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Each urologist can best form his or her own set of indications for and techniques of urodynamic evaluation or referral. Thus, what constitutes "office urodynamics" in one practice does not in another. The practicing urologist should at least have access to filling cystometry, flowmetry, residual urine determination, and voiding cystourethrography. All but the last named are certainly compatible with any office practice.
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Complications of the gastrointestinal tract in patients with diabetes mellitus can cause marked discomfort and may modify the ability of the patient to maintain normal glucostasis. In an attempt to elucidate some of the factors causing gastrointestinal dysfunction in experimental diabetes we examined the responses of jejunal smooth muscle in streptozotocin-induced diabetes in rats to some of the neurotransmitters and autocoids found in the enteric nervous system. Jejunal tissues from 4- to 5-week diabetic rats were examined for their responses to neurokinin (NK) A, NKB, substance P (SP), bradykinin, neurotensin, bethanechol, isoproterenol and phenylephrine. The affinities for all these agonists, except for SP which increased slightly with diabetes, were the same in both control and diabetic tissues. NKA was the most potent neurokinin and elicited the largest contractile responses from jejunal tissues of both control and diabetic animals. The contractile response to NKA, but not that to NKB or SP, was increased in the jejunum from diabetic animals. Part of this increased responsiveness was antagonized by atropine. The contractile effects of the cholinergic agonist, bethanechol, were not altered by the diabetic state. Decreased relaxation responses in the jejunum from diabetic animals were observed for bradykinin, neurotensin and isoproterenol, but not for phenylephrine. These results suggest that the myogenic actions of several agonists are modified in experimental diabetes.
Calcium secretion and chymotrypsin (CHT) outputs in pancreatic juice from mice were studied "in vivo". Pancreatic juice was collected after stimulation with secretin 32 mU/g. Secretin 32 mU/g plus cholecystokinin 16 mU/g (CCK) or secretin 32 mU/g plus bethanechol 0.2 ug/g. Calcium and CHT outputs were lower in mice treated with secretin alone than in those treated either with secretin plus CCK or with secretin plus bethanechol. Bethanechol or CCK addition to secretin produced a positive correlation between both parameters. Extrapolation of the regression line correlating calcium and CHT outputs indicates that at zero CHT output pancreatic juice contains calcium. These results suggest that calcium in mice pancreatic juice is produced by two different sources.
Effects of a synthetic prostaglandin analog--16,16-dimethyl prostaglandin E2 methyl ester (16-diMe-PGE2)--on parotid secretion were evaluated in eight dogs under anesthesia. Graded doses of 16-diMe-PGE2 (0.3, 0.5, 1.0 and 2.5 microgram./kg.) were administered intravenously with the parotid in the resting state or in response to urecholine (intravenous infusion or subcutaneous injections). Profound and prolonged inhibition of volume occurred. Amylase concentration was increased but output was unchanged. Bicarbonate concentration was increased but output was decreased. Nonsteroid inhibitors of endogenous prostaglandin synthesis did not alter these effects. Although these studies do not establish a physiologic role for prostaglandins in the regulation of salivary secretion, they do demonstrate a wide-ranging effect of prostaglandins on the gastrointestinal tract.
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Parotid saliva secretion was studied in conscious dogs in which a chronic fistula of the parotid duct was provoked by a simple surgical procedure. To validate the technique employed, the responsiveness of the gland to various stimuli was examined. The volume of secretion was measured as well as the concentrations of Na+, K+ and calcium. Secretion was elicited by administering bethanechol i.v. or by feeding a meat meal. These stimuli, applied repetitively in the same animal, evoked reproducible secretory responses. In addition, the dose-response curve to bethanechol could also be constructed. The parotid secretion is controlled by muscarinic receptor activation, as illustrated by atropine blockade and its insensitivity to adrenergic drugs. The preparation is a versatile model which allows to investigate secretion evoked by both direct and reflex activation. The advantages of the preparation, which avoids invasive techniques, are accurate measurements and reproducible responses over long periods in a conscious animal.
The spontaneous activity exhibited in vitro by smooth muscle strips from the urinary bladder of the rabbit under the influence of Urecholine in concentrations from 0.3 to 30 muM has been characterized in terms of three parameters: mean tension, frequency of contraction, and contractile deviation, all obtained by computer an alysis. While mean tension and frequency monotonically increased with concentration, the contractile deviation rose to a peak in the vicinity of 3.0 to 6.0 muM and thereafter decreased. At concentrations less than 10 muM the contractile patterns were almost periodic, while at 10 and 30 muM, the patterns became highly erratic. Histologic examination of a limited number of tissues showed longitudinally oriented muscle bundles with multiple anastomosing.
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The histamine H-2 receptor antagonist cimetidine was given for 90 minutes to four fistula dogs during a steady dose 270-minute infusion of histamine (50 microgram. base/kg.hr.), urecholine (80 microgram./kg.hr.) or pentagastrin (1.5 microgram./kg.hr). In each case there was gradual but marked (75-95%) inhibition of acid secretion with maximal effects after 60-90 minutes while pepsin secretion was also suppressed but to a lesser extent. These effects persisted for at least the 90 minutes after the end of cimetidine infusion. Serum gastrin was not significantly changed by cimetidine. Kinetics of effect of cimetidine were derived from stepdose responses to histamine (2-150 microgram./kg.hr.), pentagastrin (0.1 to 10 microgram.kg.hr.) and urecholine 20-160 microgram./kg.hr.) which were made alone and with background infusions of cimetidine. Cimetidine acted competitively for acid output with histamine as the stimulus and noncompetitively for pentagastrin or urecholine. With histamine or pentagastrin pepsin was less inhibited than H+ and in the case of urecholine, pepsin secretion was not inhibited by cimetidine.
After reviewing its mechanism of action, the author summarises the action of Primperan in gastro-oesophageal reflux. Various studies have shown that the intravenous or oral administration of a single dose of Primperan induces an increase in the tone of the inferior oesophageal sphincter and an acceleration of gastric emptying in patients with gastro-oesophageal reflux. A dose of at least 10 mg is required. Long term Primperan treatment, at a dose of 40 mg/day in 4 doses, before each meal and at bedtime, significantly reduces the symptoms of gastro-oesophageal reflux and the consumption of antacids.
The effect of a novel imidazoline derivative (tizanidine) on stimulated gastric acid secretion was studied in the perfused stomach of anesthetized rats. Tizanidine, which did not prevent peripherally-stimulated gastric acid secretion, inhibited 2DG- or TRH-stimulated gastric acid secretion. Yohimbine and phentolamine reduced the inhibition of TRH-stimulated acid secretion by tizanidine. Clonidine was found to have similar effects to tizanidine at a lower dose. These results indicate that tizanidine may inhibit gastric acid secretion via the central alpha-adrenergic system similar to clonidine in anesthetized rats.
A 43-year-old man who experienced profound dose-related erectile and ejaculatory dysfunction without loss of libido on three separate antidepressants and on the anorectic agent mazindol is described. Bethanechol chloride 20 mg p.o., taken 1 to 2 hours prior to sexual activity, permitted satisfactory erection and ejaculation during sexual intercourse, while the patient continued to take protriptyline or mazindol. Bethanechol chloride may prove to be of use in treating sexual dysfunction associated with drugs or conditions which increase sympathetic tone.
Intense muscarinic stimulation of the monkey ciliary muscle causes long-lasting muscarinic subsensitivity. This could be due to changes in number or affinity of muscarinic receptors which would cause a threshold elevation detectable in vivo. Since plasma levels of the agonists causing contraction in vivo were not available, the accommodation response to systemic muscarinic agents in subsensitized eyes was compared with that in the normal fellow eyes, usually seven days after a single subsensitizing dose of 100 micrograms carbachol to cornea. Subsensitivity was present whether the agonist tested was pilocarpine, carbachol or bethanechol but no evidence for threshold elevation was found. The conclusion is that changes in the muscarinic receptors are of minor importance for the kind of subsensitivity studied.