.375 mg/kg) followed by iv infusion of ketamine (200 μg/kg/min) and midazolam (10 μg/kg/min) for 60 minutes was determined in 6 dogs. Ketamine-midazolam combination was administered to dogs on 3 occasions to determine effects of prior administration of iv administered saline solution (1 ml), butorphanol (0.2 mg/kg), or oxymorphone (0.1 mg/kg). The infusion rate of ketamine and midazolam was decreased by 25% for anesthetic maintenance after opioid administration. There were no significant differences in cardiorespiratory variables after saline solution or butorphanol administration; however, oxymorphone caused significant (P &lt; 0.05) increases in mean arterial blood pressure, systemic vascular resistance, and breathing rate. Bolus administration of ketamine-midazolam combination after saline solution caused significant (P &lt; 0.05) increases in heart rate, mean arterial blood pressure, cardiac index, mean pulmonary blood pressure, venous admixture, and significant decreases in stroke index, pulmonary capillary wedge pressure, arterial and mixed venous oxygen tension, arterial oxygen content, and alveolar-arterial oxygen gradient. Opioid administration was associated with significantly (P &lt; 0.05) lower values than was saline administration for heart rate, mean arterial blood pressure, and arterial and mixed venous pH and with higher values for stroke index, pulmonary capillary wedge pressure, and arterial and mixed venous carbon dioxide tension. Prior oxymorphone administration resulted in the highest (P &lt; 0.05) values for mean pulmonary blood pressure, venous admixture, and arterial and mixed venous carbon dioxide tension, and the lowest values for arterial oxygen tension, and arterial and mixed venous pH. Each treatment provided otherwise uncomplicated anesthetic induction, maintenance, and recovery. Time to extubation, sternal recumbency, and walking with minimal ataxia was similar for each treatment.

Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis

The role of reactive oxygen metabolites in extrapancreatic organ dysfunction associated with acute hemorrhagic pancreatitis was studied in dogs. Experimental pancreatitis was induced by the intraductal infusion of activated trypsin and taurocholate. Cardiac output, pulmonary and systemic blood pressure, pulmonary wedge pressure, central venous pressure, heart rate, blood gases and serum amylase were measured. Cardiac index, pulmonary and systemic vascular resistance, and the right and left stroke work were calculated. Systemic arterial and venous blood pressure and cardiac index gradually declined over 6 hr, while pulmonary mean blood pressure and pulmonary vascular resistance increased. Pretreatment of pancreatitis with catalase and superoxide dismutase prevented the rise in mean pulmonary blood pressure, moderated the rise in pulmonary vascular resistance, and decreased the rate and extent of the fall in cardiac index. These data suggest that reactive oxygen metabolites may play some role in the extraabdominal organ manifestations of acute pancreatitis.

Ventricular outflow dynamics in the lizard, Varanus niloticus: responses to hypoxia, hypercarbia and diving.

ABSTRACT Blood flow and blood pressure have been measured in the right aorta and left pulmonary artery of the semi-aquatic lizard, Varanus niloticus, during normal breathing, during hypercarbic and hypoxic breathing and during voluntary diving. Mean pulmonary blood pressure during normal breathing was 19 · 5 ± 2 · 0 cmH2O while right aortic pressure was 118 · 0± 3·0 cmH2O. The high systemic blood pressure and high ratio of systemic to pulmonary vascular resistance (4·0−6·0) stand out among reptiles and approach values in homeotherm vertebrates. Pulmonary pressure rise preceded right aortic pressure rise by 120 msec at a heart rate of 25/min. Pulmonary ejection lasted 50% of the cardiac cycle compared to 25 % for aortic ejection during normal breathing. CO2 breathing increased right aortic vascular resistance by 120% while pulmonary resistance increased moderately by 30%. Carotid vascular resistance decreased during CO2 breathing. The pulmonary blood pressure increase was however much higher than the systemic, but at no time did systemic and pulmonary blood pressures overlap. Hypoxic breathing increased pulmonary blood pressure to 36·0 ± 4·0 cmH2O while right aortic pressure fell to 100·0± 10·0 cmH2O. Ejection time remained unchanged in the right aorta while pulmonary flow became continuous. Overall pulmonary vascular resistance increased markedly while systemic resistance changed little. Voluntary diving increased pulmonary blood pressure while the systemic blood pressure fell markedly. The results obtained are discussed in the light of ventricular outflow distribution in reptiles. Directional shunting of blood inside the heart of V. niloticus during cardiac systole must be reduced or absent. Intracardiac shunting during cardiac filling or by systolic residual volumes is small, placing varanid lacertilians haemodynamically closer to homoetherm vertebrates than other reptiles studied.