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Biomedical subjects

P L Gross

Publications and source records attributed to P L Gross.

13 recordsLinked to original sources
PubMed1992

Acute in vitro effects of ethanol on responses of platelets from cholesterol-fed and Watanabe heritable hyperlipidemic rabbits.

The effects of ethanol on platelets from rabbits with two different types of hypercholesterolemia, diet-induced and genetically determined, were investigated. There were no differences between the hypercholesterolemic groups and their controls in the extent of (primary) ADP-induced aggregation of washed platelets, and this aggregation was not inhibited by ethanol. Platelets from cholesterol-fed rabbits were more sensitive to aggregation and secretion induced by collagen, whereas platelets from Watanabe heritable hyperlipidemic (WHHL) rabbits were less sensitive. Ethanol inhibited collagen-induced responses of platelets from both hypercholesterolemic groups, but the extent of inhibition of aggregation was not different compared with controls. Because ethanol did not affect U46619-induced responses of aspirin-treated platelets, ethanol does not inhibit aggregation and secretion stimulated by collagen via an effect on thromboxane A2 (TxA2)-induced responses. Platelets from cholesterol-fed rabbits were more sensitive to thrombin even when TxA2 formation was blocked by aspirin, and inhibition of aggregation by ethanol was less in cholesterol-fed rabbits than in controls. However, neither the extent of thrombin-induced responses nor the inhibitory effect of ethanol was different in platelets from WHHL rabbits compared with controls. Thus, different etiologies of hypercholesterolemia produce different changes in platelet function, and ethanol has different effects on the platelets from cholesterol-fed rabbits compared with the platelets from WHHL rabbits. The inhibitory effect of ethanol on the thrombin-induced aggregation of platelets from cholesterol-fed rabbits is attenuated compared with controls, and this finding contrasts with the reported greater inhibitory effect of ethanol on platelets enriched with saturated fats.

Adenosine Diphosphate↗
PubMed1991

Platelet hypersensitivity in cholesterol-fed rabbits: enhancement of thromboxane A2-dependent and thrombin-induced, thromboxane A2-independent platelet responses.

Hypercholesterolemia (mean plasma cholesterol: 15 mM) was induced in rabbits by the feeding of a chow diet enriched with a low amount (0.25%, w/w) of cholesterol only. Platelet size and protein content decreased significantly, but the whole blood platelet count did not change. The platelets became enriched in cholesterol, as indicated by a significant increase in the cholesterol:phospholipid molar (C/P) ratio. Specific responses of washed platelets stimulated with various agonists were studied to determine the effects of hypercholesterolemia on the various pathways of platelet aggregation in the absence of plasma components. In platelets from hypercholesterolemic rabbits compared with controls: aggregation induced by ADP was not altered; collagen-induced responses (aggregation, secretion of [14C]serotonin from prelabelled platelets, thromboxane A2 (TXA2) formation, mobilization of [3H]arachidonate from prelabelled platelets) were enhanced; with aspirin-treated platelets, aggregation induced by the TXA2 mimetic U46619 was enhanced: and thrombin-induced responses of both untreated platelets (aggregation, secretion of granule contents, TXA2 formation) and aspirin-treated platelets (aggregation) were enhanced. Thus, platelets from cholesterol-fed rabbits not only form more TXA2, but they aggregate more extensively when stimulated by its mimetic. In addition, it has not been previously recognized that these platelets are also hypersensitive to thrombin-induced aggregation that is independent of TXA2.

Adenosine Diphosphate↗
PubMed1990

Quantitative serum toxic screening in the management of suspected drug overdose.

Data were collected on 176 consecutive cases of drug overdose evaluated in an emergency department. Quantitative serum toxic screening (TS) was performed for 164 (93%) of these patients; positive results were noted for 133 patients (81%). Six classes of drugs (ethanol, benzodiazepines, salicylates, acetaminophen, barbiturates, and tricyclic antidepressants) were responsible for nearly 70% of all drug detections and were associated with 80% of all admissions in this patient sample. Only two patients (1%) had drug-specific treatment initiated because of TS results. In 12 patients (7%), TS confirmed substances for which specific treatments had been initiated on clinical grounds. Four patients (2%) had drug-specific treatment discontinued because of TS results. Thirty-two patients (19%) were admitted to a medical service; however, only seven patients (4%) were admitted primarily because of TS results. All other patients were admitted because of clinical abnormalities that required inpatient care. It is concluded that only a few drugs are responsible for most drug overdoses. Moreover, TS results rarely change the treatment or disposition of overdose patients; these decisions are typically based on clinical parameters.

Acetaminophen↗
PubMed1989

In vitro effects of ethanol on rabbit platelet aggregation, secretion of granule contents, and cyclic AMP levels in the presence of prostacyclin.

Ethanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin-treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Adenosine Diphosphate↗
PubMed1989

Depression.

Explore the source record for details and available documents.

Aged↗
PubMed1985

Fatal systemic fluorosis due to hydrofluoric acid burns.

A patient with a 70% hydrofluoric acid burn developed systemic dissemination of fluoride ion from a 9% to 10% body surface area exposure on the lower extremities. Severe hypocalcemia and intractable ventricular arrhythmias resulted. This case is the second documented occurrence of hypocalcemia from hydrofluoric acid burns. It is the first case to document myocardial injury and systemic fluorosis from a skin burn.

Acidosis↗
PubMed1985

Malignant lymphoma presenting as Kaposi's sarcoma in a homosexual man with the acquired immunodeficiency syndrome.

A homosexual man had Kaposi's sarcoma of the skin and lymph nodes. After a brief response to interferon, the patient developed new skin lesions. Massive bleeding in the gastrointestinal tract prompted endoscopy, which showed tumor involvement of the stomach, believed to be Kaposi's sarcoma. At autopsy, a diffuse lymphoma was found involving the skin and gastrointestinal tract, forming collision tumors in regions that contained Kaposi's sarcoma. Lymphomatous tissue, but not uninvolved lymph node or spleen, contained Epstein-Barr virus DNA, as shown by DNA hybridization studies. Epstein-Barr virus may play a role in the development of lymphoma in immunosuppressed patients. Unusual manifestations of tumors, such as the massive gastrointestinal bleeding seen in this case, may indicate the development of a second neoplasm.

Acquired Immunodeficiency Syndrome↗
PubMed1978

Fatal hyperthermia following haloperidol therapy of sedative-hypnotic withdrawal.

A 30 year old male, with a history of methalqualone and barbiturate abuse, developed a delirium tremens-like syndrome following discontinuation of the medications. Shortly following high doses of parenteral haloperidol administered for treatment of the withdrawal syndrome, the patient developed severe hyperthermia, with body temperatures reaching as high as 108 degrees F. The hyperthermic episode was followed by cardiovascular collapse, multiple complications, and death. The sequence of events strongly suggests that haloperidol therapy was casually related to the development of fatal hyperthermia. Thus the butyrophenone haloperidol, like the phenothiazine derivatives, can produce clinically important impairment of thermoregulation.

Adult↗
PubMed1976

Pharmacotherapy of cardiopulmonary arrest.

The assessment and treatment of patients requiring cardiopulmonary resuscitation (CPR) is discussed. Cardiovascular pharmacotherapy is discussed as suppressive therapy, stimulant therapy and treatment of hypotension. Special situations covered include hyperkalemia, anaphylaxis and drug overdosages. It is concluded that the likelihood of success of CPR depends on the rapid initiation of ventilation and restoration of circulation, and is inversely dependent on the severity of the underlying disease or injury.

Acidosis↗
PubMedDate not supplied

Platelet function in Watanabe heritable hyperlipidemic rabbits. Decreased sensitivity to thromboxane A2.

The characteristics of platelets from seven 5-7-month-old homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits (plasma cholesterol, 13.9 +/- 1.7 mM, mean +/- SEM) were compared with those of platelets from normocholesterolemic age/weight- and sex-matched control rabbits (plasma cholesterol, 2.2 +/- 0.3 mM). Whole-blood platelet count and platelet size and protein content were not different in the two groups of rabbits, and the platelets from the WHHL rabbits were not enriched in cholesterol as indicated by identical mean cholesterol:phospholipid molar ratios (C/P). Responses of washed platelets stimulated with various agonists were studied to determine the effects of the genetically determined hypercholesterolemia on the various pathways of platelet aggregation in the absence of plasma components. In platelets from WHHL rabbits compared with controls, aggregation induced by ADP (0.5-5 microM) did not differ; collagen-induced (0.25-1.5 micrograms/ml) responses (aggregation, secretion of carbon-14-labeled serotonin from the amine storage granules of prelabeled platelets, and thromboxane A2 [TxA2] formation) were significantly less extensive; with aspirin-treated platelets, aggregation and secretion of granule contents induced by the TxA2 mimetic U46619 (0.25-1 microM) were significantly less extensive; and thrombin-induced (0.005-0.1 unit/ml) responses of untreated platelets (aggregation, secretion of granule contents, and TxA2 formation) or aspirin-treated platelets (aggregation and secretion of granule contents) did not differ. These observations are in direct contrast with previous studies of platelets from rabbits with diet-induced hypercholesterolemia, in which responses to TxA2 and thrombin were enhanced. Platelets from WHHL rabbits are hyposensitive to aggregation induced by TxA2.

Adenosine Diphosphate↗