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Infections of the Gastrointestinal Tract

It has been known for over 100 years that acidosis decreases the contractility of cardiac muscle. However, the mechanisms underlying this decrease are complicated because acidosis affects every step in the excitation-contraction coupling pathway, including both the delivery of Ca2+ to the myofilaments and the response of the myofilaments to Ca2+. Acidosis has diverse effects on Ca2+ delivery. Actions that may diminish Ca2+ delivery include 1) inhibition of the Ca2+ current, 2) reduction of Ca2+ release from the sarcoplasmic reticulum, and 3) shortening of the action potential, when such shortening occurs. Conversely, Ca2+ delivery may be increased by the prolongation of the action potential that is sometimes observed and by the rise of diastolic Ca2+ that occurs during acidosis. This rise, which will increase the uptake and subsequent release of Ca2+ by the sarcoplasmic reticulum, may be due to 1) stimulation of Na+ entry via Na(+)-Ca2+ exchange; 2) direct inhibition of Na(+)-Ca2+ exchange; 3) mitochondrial release of Ca2+; and 4) displacement of Ca2+ from cytoplasmic buffer sites by H+. Acidosis inhibits myofibrillar responsiveness to Ca2+ by decreasing the sensitivity of the contractile proteins to Ca2+, probably by decreasing the binding of Ca2+ to troponin C, and by decreasing maximum force, possibly by a direct action on the cross bridges. Thus the final amount of force developed by heart muscle during acidosis is the complex sum of these changes.

Effects of changes of pH on the contractile function of cardiac muscle

We systematically modified isoproterenol's chemical structure to reduce chronotropic, arrhythmogenic, and vascular side effects. Experiments on dogs showed that the resulting drug, dobutamine, had an inotropic efficacy as great as that of epinephrine due to a direct action on beta1 cardiac receptors. However, unlike epinephrine, dobutamine's effect on alpha and beta2 vascular receptors was slight. At equivalent inotropic doses, dobutamine had less than a fourth of the chronotropic effect of isoproterenol. Desmethylimipramine (DMI), which blocks the sympathetic nerve fiber uptake mechanism, had no effect on dobutamine's actions. In contrast, DMI antagonized dopamine's inotropic effect, and marked chronotropic and pressor responses occurred when we used doses of dopamine large enough to elicit a direct inotropic effect. Dobutamine increased the contractility of isolated cat papillary muscles more but the automaticity less than did isoproterenol. In ischemic dog hearts, dobutamine lacked significant arrhythmic activity, whereas dopamine, norepinephrine, and isoproterenol caused severe ectopic activity. In dogs with experimentally induced low cardiac contractility, low cardiac output, and hypotension, dobutamine produced dose-related increases in cardiac contractility and output, restored arterial blood pressure, and reduced total peripheral resistance slightly. In contrast, isoproterenol failed to restore blood pressure, had only a meager effect on cardiac contractility and output, cuased extreme tachycardia, and lowered peripheral resistance more than did dobutamine. Norepinephrine, which did not increase cardiac contractility or output as much as dobutamine, excessively elevated peripheral resistance and arterial blood pressure.

Dobutamine: development of a new catecholamine to selectively increase cardiac contractility.

The drastic intestinal secretion of fluid and electrolytes that is characteristic of cholera is the result of reasonably well understood cellular and biochemical actions of the toxin secreted by Vibrio cholerae. Based on this understanding it is possible to devise new techniques for the treatment and prophylaxis of cholera to complement those based on fluid replacement therapy and sanitation.

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Actions of cholera toxin and the prevention and treatment of cholera

An epidemic of 110 sudden sniffing deaths without plastic bag suffocation which occurred in American youths during the 1960's, appears to have originated on the West Coast. The incidence rate showed a sharp rise during the late 1960's. Volatile hydrocarbons most frequently involved were trichloroethane and fluorinated refrigerants. Sudden sniffing death occurred in all socioeconomic groups, with a preponderance in the suburban middle-income white family. Severe cardiac arrhythmia, resulting from light plane anesthesia, and intensified by hypercapnia or stress or activity or a combination of these, is the most likely explanation for sniffing death.

Sudden Sniffing Death

BENNETT1 has suggested that cholera toxin stimulates the release or synthesis of prostaglandins (PG) which, in turn, interact with the cyclic 3′,5′-adenosine monophosphate system to produce diarrhoea. PGs might also be involved in the diarrhoea associated with medullary carcinoma of the thyroid, the carcinoid syndrome and ganglioneuroma2–4. Diarrhoea has also been observed in patients with phaeochromocytoma (unpublished results of R. L. K.) and large amounts of PGE2 and PGF2α have been reported in phaeochromocytoma2. Vane5, Smith and Willis6, and Ferreira et al.7 showed that aspirin inhibits the synthesis of PGs in several in vitro systems. Bennett1 therefore suggested that aspirin might prevent the diarrhoea associated with cholera. Our study was undertaken to investigate this possibility in cats.

Prevention of Cholera-induced Intestinal Secretion in the Cat by Aspirin

In an effort to reconcile conflicting reports in the literature concerning suxamethonium and tubocurarine, we studied the effects of these agents on the adductor pollicis mechanical twitch, adductor pollicis brevis compound action potential and abductor digiti quinti compound action potential. It was observed that the magnitude of block of the adductor pollicis differed from that of the abductor digiti quinti. In addition the magnitude of adductor pollicis block recorded mechanically differed from that recorded electrically. It was further observed that the presence or absence and magnitude of fade and post-tetanic potentiation depended upon the muscle studied, the rate of stimulation, the anaesthetic technique employed, the degree of block and whether electrical or mechanical responses were recorded. Nevertheless, by recording electrical and mechanical effects, it was possible to distinguish clearly the depolarizing block produced by suxamethonium from the desensitizing block produced by this agent as well as from the non-depolarizing block produced by tubocurarine.

Electromyographic and mechanical effects of suxamethonium and tubocurarine on twitch, tetanic and post-tetanic responses

The effects of localized acidosis and alkalosis on coronary blood flow, myocardial contractile force, and heart rate were studied in anesthetized, open-chest dogs. Acidosis of the coronary vascular bed was induced by infusion of 5,5-dimethyl-2, 4-oxazolidinedion (DMO) into the total coronary artery inflow, and alkalosis by infusion of tris hydroxymethyl aminomethane (THAM), Na2CO3 or NaHCO3. DMO infusion caused an initial slight increase of coronary blood flow, followed by a decrease. The decrease was accompanied by and attributed to a moderate to marked decrease of myocardial contractile force and bradycardia. THAM and Na2CO3 infusion caused a marked increase of coronary blood flow, associated with a decrease of coronary oxygen A-V difference, indicating coronary vasodilation. A slight to moderate increase of myocardial contractile force but little or no change in heart rate was noted. NaHCO3 infusion caused changes similar to those induced by DMO but of smaller magnitude. It was suggested that the direc...

Effects of Changes in Coronary Blood pH on the Heart

SUMMARY The effects of suxamethonium and tubocurarine were studied in London and New York patients anaesthetized with thiopentone, nitrous oxide and halothane. The action of tha muscle relaxants were assessed by measurement of the twitch respone of the adductor pollicis muscle to supramaximal stimulation of the ulnar nerve. The duration of action of suxamethonium (1 mg/kg) was less in London patients than in a comparable group of New York patients. With tubocurarine (0.1 mg/kg) the magnitude and duration of action was less in London than in New York patients. In a group of Amercian patients at a United States Air Force (USAF) hospital the magnitude and duration of action of tubocurarine (0.1 mg/kg) was similar to that seen in New York patients. It was also observed that the response to tubocurarine (0.1 mg/kg) was affected by the prior administration of suxamethonium (1 mg/kg). Both the magnitude and duartion of action of tuborcurarine were greater in patients who had previously received suxamethonium than in those who had not.

A comparison of the effects of suxamethonium and tubocurarine in patients in london and new york

SUMMARY The neuromuscular effects of suxamethonium (single dose and continuous infusion) were determined in anaesthetized patients. A marked variation in patient response was observed. The block was initially depolarizing but with increasing dosage and time became desensitizing. Tachyphylaxis was observed with repeated doses of suxamethonium but not with continuous infusion. The depth of anaesthesia was an important factor in determining the amount of suxamethonium required to produce satisfactory operating conditions. If suxamethonium was infused continuously for no more than 1 hour or infused intermittently for several hours, recovery was always rapid (3–21 minutes). However, in four of nine patients who received suxamethonium by continuous infusion for 2 hours recovery required 51–69 minutes.

Ronald L. Katz

Papers

Prevention of Cholera-induced Intestinal Secretion in the Cat by Aspirin

Electromyographic and mechanical effects of suxamethonium and tubocurarine on twitch, tetanic and post-tetanic responses

Effects of Changes in Coronary Blood pH on the Heart

A comparison of the effects of suxamethonium and tubocurarine in patients in london and new york

The neuromuscular effects of suxamethonium in man