The list of drugs for the physician's bag depends on several factors, including practice location, conditions most likely to be found, costs and availability of drugs, organization of the emergency medicine in the region, shelf life and climatic vulnerability of certain drugs, population age, and size and design of the bag. Most of the drugs carried should be in an injectable form. However, the non-injectable drugs with relatively rapid systemic onset may be also included. Separation of drugs in the bag according to their usage may help in providing an organized treatment. For example, one could separate drugs for treatment of the following emergencies: cardiovascular, altered mental status, respiratory, gastrointestinal, bleeding, infections, and toxicological emergencies. The list of drugs needed for medical emergencies when physician makes house-calls is presented with short notes on their usage. Oncologic, toxicologic and pediatric emergencies are commented.

Alterations of autonomic tone can induce cardiac dysrhythmias. In the present experiments intravenous administration of epinephrine (15 micrograms/kg) caused dysrhythmias in rat hearts. Bilateral vagotomy or yohimbine treatment did not suppress the dysrhythmic effects of epinephrine. Atropine, glycopyrrolate, and pertussis toxin reduced the number of premature ventricular contractions and eliminated missed beats caused by epinephrine. Neostigmine increased the number of missed beats but did not change the number of premature ventricular contractions. These results indicate that epinephrine induces cardiac dysrhythmias in part by local release of acetylcholine. Muscarinic receptors and pertussis toxin sensitive G proteins are involved in epinephrine-induced arrhythmogenesis.

Both human plasma carboxypeptidase N (CPN) and membrane-bound carboxypeptidase M (CPM) released the C-terminal arginine (alpha-Arg141) of the alpha chain of human adult hemoglobin. An arginase contamination present in the hemoglobin preparation, which converted the released arginine to ornithine, was removed by gel filtration. CPM was about 20 times more efficient than CPN or its active subunit in hydrolyzing oxyhemoglobin and cleaved oxyhemoglobin twice as fast as deoxyhemoglobin. The hydrolysis of the peptide bond of alpha-Arg141 accelerated the dissociation rate of the tetramer deoxy-des-alpha-Arg141 hemoglobin to dimers 2500-fold over that of deoxyhemoglobin, as measured by haptoglobin binding. Moreover, the dissociation of the deoxy-des-alpha-Arg141 hemoglobin tetramer to dimers was not affected by 2,3-diphosphoglyceric acid. Des-alpha-Arg141 hemoglobin had a higher oxygen affinity (P50, 5.51 mm Hg; control, 19.94 mm Hg [P50 is the partial pressure of oxygen that gives 50% of the saturation of hemoglobin]) and a lower apparent cooperativity (Hill coefficient: n, 1.02; control, 2.24) than unhydrolyzed hemoglobin. After hemoglobin was incubated in human plasma, its oxygen-binding parameters, the P50, and the Hill coefficient decreased drastically due to cleavage by CPN. In the perfused rat heart, des-alpha-Arg141 hemoglobin was a more effective coronary vasoconstrictor than hemoglobin, possibly because it dissociated to dimers in the coronary vascular bed. A covalently cross-linked hemoglobin was less active than native hemoglobin. The coronary vasoconstriction was caused by multiple factors, including interference with vasodilation by nitric oxide and eicosanoids. Thus, the hydrolysis of hemoglobin by CPM and CPN demonstrated the contribution of the alpha-Arg141 residue to sustaining the tetrameric structure of hemoglobin and its normal oxygen affinity and vasoactivity.

Degradation of substance P was studied in dog and rabbit aqueous humor. Substance P inactivation was followed by the bioassay using the isolated guinea pig ileum. Both rabbit and dog aqueous humor inactivated substance P. Rabbit aqueous humor inactivated the peptide faster than dog aqueous humor. Inactivation of substance P by rabbit aqueous humor was inhibited by diisopropylfluorophosphate while other enzyme inhibitors tested (captopril, phosphoramidon, mersalyl acid and p-chloromercuriphenyl-sulphonate) were practically ineffective or had a partial inhibitory effect. Our results suggest that serine proteases, rather than other peptidases, play a major role in the inactivation of substance P in aqueous humor.