Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Coca”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1993

Emphysematous gastritis secondary to ingestion of large amounts of Coca Cola.

Acute emphysematous gastritis (AEG) is a life-threatening disease in which gas-forming bacteria invade the gastric wall and cause acute inflammation of it. The clinical presentation of the patient with AEG is stormy: severe sepsis which usually leads to an early death. Presented herein is a case of a 16-yr-old boy with AEG. There were no predisposing factors to the condition in this case. Gas invaded the stomach wall and portal venous system, as well as the duodenal wall, a finding that has not been reported previously. The clinical course was very severe but, in contrast to previously reported cases, recovery was very rapid and left no sequelae.

Abdominal Pain↗
PubMed1997

["Coca-Koller" and hist friends. On the 140th birthday of the Vienna Jewish trio: Carl Koller (1857-1944), Sigmund Lustgarten (1857-1911) and Sigmund Freud (1856-1939)].

The lives of Carl Koller (1857-1944), Sigmund Lustgarten (1857-1911) and Sigmund Freud (1856-1939) are characterized by several interesting similarities. In their early achievements in medical research they were pathfinders of the first successful local anesthetic: cocaine. All three became later victims of antisemitism. Attention is paid to their personal relationship during their time in Vienna, on occasion of the 140th anniversary of their birth.

Anesthetics, Local↗
PubMedDate not supplied

Antidotal effects of buprenorphine on the behavioral alterations accompanying cocaine and combined cocaine-ethanol toxicity.

The present study examined the effects of buprenorphine (BUP), a mixed opioid agonist-antagonist, on the behaviors accompanying cocaine (COCA) and combined cocaine-ethanol (EtOH) toxicity in the surviving mice. Using the activity-counting instrument Supermex, the relationship between the toxic signs and the corresponding behavioral alterations could be assessed. In the COCA-only group, a prolonged increase in the activity counts was caused by a high dose of COCA (75 mg/kg ip). Furthermore, this COCA-induced hyperactivity included ataxic behaviors that were accompanied by visible toxic signs, which were not observed in the mice with no drug treatment. A depressive dose of EtOH (3 g/kg ip) did not significantly modify the mortality rate in the COCA-only group in spite of its anticonvulsant effects. However, the peak activity counts in the survivors were attenuated in the COCA-EtOH group as compared to the COCA-only group. BUP attenuated the mortality rate in both COCA and COCA-EtOH groups, even without any anticonvulsant effects, but the most effective dose differed between the COCA (BUP: 0.25 mg/kg ip) and COCA-EtOH (BUP: 0.5 mg/kg ip) groups. At these BUP doses, the prolonged suppression of the morbid hyperactivity in the COCA-BUP group and the restoration of normal behavior in the COCA-EtOH-BUP group both seemed to be correlated with a good prognosis in the survivors; there was an early recovery from an increased blood pressure (BP), increased heart rate (HR) and decreased respiratory rate (RR) in the COCA-BUP group, and an early recovery from a decreased BP, decreased HR and decreased RR in the COCA-EtOH-BUP group.

Animals↗
PubMed2003

Identification of Erythroxylum taxa by AFLP DNA analysis.

Erythroxylum coca, indigenous to the Andean region of South America, is grown historically as a source of homeopathic medicine. However, in the last century, cultivation of E. coca and several closely-related species for the production of illicit cocaine has become a major global problem. Two subspecies, E. coca var. coca and E. coca var. ipadu, are almost indistinguishable phenotypically; a related cocaine-bearing species also has two subspecies (E. novogranatense var. novogranatense and E. novogranatense var. truxillense) that are phenotypically similar, but morphologically distinguishable. The purpose of this research was to discover unique AFLP DNA patterns ("genetic fingerprinting") that characterize the four taxa and then, if successful, to evaluate this approach for positive identification of the various species of coca. Of seven different AFLP primer pairs tested, a combination of five proved optimal in differentiating the four taxa as well as a non-cocaine-bearing species, E. aerolatum. This method of DNA fragment separation was selective, and faster, for coca identification, compared with analyses based on flavonoid chemotaxonomy. Using the 5-primer AFLP approach, 132 known and unknown coca leaf accessions were evaluated. Of these, 38 were collected in 1997-2001 from illicit coca fields in Colombia, and all were genetically differentiated from coca originating in Peru and Bolivia. Based on the DNA profiling, we believe that the Colombian coca now represents a hybridization of E. coca var. ipadu. Geographical profiling within Colombia also seems feasible as new coca production areas are developed or new types of coca are introduced within traditional growing areas.

Alkaloids↗
PubMed2005

Inter- and intra-specific variation among five Erythroxylum taxa assessed by AFLP.

BACKGROUND: and Aims The four cultivated Erythroxylum taxa (E. coca var. coca, E. novogranatense var. novogranatense, E. coca var. ipadu and E. novogranatense var. truxillense) are indigenous to the Andean region of South America and have been cultivated for folk-medicine and, within the last century, for illicit cocaine production. The objective of this research was to assess the structure of genetic diversity within and among the four cultivated alkaloid-bearing taxa of Erythroxylum in the living collection at Beltsville Agricultural Research Center. METHODS: Amplified fragment length polymorphism (AFLP) fingerprinting was performed in 86 Erythroxylum accessions using a capillary genotyping system. Cluster analysis, multidimensional scaling (MDS) and analysis of molecular variance (AMOVA) were used to assess the pattern and level of genetic variation among and within the taxa. KEY RESULTS: A clear distinction was revealed between E. coca and E. novogranatense. At the intra-specific level, significant differentiation was observed between E. c. var. coca and E. c. var. ipadu, but the differentiation between E. n. var. novogranatense and E. n. var. truxillense was negligible. Erythroxylum c. var. ipadu had a significantly lower amount of diversity than the E. c. var. coca and is genetically different from the E. c. var. ipadu currently under cultivation in Colombia, South America. CONCLUSIONS: There is a heterogeneous genetic structure among the cultivated Erythroxylum taxa where E. coca and E. novogranatense are two independent species. Erythroxylum coca var. coca is most likely the ancestral taxon of E. c. var. ipadu and a founder effect may have occurred as E. c. var. ipadu moved from the eastern Andes in Peru and Bolivia into the lowland Amazonian basin. There is an indication of artificial hybridization in coca grown in Colombia.

Coca↗
PubMed1999

Effects of ethanol and/or cardiovascular drugs on cocaine- and methamphetamine-induced fatal toxicities in mice.

The antidotal effects of antihypertensive cardiovascular (CV) drugs against cocaine (COCA)- and methamphetamine (MA)-induced fatal toxicities were examined in mice. Considering the previously-reported favorable interactions, the effects of CV drugs against combined COCA-ethanol (EtOH) or MA-EtOH toxicities were also evaluated. COCA (75 mg/kg) or MA (18 mg/kg) was administered 5 min after an injection of CV drugs, with or without EtOH (3 g/kg); all drugs were injected intraperitoneally. The CV drugs used were 10 mg/kg diltiazem (DIL), 5 mg/kg nimodipine (NIMO) and 5 mg/kg nitrendipine (NITRE) as calcium channel blockers, 5 mg/kg prazosin (PRA) and 5 mg/kg phentolamine (PHEN) as alpha-adrenergic blocking agents, 10 mg/kg propranolol (PRO) as a beta-adrenergic blocking agent, and 10 mg/kg enalapril (ENA) as an angiotensin converting-enzyme inhibitor. In both the COCA (n = 10) and MA (n = 6) groups, regardless of EtOH or CV drug cotreatment, the fatalities could be divided into the early and late deaths, depending on the survival times, the presence of a temporary recovery from acute toxic symptoms such as observable respiratory and locomotive symptoms, and the presence of the drugs (COCA or MA) in blood samples. The acute toxic symptoms included seizures in both the COCA and MA groups, but they were generally suppressed by EtOH regardless of the mortality rate. Some of the CV drugs, such as PRA and PHEN in the COCA groups and DIL, NIMO, NITRE, PRA and PHEN in the MA groups, also suppressed the seizures. The mortality rate was attenuated by PRA in the COCA groups, and by NIMO, NITRE, PRA and PHEN in the MA groups. In the groups cotreated with EtOH, which has been reported to exacerbate the COCA- and MA-induced cardiotoxicity, the frequency of late deaths was increased. Nevertheless, antidotal effects due to NIMO, NITRE, PRA and ENA in the COCA-EtOH groups, and NIMO, NITRE and PRA in the MA-EtOH groups were observed.

Animals↗
PubMed2000

Stress-related behavioral alterations accompanying cocaine toxicity: the effects of mixed opioid drugs.

The present study evaluated the effects of mixed opioid drugs on the severity of cocaine (COCA) toxicity by examining stress-related behavioral alterations in mice. In order to ascertain the strength of the stress, the continuous observation of the behavioral symptoms in the cage and the forced swimming test (Porsolt test) were performed in the COCA (75 mg/kg, i.p.)-treated groups, with or without the mixed mu-kappa receptor-related opioid drugs, buprenorphine (BUP) and pentazocine (PEN). Using the high-sensitivity activity measuring instrument Supermex, both the spontaneous behaviors in the cage and the forced swimming behaviors in the water were assessed as activity counts. The behavioral alterations in the COCA-treated groups were compared with a group of mice given a 10 min immobilization stress (IM group). In the COCA-only group, a prolonged increase in the spontaneous behaviors accompanied by convulsive seizures was observed even in the surviving mice, unlike in the IM group. However, an acceleration of behavioral despair in the Porsolt test similar to that observed in the IM group was observed in the COCA group after the disappearance of the acute toxic symptoms (5 hours after the COCA treatment). Among the opioid-treated groups, the mortality rate was attenuated only in the COCA-BUP (0.25 mg/kg, i.p.) group. In the COCA-BUP group, a prolonged suppression of the morbid hyperactivity in the cage except for the convulsive seizures, and a normalization of the swimming behavior in the Porsolt test were observed in the survivors. On the other hand, in the COCA-PEN (5 mg/kg, i.p.) group, the swimming behavior in the Porsolt test was abnormally increased in addition to the prolonged morbid hyperactivity in the cage. Therefore, the COCA-induced stress-related behaviors were normalized in the group of mice treated with BUP, a group with a good prognosis.

Analgesics, Opioid↗
PubMed2000

Comparison of effect of ethanol and anticonvulsants on cardiovascular drug-modified cocaine toxicity.

The anticonvulsant (AC drug)- or ethanol (EtOH)-modified effects of cardiovascular (CV) drugs against cocaine (COCA)-induced toxicity were examined in male ICR mice. Nontoxic doses of the CV drugs nimodipine (NIMO), prazosin (PRA), phentolamine (PHEN), propranolol (PRO), and enalapril (ENA) were used with or without the AC drugs diazepam (DZP), phenobarbital (PHB), phenytoin (PHY), and EtOH. Each CV drug combined with or without each AC drug was administered intraperitoneally (IP) 5 min before an IP injection of COCA 75 mg/kg. Of the CV drugs examined, PRA 5 mg/kg and PHEN 5 mg/kg protected against COCA-induced seizures, but only the alpha1-adrenergic blocking agent PRA protected against COCA-induced deaths. Of the AC drugs examined, DZP 5 mg/kg and PHB 50 mg/kg, as well as EtOH 3 g/kg, attenuated the severity of the COCA-induced seizures, but only PHB protected against COCA-induced deaths. The total mortality rate was significantly, often synergistically, decreased compared to the COCA-only group when the appropriate CV drugs were combined with the AC drugs: PRA 5 mg/kg in the EtOH-cotreated groups, PRA 5 mg/kg, PHEN 5 mg/kg or ENA 10 mg/kg in the DZP-cotreated groups, and NIMO 5 mg/kg, PRA 5 mg/kg, PHEN 5 mg/kg, or PRO 10 mg/kg in the PHB-cotreated groups. The decrease in the COCA concentration in the blood and/or brain was not always accompanied by an attenuation of the mortality rate. However, the attenuation of severe seizures by a single PRA, PHEN, DZP, or PHB cotreatment was accompanied by a decrease in the brain COCA concentration.

Animals↗
PubMed2000

The effect of cola consumption on oral mucosa in rats.

Drinks that contain phosphoric acid have been shown to have erosive effects and cola drinks are strongly acidic (pH 2.5). Gingivitis may be caused by dietary acids. Therefore, this study analyses the interaction of Coca Cola consumption and oral mucosal damage. Thirty rats were divided into three groups of 10. The animals received saline (pH 7.0) or HCl acid buffered to pH 2.6 or Coca Cola (pH 2.6) per os with 24-h free access to these solutions. A biopsy was taken from the front of the gingiva and the tongue. Histopathological analysis showed no specific lesion and there were no differences among saline, Coca Cola and HCl groups. Flow cytometric analysis was used to assess proliferative activity. In the HCl acid and Coca Cola groups, cell cycle analysis showed that the effects of Coca Cola and HCl acid in inducing oral mucosal damage are similar. In both Coca Cola [G0/G1, 70.38+/-7.9; S, 28.06+/-10.13; G2/M, 1.62+/-2.80; proliferative index (PI), 28.68+/-7.981 and HCI (G0/G1, 67.7+/-18.9; S, 27.8+/-17.5; G2/M, 4.4+/-3.8; PI, 30.9+/-20.98), the rat cell population G0/G1 and G2/M phases were found to be low (p < 0.05) and the cell population S and PI phases were found to be significantly elevated compared with the control group (p < 0.05) (G0/G1, 86.92+/-8.69; S, 9.8+/-1.21; G2/M, 3.25+/-2.87; P1, 13.2+/-8.7). This result was reflected in the proliferative index, which is used as a measure of the regeneration index. The data show that Coca Cola and HCl acid have similar proliferative and regenerative effects on oral mucosa, and it is possible that their regenerative effects are caused as a result of an irritant effect.

Animals↗