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Biomedical subjects

J Sassano

Publications and source records attributed to J Sassano.

4 recordsLinked to original sources
PubMed1998

Delayed death after uncomplicated hot tub bathing in dogs and monkeys.

Prolonged heat exposure as in hot tub bathing, although frequently practiced, has occasionally resulted in fatalities that have been explained by an underlying disease. We explored the tolerance of hot water immersion of 60 min in five previously healthy animals (three dogs and two monkeys). With invasive monitoring, experimental body immersion in water at 40-45 degrees C, with core temperature kept at 40-42 degrees C for 60 min, caused no significant cardiovascular, pulmonary or metabolic changes during hyperthermia or for 2 h after return to normothermia. Then secondary deterioration occurred with progressive hypotension, petechial hemorrhages throughout the viscera, gross gastrointestinal hemorrhages and irreversible (hypovolemic) shock. These effects occurred earlier in the monkeys than in the dogs. This shock state did not respond to standard resuscitation attempts. One dog survived the secondary shock state. We conclude that during and after hot tub immersion, good initial tolerance to heat exposure can, several hours after return of normothermia, result in delayed secondary deterioration and death. We recommend that the mechanism of this delayed shock state with apparent capillary leakage be clarified.

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↗
PubMed1980

Effect of postcirculatory-arrest life-support on neurological recovery in monkeys.

The existence of treatable postischemic (PI) changes which influence neurological outcome has been documented by this group before. A global brain ischemia model without cardiac arrest was developed in monkeys. It includes high-pressure neck tourniquet inflation plus hypotension for a reproducible ischemic insult; survival with reproducible neurological deficit (ND) under continuous PI life-support for 7 days with control of extracranial variables; and new ND and histopathological damage scoring systems. Hypoxemia, hypercarbia, hypotension, uremia, sepsis, and other extracranial complications PI in 50 unsatisfactory experiments led to immediate worsening in ND and brain death (ND = 100%) in most of these monkeys. In contrast, all monkeys with the same initial insult, with life-support according to protocol, survived with a 7 day ND of 60% or less. In 46 experiments of seven treatment groups, after 16 or 18 min ischemia, life support was according to protocol for 7 days. The control 1 protocol (spontaneous breathing when feasible) resulted in a mean 7-day ND score of 53% (including quadriplegia). Immobilization with pancuronium and controlled ventilation ameliorate deficit to an ND score of 19% (P less than 0.05) (including quadriparesis); this became control 2 protocol. Immobilization resulted in less neuronal damage in the neocortex. Severe repetitive hypertension worsened ND to 46%, versus 19% in controls (P less than 0.05). In separate series, neither heparinization over 72 hours PI, nor hemodilution to hematocrit 25% with dextran 40, changed final ND significantly from that of their control groups. Histopathological damage scores correlated with ND scores.

Animals↗