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Biomedical subjects

C F Babbs

Publications and source records attributed to C F Babbs.

At least 73 records · Page 4Linked to original sources
PubMed1988

Reperfusion injury of postischemic tissues.

Reperfusion injury, occurring when blood circulation is restored to previously ischemic tissues, is now demonstrable as a pathophysiologic entity distinct from the primary ischemic injury that develops during ischemia per se. The primary pathogens that cause reperfusion injury are thought to be partially reduced oxygen species, including superoxide radicals, hydrogen peroxide, and hydroxyl radicals, which initiate lipid peroxidation and other deleterious oxidation reactions during the reperfusion period. Antioxidant drugs, given at the end of ischemia or at the very onset of reperfusion, can improve the postischemic function of isolated organs and the survival of intact animals subject to a cycle of circulatory arrest and reperfusion, suggesting that reperfusion injury is both a real and a preventable pathophysiologic entity.

Animals↗
PubMed1987

Colorimetric assay for methanesulfinic acid in biological samples.

We describe a simple colorimetric method to measure 30 to 300 microM concentrations of sulfinic acids in biologic samples. The procedure employs the coupling reaction of an aromatic diazonium salt (Ar--N = N+) with the sulfinic acids (RSOOH) to produce a colored diazosulfone derivative (Ar-N = N-SOOR), which can be selectively extracted into an organic solvent. Linearity as well as noninterference by liver homogenate, phenols, amines, and thousandfold or greater excesses of sulfate, thiol, and dimethyl sulfoxide is demonstrated. Sensitivity of the method is about 10 nmol per sample. Because methanesulfinic acid is the principal product of the action of hydroxyl radicals upon dimethyl sulfoxide, and because intact animals can tolerate dimethyl sulfoxide in millimolar concentrations, the method may prove widely useful for detecting the involvement of hydroxyl radicals in pathologic processes in vivo.

Animals↗
PubMed1987

Hemodynamic mechanisms in CPR: a theoretical rationale for resuscitative thoracotomy in non-traumatic cardiac arrest.

Experimental work over the past decade has revealed three distinct mechanisms for generating artificial circulation during cardiac arrest and resuscitation. To isolate these mechanisms and study them in pure form, and in particular to characterize circulation during open vs. closed chest cardiopulmonary resuscitation (CPR), we developed an electrical model of the human circulatory system. Heart and blood vessels were modeled as resistive-capacitive networks, pressures in the chest, abdomen, and vascular compartments as voltages, blood flow as electric current, blood inertia as inductance, and the cardiac and venous valves as diodes. External pressurization of thoracic and abdominal vessels, as would occur in CPR, was simulated by application of half-sinusoidal voltage pulses. Simulations included two modes of creating artificial circulation: the cardiac pump mechanism, in which the atria and ventricles of the model were pressurized simultaneously, as occurs during open chest cardiac massage, and the thoracic pump mechanism, in which all intrathoracic elements of the model were pressurized simultaneously, as is likely to occur in closed chest CPR. The two mechanisms were compared for the same peak applied pressure (80 mmHg). Pure cardiac pump CPR generated near normal systemic perfusion pressures throughout the compression cycle. Pure thoracic pump CPR generated much lower systemic perfusion pressure only during the diastolic phase of the compression cycle. Simulation of cardiac compression at rates from 40 to 100/min produced total flows of 2500-3300, myocardial flows of 150-250 and cranial flows of 600-800 ml/min, depending on the compression rate. In contrast, thoracic pump CPR produced a total flow of approx. 1200, myocardial flow of 70, and cranial flow of 450 ml/min, independently of the compression rate. Direct cardiac compression is an inherently superior hemodynamic mechanism, because it can generate greater perfusion pressure throughout the compression cycle. If one presumes that improved blood flow during CPR is the key to more successful resuscitation, then it is reasonable to conclude that direct heart massage is the most effective available way to achieve this end.

Computer Simulation↗
PubMed1987

Comparison of mechanical techniques of cardiopulmonary resuscitation: survival and neurologic outcome in dogs.

Three currently available mechanical devices for cardiopulmonary resuscitation (CPR) were compared using a canine cardiac arrest model. Twenty-four-hour survival without neurologic deficit was the goal. A group of 30 large mongrel dogs was divided equally among Thumper CPR, simultaneous compression and ventilation (SCV) CPR, and vest CPR. Ventricular fibrillation was induced electrically, and after 3 minutes of no intervention, one of the three types of mechanical CPR was performed for 17 minutes. SCV CPR and vest CPR produced significantly greater aortic and right atrial systolic pressures than Thumper CPR (P less than .03). The SCV CPR technique also produced significantly higher aortic diastolic pressure and right atrial diastolic pressure than either of the other methods (P less than .03). However, coronary perfusion pressure was not different among the three mechanical methods. No differences in immediate resuscitation, 24-hour survival, or neurologic deficit scores at 24 hours were found. Neither SCV nor the vest techniques of CPR appear better for survival or neurologic outcome than standard cardiopulmonary resuscitation performed with the Thumper.

Animals↗
PubMed1987

Protection from reperfusion injury in the isolated rat heart by postischaemic deferoxamine and oxypurinol administration.

A Langendorff isolated rat heart preparation was used to determine the effect of oxypurinol, a xanthine oxidase inhibitor, and deferoxamine, an iron binding agent, on the extent of myocardial reperfusion injury after 60 minutes of ischaemia. Thirty rats were divided into three groups of 10, and an isolated heart preparation made from each rat. The isolated hearts were perfused for 15 minutes with a modified Krebs-Henseleit perfusate solution to permit stabilisation of the preparation. Each heart was then subjected to 60 minutes of total ischaemia at 37 degrees C followed by 60 minutes of reperfusion with either saline treated perfusate, oxypurinol treated perfusate (1.3 mmol.litre-1), or deferoxamine treated perfusate (0.61 mmol.litre-1). Reperfusion injury was assessed by the total amount of creatine phosphokinase released into the perfusate, by changes in myocardial vascular resistance, and by morphological examination. The saline treated group released significantly more creatine phosphokinase into the perfusate than either the oxypurinol treated group (p less than 0.05) or the deferoxamine treated group (p less than 0.05). The mean vascular resistance increased for all groups during the 60 minutes of reperfusion compared with that just before ischaemia but was significantly greater in the saline treated group than in the drug treated groups (p less than 0.01). Ultrastructural examination of a randomly selected heart from each group after 60 minutes of reperfusion showed pronounced attenuation of mitochondrial and endoplasmic reticulum swelling, increased maintenance of membrane integrity, and diminished separation of myofilaments in the oxypurinol treated and deferoxamine treated hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The effect of carbon dioxide, lidoflazine and deferoxamine upon long term survival following cardiorespiratory arrest in rats.

This study examined the effect of carbon dioxide, lidoflazine and deferoxamine therapy upon the 10-day survival incidence and subsequent neurologic function of rats subjected to 7 min of cardiorespiratory arrest with resuscitation. Cardiac arrest (asystole) was induced at time zero by injection of cold, 1% KCl into the left ventricle of ketamine-anesthetized rats pretreated with succinylcholine. Positive pressure ventilation was discontinued at time zero. Cardiopulmonary resuscitation (CPR) was begun at 7 min, and animals with return of spontaneous circulation were entered into the study. Twenty treated rats were ventilated for 1 h with 7% carbon dioxide-93% oxygen and given lidoflazine (2.0 mg/kg, i.v.) and deferoxamine (50 mg/kg, i.v.) 5 min after CPR. Twenty control rats were ventilated for 1 h with 100% oxygen and given lidoflazine vehicle and deferoxamine vehicle. Lidoflazine treatment (1.0 mg/kg) for the treated group, or lidoflazine vehicle for the control group, was repeated at 8 h postresuscitation. At 2 days postresuscitation, 75% of treated rats vs. 25% of control rats were alive (CHI2 = 10.0, d.f. = 1, P less than 0.01), and at 10 days, 60% of treated rats vs. 25% of control rats were alive (CHI2 = 5.01, d.f. = 1, P less than 0.05). There was no detectable neurologic deficit among survivors in either group at 15 days. The combination of carbon dioxide, lidoflazine and deferoxamine, administered after return of spontaneous circulation, is a simple and easily administered treatment regimen that improves the survival incidence without neurologic deficits in this animal model of cardiorespiratory arrest and CPR.

Animals↗
PubMed1986

Neurologic outcome following successful cardiopulmonary resuscitation in dogs.

Successful cardiopulmonary resuscitation necessitates that both myocardial and central nervous system function be restored with minimal long-term damage. Recent resuscitation research has emphasized minimizing neurologic damage during and after cardiopulmonary resuscitation. However, whether neurologic damage is a major cause of death or morbidity following successful cardiopulmonary resuscitation is unknown. This study examined the role of neurologic injury as a cause for morbidity and mortality following cardiopulmonary resuscitation, and if parameters used successfully during resuscitation for assessing the potential for myocardial salvage, could also be used to predict neurologic outcome. Eighty-eight mongrel dogs underwent 3 min of untreated ventricular fibrillation and either 15 or 17 min of cardiopulmonary resuscitation. Twenty-four hour survivors were evaluated with a neurologic deficit scoring system. Thirty-one percent of these animals were never resuscitated. Twenty-eight percent were resuscitated, but expired prior to 24 h. Approximately half of those who expired after resuscitation died from apparent neurologic sequellae. Forty-one percent of the 88 animals survived for 24 h. Two-thirds of these survivors were completely neurologically normal, while one-third were neurologically impaired. Hemodynamic parameters useful in assessing cardiovascular prognosis were not helpful in predicting neurologic outcome. Hence, although the majority of resuscitated animals did not suffer neurologic damage, up to one-third did exhibit neurologic impairment following resuscitation. Neurologic injury is also a major contributor to early death following successful resuscitation. Hemodynamic parameters of cardiovascular recovery do not predict neurologic outcome after prolonged cardiopulmonary resuscitation.

Animals↗
PubMed1986

Effect of allopurinol and dimethylsulfoxide on long-term survival in rats after cardiorespiratory arrest and resuscitation.

The effects of allopurinol and dimethylsulfoxide (DMSO) upon reperfusion injury were tested in separate studies that utilized a rat model of cardiorespiratory arrest and resuscitation. The rats were subjected to 7 minutes of arrest followed by resuscitation, and then were alternately assigned to either a drug-treated group or a vehicle-treated group (n = 22 for all groups). Drug treatment was given after the return of spontaneous circulation, and survival was monitored for a ten-day period. Study 1 utilized DMSO (50% solution, 1 ml/kg) as the test drug and saline solution as the vehicle. The percentages of surviving rats in the DMSO-treated and vehicle-treated groups were never statistically significantly different. There were 59% (13/22) of the DMSO-treated rats and 63% (14/22) of the vehicle-treated rats alive at one hour after resuscitation. Survival rates decreased to 18% (4/22) of DMSO-treated rats and 22% (5/22) of vehicle-treated rats on days 3 through 10. Allopurinol (25 mg/kg) was the test drug in study 2, and 0.18-M sodium hydroxide was the vehicle. The survival rate of resuscitated rats was statistically significantly greater at two days in the drug-treated group (68%, 15/22) than in the vehicle-treated group (36%, 8/22) (chi 2 = 4.46, df = 1, P less than 0.05). The difference increased to a maximum of 68% (15/22) of the allopurinol-treated group versus 27% (6/22) of the vehicle-treated group at days 7 and 8 (chi 2 = 7.38, df = 1, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1986

Effect of deferoxamine on late deaths following CPR in rats.

The iron-chelating agent deferoxamine was studied in an animal model as postresuscitation therapy to prevent late deaths and brain damage following total circulatory arrest and resuscitation. Cardiorespiratory arrest was induced by injection of cold, 1% KCl into the left ventricles of ketamine-anesthetized rats pretreated with succinylcholine, and by discontinuation of positive pressure ventilation. CPR was begun after six minutes, and animals with return of spontaneous circulation were entered into the study. Within five minutes after return of spontaneous circulation, treated animals received deferoxamine (50 mg/kg, IV). At ten days, 16 of 25 (64%) of treated animals had survived without neurologic deficit, compared to nine of 25 (36%) of controls (chi square = 3.92, P less than .05). Chelation of intracellular iron by deferoxamine may have prevented free-radical-mediated reactions that led to late deaths in control animals.

Animals↗
PubMed1986

CPR-induced trauma: comparison of three manual methods in an experimental model.

Cardiopulmonary resuscitation (CPR) often results in traumatic injury to the patient. Differences in CPR-induced trauma among various forms of manual, external CPR, however, are unknown. We compared CPR-induced trauma among manual standard (STD) CPR at 60 compressions per minute; high-impulse compression (HIC) CPR at 120 compressions per minute; and interposed abdominal compression (IAC) CPR at 60 compressions per minute. A large (24 +/- 3 kg) mongrel canine model was used. Ten animals were assigned to each type of CPR. Each received 17 minutes of CPR, applied to produce the best possible coronary perfusion pressure without obviously damaging the dog. Defibrillation was attempted at 20 minutes. Necropsy was performed at the time of death or after sacrifice at 24 hours. Careful postmortem examination of the thorax, lungs, heart, abdomen, and great vessels was performed. A semiquantitative trauma score of 0 to 5 was assigned to each area with a possible maximal score of 25. There was no difference in trauma scores among STD (6.4 +/- 1.5), HIC (9.4 +/- 1.4), and IAC (8.1 +/- 1.3) methods. No significant correlation was found between the method of CPR and the different types of trauma. Specifically, IAC did not produce an increase in liver lacerations nor did HIC produce a significant increase in thoracic or pulmonary injuries. Six of 20 initially resuscitated animals expired during the 24-hour follow-up period due to CPR-induced injuries. Four of these six had extensive pulmonary trauma, including pulmonary hemorrhage or edema. Liver lacerations were the second most lethal injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1986

Twenty-four hour survival in a canine model of cardiac arrest comparing three methods of manual cardiopulmonary resuscitation.

Two new modifications of manual cardiopulmonary resuscitation, high impulse compression at a rate of 120/min and interposed abdominal compression at a rate of 60/min, have been reported to produce better hemodynamic responses than standard cardiopulmonary resuscitation at 60/min. However, the effect of these two new methods on initial resuscitation success and 24 hour survival is unknown. In this study, 30 mongrel dogs were divided into three equal groups, each treated with one of three types of manual cardiopulmonary resuscitation. Ventricular fibrillation was induced electrically in morphinized, endotracheally intubated dogs emerging from halothane anesthesia. After 3 minutes of circulatory arrest without intervention, one of the three techniques of manual cardiopulmonary resuscitation was begun, and continued for 17 minutes. Defibrillation was performed at 20 minutes. Successful resuscitation was defined as a mean arterial blood pressure of at least 60 mm Hg, without chest compressions, 10 minutes after the initial defibrillation attempt. Intensive care was provided for 2 hours, including hemodynamic and respiratory monitoring, and drug intervention when required. Twenty-four hour survival and neurologic deficit were used as critical measures of outcome. Ten of 30 animals survived 24 hours with a mean neurologic deficit score of 5% (normal = 0, brain dead = 100). There was no difference in initial resuscitation success, 24 hour survival or neurologic deficit of the survivors among the three manual cardiopulmonary resuscitation methods. Aortic diastolic and calculated coronary perfusion pressures were similar for all three methods. Well performed standard manual cardiopulmonary resuscitation is as effective as these modified versions (high impulse compression and interposed abdominal compression) when compared in the same animal model.

Animals↗
PubMed1986

Abdominal binding and counterpulsation in cardiopulmonary resuscitation.

During the past 15 years, many different studies have documented improved blood pressure and blood flow above the diaphragm when some type of abdominal compression was added to conventional CPR, either in animals or in humans. Rhythmically interposed abdominal compressions seem to provide even greater hemodynamic benefit than continuous abdominal binding. Both total flow and the distribution of flow to vital organs above the diaphragm are improved, while the chances of liver entrapment and damage during chest compression are reduced. The technique of interposed abdominal compression can be performed with the bare hands of a second or third rescuer. It requires no special equipment, and could be easily incorporated into existing training programs for basic rescuers. In this sense the technique may constitute a logical evolution in basic life support, if subsequent clinical research confirms that it improves outcome.

Abdomen↗
PubMed1986

Cardiopulmonary resuscitation with interposed abdominal compression.

The addition of interposed abdominal compressions (IACs) to otherwise standard CPR enhances artificial circulation both in anesthetized dogs with ventricular fibrillation and in electrical models of the circulation that demonstrate fundamental mechanisms generating flow. Manual abdominal compressions cause both central aortic and central venous pressure pulses but, because of differences in venous and arterial capacitance, the former are usually greater than the latter. Thus mean perfusion pressure is enhanced. Limited clinical studies confirm that IAC-CPR can improve perfusion pressures in humans, and reported complications of the technique are rare in animals and man. However, no study has demonstrated that IAC-CPR improves either short- or long-term survival after cardiac arrest in man. Accordingly, the method remains experimental and cannot be recommended for basic life support at the present time.

Abdomen↗
PubMed1985

Hyperthermia-induced vascular injury in normal and neoplastic tissue.

The sequential morphologic alterations in normal skeletal muscle in rats, Walker 256 tumors in rats, and transmissible venereal tumors (TVT) in dogs following microwave-induced hyperthermia (43 degrees C and 45 degrees C for 20 minutes), were studied by histologic and ultrastructural examination. Normal muscle and Walker 256 tumors showed edema, congestion, and hemorrhage at 5 minutes post-heating (PH), followed by suppuration, macrophage infiltration, and thrombosis at 6 and 48 hours PH, and finally by regeneration and repair by 7 days PH. Vascular endothelial damage and parenchymal degeneration were present 5 minutes PH. Progressive injury occurred for at least 48 hours PH. Two hyperthermia treatments separated by a 30- or 60-min cooling interval, were applied to Walker 256 tumors in a subsequent study. Increased selective heating of tumor tissue versus surrounding normal tissue, and increased intratumoral steady state temperatures were found during the second hyperthermia treatment. Canine TVTs were resistant to hyperthermia damage. These results suggest that vascular damage contributes to the immediate and latent cytotoxic effects of hyperthermia in normal tissue and some types of neoplastic tissue, and that selective heating of neoplastic tissue occurs in tumor tissue with disrupted microvasculature.

Animals↗