PubMed Health⌕ Search

Biomedical subjects

W Stezoski

Publications and source records attributed to W Stezoski.

16 recordsLinked to original sources
PubMed2001

The role of the gut in the pathogenesis of death due to hyperthermia.

Pathologic data from the gastrointestinal tract in heat-stroke victims, although documented, are confusing. The object of this study was to document the gastrointestinal changes observed during induced total body hyperthermia (42 degrees C) followed by cooling. An established heat-stroke model was used in a university animal laboratory. Group A underwent immersion hyperthermia for 1 hour, followed by cooling to normothermia. Group B underwent hyperthermia to cardiac arrest, followed by resuscitation plus cooling to normothermia. The postmortem findings in the gastrointestinal tract were evaluated. In group A, several hours after return to normothermia and stable vital signs, delayed secondary deterioration with massive gastrointestinal bleeding occurred. The postmortem findings revealed bleeding into the whole intestine and serosanguineous fluid in the peritoneal cavity. In group B, an adynamic gut was observed after 165 +/- 21 minutes (range 125-174) of heating when mean arterial pressure (MAP) decreased to 38 +/- 21 mm Hg (range 30-70). Cardiac arrest occurred at 178 +/- 26 minutes (range 140-208) of immersion. Eight monkeys could be resuscitated to spontaneous circulation with return of normal gut motility, then they rearrested at 158 +/- 68 minutes (range 45-228). The postmortem findings resembled those in group A. The Postmortem findings in the four monkeys in which restoration of spontaneous circulation failed, revealed only some intestinal wall edema and occasional petechial hemorrhages. It is concluded that after a hyperthermic event, tissue injury continues to develop. The pathologic findings are related to the time lapse between hyperthermia, cooling, and death. The similarity to the descriptions of septic shock, multiple organ failure, and the gut reperfusion syndrome is striking. An immunologic response as a mechanism for all these syndromes is discussed.

Animals↗
PubMed1995

Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock.

BACKGROUND: Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, long-term studies evaluating the consequences of fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effects of deliberate hypotension in the treatment of uncontrolled hemorrhage. STUDY DESIGN: Uncontrolled hemorrhagic shock was produced in 40 rats by a preliminary bleed (3 mL per 100 g) followed by 75 percent tail amputation. Experimental design consisted of three phases: a "prehospital phase" (90 minutes of uncontrolled bleeding with or without treatment with lactated Ringer's [LR] solution), followed by a "hospital phase" (60 minutes, including control of hemorrhage and fluid resuscitation including blood), and a three day observation phase. Forty rats were studied in four treatment groups (ten rats per group). Group 1 consisted of untreated controls (no resuscitation). Group 2 had no fluid during the prehospital phase. Group 3 had prehospital resuscitation to a mean arterial pressure (MAP) of 40 mm Hg with LR, and group 4 had prehospital resuscitation to MAP of 80 mm Hg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mm Hg and hematocrit of 30 percent in the hospital phase. RESULTS: All rats in group 1 (untreated) died within 2.5 hours. Five rats in group 2 (no prehospital FR) survived 90 minutes; however, only one survived three days. In group 3, all ten rats survived 2.5 hours and six survived three days. In group 4, eight rats died within 90 minutes, but none survived long-term. Blood loss (mL per 100 g) for each group was 3.75 0.6 for group 1, 3.35 0.1 for group 2, 4.15 0.8 for group 3, and 8.45 0.6 for group 4, (p < 0.05, group 4 compared with groups 1, 2, and 3). CONCLUSIONS: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality. Hypotensive resuscitation resulted in less acidemia and improved long-term survival.

Animals↗
PubMed1993

The effect of resuscitative moderate hypothermia following epidural brain compression on cerebral damage in a canine outcome model.

A canine model of temporary epidural cerebral compression and standardized intensive care was developed to evaluate the effect of resuscitative (postinsult) moderate systemic hypothermia. A balloon was inflated over the temporal region to maintain contralateral intraventricular pressure (IVP) at 62 mm Hg for 90 minutes. For a 66-hour period after initiation of brain compression, the intubated dogs received controlled ventilation and standard intensive care. From 66 to 90 hours postinjury, the extubated dogs were evaluated as to functional outcome. Morphological brain damage was evaluated at 90 hours or earlier if brain death occurred. Eight dogs in a control group were maintained at a body of temperature of 38 degrees C. Eight treated dogs had core body temperature reduced by surface cooling starting 15 minutes after balloon inflation, first to 31 degrees C for 5 hours and then to 35 degrees C from 5 to 62 hours after insult. Intraventricular pressure increased to 20 mm Hg or greater in the control group at a mean of 2.9 hours (range 2 to 4 hours) following the insult, and in the hypothermic group at a mean of 14.8 hours (range 5 to 30 hours)--that is, during the time period when the body temperature was 35 degrees C, not 31 degrees C (p = 0.01). There was no difference in peak pressures between the two groups. Brain death occurred in four of the eight dogs in the normothermic group at 18, 24, 24, and 48 hours (mean +/- standard deviation 28 +/- 13 hours) and in three of the eight in the hypothermic group at 27, 42, and 45 hours (mean 38 +/- 10 hours) (not significant). The animals surviving 90 hours (four in the normothermic and five in the hypothermic group) were neurologically near normal. The total mean macroscopically damaged brain volume was 2584 +/- 1890 cu mm in the normothermic versus 765 +/- 611 cu mm in the hypothermic group (p = 0.03). The mean necrotic volume was 741 +/- 599 cu mm in the normothermic versus 263 +/- 346 cu mm in the hypothermic group (p = 0.07). Microscopically, the damaged regions consisted of ischemic neurons, reactive glia, edema, vascular endothelial hypertrophy, and erythrocyte extravasation. It is concluded that, in this model, immediate postinsult hypothermia of 31 degrees C (not 35 degrees C) for 5 hours prevents a rise in IVP and significantly decreases cerebral tissue damage, but does not prevent brain herniation during rewarming.

Animals↗
PubMed1992

Dynamic heterogeneity of cerebral hypoperfusion after prolonged cardiac arrest in dogs measured by the stable xenon/CT technique: a preliminary study.

After prolonged cardiac arrest and reperfusion, global cerebral blood flow (gCBF) is decreased to about 50% normal for many hours. Measurement of gCBF does not reveal regional variation of flow or permit testing of hypotheses involving multifocal no-flow or low-flow areas. We employed the noninvasive stable Xenon-enhanced Computerized Tomography (Xe/CT) local CBF (LCBF) method for use in dogs before and after ventricular fibrillation (VF) cardiac arrest of 10 min. This was followed by external cardiopulmonary resuscitation (CPR) and control of cardiovascular pulmonary variables to 7 h postarrest. In a sham (no arrest) experiment, the three CT levels studied showed normal regional heterogeneity of LCBF values, all between 10 and 75 ml/100 cm3 per min for white matter and 20 and 130 ml/100 cm3 per min for gray matter. In four preliminary CPR experiments, the expected global hyperemia at 15 min after arrest, was followed by hypoperfusion with gCBF reduced to about 50% control and increased heterogeneity of LCBF. Trickle flow areas (LCBF less than 10 ml/100 cm3 per min) not present prearrest, were interspersed among regions of low, normal, or even high flow. Regions of 125-500 mm3 with trickle flow or higher flows, in different areas at different times, involving deep and superficial structures migrated and persisted to 6 h, with gCBF remaining low. These preliminary results suggest: no initial no-reflow foci (less than 10 ml/100 cm3 per min) larger than 125 mm3 persisting through the initial global hyperemic phase; delayed multifocal hypoperfusion more severe than suggested by gCBF measurements; and trickle flow areas caused by dynamic factors.

Animals↗
PubMed1990

Hyperthermia-induced cardiac arrest in dogs and monkeys.

The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45 degrees C, which was subsequently adjusted to control brain (parietal epidural) temperature at 42 +/- 0.5 degrees C. Transient initial hypertension, tachycardia, tachypnea and hypocarbia were followed by progressive hypotension with decreasing central venous pressure and pulmonary artery occlusion pressures (measured in three dogs only), bradycardia and bradypnea. Cardiac arrest occurred in the dogs after immersion of 288 +/- 66 min and more rapidly (P less than 0.02) in the rhesus monkeys (at 137 +/- 75 min) and pigtail monkeys (at 178 +/- 26 min). EEG silence occurred in the monkeys at MAP 40 mmHg and in the dogs at MAP 25 mmHg. Cardiac arrest occurred in form of sudden ventricular fibrillation (2/5 dogs, 2/9 rhesus monkeys, 3/12 pigtail monkeys), or later in electromechanical dissociation leading to electric asystole (3/5 dogs, 7/9 rhesus monkeys, 9/12 pigtail monkeys). The mean blood glucose levels decreased to less than 30 mg/dl (P less than 0.002), whereas hematocrit, serum osmolality, lactate and potassium levels increased. Necropsies revealed macroscopic petechial hemorrhages in all extracerebral organs, but not in the brain. There was no gross evidence of cerebral edema. Death seemed to be the result of primary cardiovascular failure leading to secondary (ischemic) cerebral failure (EEG silence) and apnea, which coincided with pulselessness.

Acid-Base Equilibrium↗
PubMed1990

Evaporative cooling as an adjunct to ice bag use after resuscitation from heat-induced arrest in a primate model.

Heat stroke and other hyperthermia-related crises are serious clinical problems in childhood and adolescence. Rapid cooling is required to reduce morbidity and mortality. A variety of effective cooling methods exist, and some may interfere with monitoring and resuscitation or are not readily available. We studied in 12 pigtail monkeys the pathophysiology of immersion hyperthermia (42 degrees C) to cardiac arrest (1 min no flow) and CPR plus cooling to normothermia for restoration and stabilization of spontaneous normotension. This was followed by intractable shock and secondary arrest. These studies gave us the opportunity to compare two simple cooling methods applied during and after CPR: group I (n = 6) received application of ice bags to the groins, axillae, and neck. Group II (n = 6) received ice bags plus cold water wetting (sponging) over the entire anterior surface of trunk and extremities, plus fanning. CPR restored spontaneous circulation in four of six in each group, after CPR of 1.5-16 min (NS between groups). Speed of cooling correlated with speed of stabilization of spontaneous normotension. After cardiac arrest and during and after CPR, rectal temperature had declined from a lethal level of 42.2 degrees C to a safe level of 38.5 degrees C within 45 +/- 6 (38-53) min in group I, and within 28 +/- 4 (23-32) min in group II (p less than 0.05). Epidural and esophageal temperatures declined more rapidly than rectal temperature. For critical hyperthermia, we recommend immediate application of ice bags, cold water wetting (sponging), fanning, and head cooling combined when invasive blood cooling (the most effective method) is not immediately available.

Animals↗
PubMed1987

Cardiopulmonary bypass after prolonged cardiac arrest in dogs.

Ventricular fibrillation (VF) cardiac arrest of more than ten minutes can be survived by cerebral neurons, but restoration of spontaneous circulation (ROSC) by external CPR is unreliable. Cardiopulmonary bypass (CPB) permits control of pressure, flow, oxygenation, temperature, and composition of blood. After 12 1/2 minutes of normothermic VF cardiac arrest, CPB was used as a research tool for reperfusion and assisted circulation for two hours in ten dogs without thoracotomy, with plasma substitute priming, and without preceding CPR (a deliberately nonclinical scenario). Recovery was compared with that in ten control dogs in which standard CPR with advanced life support (ALS) for up to 30 minutes was used to achieve ROSC. Both groups subsequently had blood pressure, blood gases, ventilation, and other parameters controlled for 20 hours, and intensive therapy to 72 hours. CPB achieved ROSC more successfully (ten of ten vs six of ten controls) (P less than .05), and more rapidly, with fewer defibrillation attempts and with less epinephrine (P less than .05). CPB improved 72-hour survival (seven of ten vs two of ten controls) (P = .025). Between two and 24 hours, of those with ROSC, intractable cardiogenic shock killed four of six control dogs (NS). CPB was followed by fewer arrhythmias. CPB increased recovery of consciousness (five of ten CPB vs zero of six controls with ROSC) (P = .037), but achieved neurologic normality in only one of ten. Cardiac arrest and CPB (without CPR) resulted in less myocardial morphologic damage than did standard CPR (P less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Cardiopulmonary bypass after cardiac arrest and prolonged closed-chest CPR in dogs.

We studied a clinically realistic field-to-hospital scenario in dogs with four-minute ventricular fibrillation (VF) cardiac arrest followed by 30-minute standard external CPR basic life support (BLS). At the end of this 34-minute insult, cardiopulmonary bypass (CPB) was used for early defibrillation and assisted circulation for one hour (n = 10). Recovery was compared with that of control dogs (n = 10) in which standard CPR with advanced life support (ALS) for another 30 minutes was used for restoration of spontaneous circulation (ROSC). Both groups had hemodilution and heparinization; controlled blood pressure, blood gases, ventilation, and other parameters for 20 hours; and intensive care to 72 hours. During CPR-BLS of 30 minutes in both groups signs of cerebral viability returned. CPB achieved ROSC more successfully (ten of ten vs five of ten CPR-ALS controls) (P less than .02); and more rapidly, with less defibrillation energy (first countershock in eight of ten) and with less epinephrine (P less than .01). CPB improved 72-hour survival (seven of ten vs three of ten controls) (P less than .05). Between two and 24 hours, of those with ROSC, cardiac complications killed three of ten CPB dogs (after weaning), and two of five CPR-ALS dogs (NS). All seven CPB survivors to 72 hours were neurologically normal; of the three CPR-ALS survivors, one remained with severe neurologic deficit and two were neurologically normal (seven of ten CPB vs two of ten controls, P = .025). Starting CPR-BLS within four minutes of arrest can maintain cerebral viability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Resuscitation of dogs from cold-water submersion using cardiopulmonary bypass.

In cold-water drowning, attempts at restoration of spontaneous circulation (ROSC) by external cardiopulmonary resuscitation (CPR) often fail. We explored the longest period of asphyxial cardiac arrest from cold-water submersion (without inhalation of water) from which ROSC is possible using cardiopulmonary bypass (CPB). In 19 lightly anesthetized dogs the tracheal tube was clamped (simulating laryngospasm) and the dogs were immersed in ice water from 20, 40, 60, 90, or 120 minutes. Cardiac arrest occurred after six to 11 minutes of submersion. At start of resuscitation, rectal temperature ranged from 21 C (after 60 minutes) to 34 C (after 20 minutes of submersion), and cerebral temperature was between 7 C (after 120 minutes) and 27 C (after 20 minutes submersion). Resuscitation attempts were performed according to protocol in 16 dogs, using only CPB by venoarterial pumping with an oxygenator and a heat exchanger. Priming was with 400 to 800 mL Dextran 40 and Ringer's solution 1:1 plus heparin. CPB flows were 10 mL/kg/min, and they increased to achieve normotension and return of rectal temperature to 32 C. After one-half to three hours, of CPB, ROSC was successful in 75%. This percentage included one of three dogs after 90 minutes submersion, but not in the one dog after 120 minutes submersion. Spontaneous breathing and EEG activity returned in 56% at two to 24 hours, after 20 to 90 minutes of submersion. Failure of ROSC attempts apparently were due to clotting in large vessels during arrest and capillary leakage during reperfusion. CPB is effective for ROSC after prolonged hypothermic cardiac arrest, and it should be evaluated in animal outcome studies.

Animals↗
PubMed1984

Amelioration of brain damage by lidoflazine after prolonged ventricular fibrillation cardiac arrest in dogs.

Calcium entry blockers can ameliorate postischemic cerebral hypoperfusion, protect the myocardium against ischemia, and may protect against early postischemic neurologic deficit. This study documents that a calcium entry blocker, given after cardiac arrest, can ameliorate late postischemic neurologic deficit (ND). Thirty-four dogs received 10 min of ventricular fibrillation, restoration of spontaneous circulation by external cardiopulmonary resuscitation, and standard postarrest intensive care. Eleven of these dogs were given lidoflazine, 1 mg/kg body weight, within 10 min postarrest and again at 8 h and 16 h. Pupillary light reflexes, EEG activity, arterial-cerebrovenous oxygen gradients (O2 demand/supply ratios) and intracranial pressure were the same in both groups. After weaning from controlled ventilation at 24 h, ND scores improved consistently through the 96-h observation period in the lidoflazine-treated dogs. In the control group, ND scores were significantly higher than in the lidoflazine-treated dogs. In the lidoflazine-treated group, 5/11 dogs achieved normal overall performance and none remained comatose, whereas all control dogs had some deficit and 4/11 remained comatose. Delayed neurologic deterioration occurred in 6/11 control and 0/11 lidoflazine-treated dogs. Total mean cerebral histopathologic damage (HD) scores at 96 h were not significantly different between the two groups; however, individual HD scores and maximum cerebro-spinal fluid (brain-specific) creatine-phosphokinase activity--which increases after brain insults--correlated well with 96-h ND scores. In the lidoflazine group, life-threatening dysrhythmias were less frequent and the norepinephrine requirement for blood pressure maintenance was the same as in the control group. Cardiac output remained at prearrest levels in the lidoflazine-treated dogs, but decreased in the control group, particularly during the first 4 h postarrest.

Animals↗
PubMed1982

Cerebral and hemodynamic variables during cough-induced CPR in dogs.

To assess the potential of self administered, cough-induced cardiopulmonary resuscitation (CICPR) to sustain cerebral function during sudden onset ventricular fibrillation (VF), the authors studied four groups of six dogs each. Cough was simulated by: spontaneous gasping (group 1); cough elicited by bilateral electrical stimulation of the vagi (group 2); gasping with artificial glottic closure (group 3); and as a control, apnea under paralysis (group 4). Sudden onset of VF during apnea (group 4) resulted in cessation of arterial blood flow in 11 +/- 3 sec (mean +/- SD) and an isoelectric EEG in 26 +/- 5 sec. Spontaneous gasping (group 1) and cough resulting from vagal stimulation (group 2) resulted in minimal systemic and cerebral perfusion pressures and common carotid artery blood flows (CCABF). CCABF became 0 in group 1 at 31 +/- 12 sec, and in group 2 at 33 +/- 16 sec after the onset of VF. EEG silence occurred at 57 +/- 9 sec and 54 +/- 19 sec in groups 1 and 2, respectively. The decay of vital parameters was delayed further when spontaneous gasping via tracheal tube was against artificial glottic closure, which augments airway pressure fluctuations (group 3); pulselessness occurred at 52 +/- 28 sec and EEG silence at 66 +/- 27 sec. Self-induced fluctuations of intrathoracic pressure generated sufficient blood flow to briefly but statistically significantly (p less than 0.001) prolong EEG activity compared to apneic controls. In this dog preparation, gasping with artificial glottic closure sustained cerebral electrical activity for a maximum of 112 sec. CICPR may offer a means of briefly sustaining consciousness after the sudden onset of VF and, thus, constitutes self-administered CPR.

Animals↗
PubMed1976

Amelioration of brain damage after 12 minutes' cardiac arrest in dogs.

To determine the efficacy of cerebral microcirculation promoting therapy in postischemic brain failure, 11 dogs awakening from methohexital sodium anesthesia were subjected to 12 minutes of reversible circulatory arrest by ventricular fibrillation. Physiological variables were controlled for six hours after resuscitation, and the dogs were observed for seven days. Six dogs without the special postresuscitative therapy did not awaken, and either died within 36 hours or remained comatose for seven days. In five dogs, a combination of the following measures was applied: (1) mean arterial pressure was raised to 150 to 180 mm Hg with norepinephrine for six hours; (2) heparinization; (3) rapid intra-aortic injection of dextran 40 (10 ml/kg body weight); and (4) normovelemic hemodilution with dextran 40 to a hematocrit reading of 25% to 30%. All five treated dogs awakened within 24 hours and appeared normal on the seventh day. Therapy enhanced constriction of pupils and normalization of the electroencephalogram (P less than .05). Postischemic neurological deficit is at least partially due to impaired reperfusion and can be ameliorated or prevented by blood flowing-promoting therapy.

Animals↗