The effects of interleukin-1 beta (IL-1), an endogenous pyrogen, on both the central and peripheral endocrine, sympathetic, and cardiovascular systems were investigated by injecting it intracisternally (IC) and intravenously (IV). Intracisternal injections of IL-1 caused dose-dependent vasopressor responses, which were accompanied by corresponding increases in the abdominal sympathetic discharge. Blood pressure increased gradually, and attained a peak response at 20 to 30 min. Heart rate also increased dose-dependently. Intracerebroventricular pretreatments with indomethacin abolished both the pressor responses and tachycardia. The IV injections similarly elicited vasopressor responses with gradual onset, which were also accompanied by corresponding increases in the abdominal sympathetic firings. However, IL-1 did not constrict the peripheral vasculature in the perfused hindlimb preparation. Both IC and IV injections of IL-1 increased plasma vasopressin and corticotropin dose-dependently after 30 min. These results indicate that IL-1 of both central and peripheral origin may cause vasopressor responses. These may be partly mediated by the release of vasopressor pituitary hormones. The site of action could be a similar region in the central nervous system.

The effect of brain L-arginine on arterial pressure was investigated by injecting L- or D-arginine into the cerebral ventricles of male Wistar rats that were anesthetized with urethane. Intracerebroventricular (I.C.V.) injection of 1 micromol L-arginine reduced the arterial pressure and the abdominal sympathetic nervous activity (SNA), whereas the injection of 10 micromol L-arginine induced a transient pressor response and reduced both the heart rate and SNA. Although I.C.V. injection of 1 micromol D-arginine had no effect on cardiovascular function or SNA, injection of 10 micromol of this enantiomer elicited a transient pressor response, similar to that induced by 10 micromol L-arginine, followed by a persistent increase in arterial pressure and a corresponding increase in SNA. I.C.V. pretreatment with the nitric oxide synthase inhibitor N(G)-monomethyl L-arginine abolished the vasodepressor response and reduced the inhibition of SNA induced by I.C.V. injection of 1 micromol L-arginine; such pretreatment increased the arterial pressure, heart rate, and SNA measured 30 min after I.C.V. injection of 10 micromol L-arginine. I.C.V. pretreatment with the angiotensin II type 1 receptor antagonist CV-11974 inhibited the pressor response to 10 micromol L-arginine and the first phase of the pressor response to 10 micromol D-arginine. Intravenous pretreatment with the alpha1-adrenoceptor blocker bunazosin hydrochloride abolished the pressor response to 10 micromol L-arginine and both phases of the pressor response to 10 micromol D-arginine. Brain L-arginine thus appears to exert pressor actions through stimulation of the brain renin-angiotensin system and peripheral SNA. However, these actions may be attenuated by L-arginine-derived nitric oxide.

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Blunt traumatic intraperitoneal bladder rupture is usually treated by surgical repair. We report a patient with intraperitoneal bladder rupture secondary to blunt abdominal trauma that responded to nonoperative conservative management using a transurethral catheter. A 58-year-old woman was admitted to our Department of Internal Medicine complaining of lower abdominal pain and urinary retention after drinking alcohol. Computed tomography (CT) scan revealed collection of fluid in the abdominal cavity and fresh blood clots in the bladder. At 2 days after admission, she was moved from the Department of Internal Medicine to Urology. Cystoscopy revealed an old hematoma in the bladder. She complained of abdominal pain when the Foley catheter was removed. At 3 days after admission, cystoscopy revealed a small tear at the bladder dome, which led to a definitive diagnosis of intraperitoneal bladder rupture. At 4 days after admission, a CT scan detected only a small amount of fluid in the abdominal cavity. Conservative therapy was continued because urine could be constantly drained. At 2 weeks after admission, the bladder rupture had healed.

The ATP-sensitive potassium channels (KATP) are activated either by a decrease in intracellular ATP content or by a lowering of the ATP-ADP ratio such as during stroke. We studied the role of cerebral KATP on arterial pressure during acute reduction of cerebral blood flow in 12-week-old male Wistar rats anesthetized with urethane by recording arterial pressure and heart rate continuously. After bilateral ligation of the common carotid arteries, glibenclamide, a specific blocker of KATP, was injected intracerebroventricularly into the cerebral lateral ventricle. Glibenclamide elicited a sustained vasopressor response in a dose-dependent manner in rats with bilateral carotid artery ligation (10 nmol, +15 +/- 2 mm Hg; 1 nmol, +5 +/- 1 mm Hg, P < .01 versus vehicle), but hemodynamic alterations were barely recorded with glibenclamide in sham-operated control rats. The abdominal sympathetic discharge was not increased significantly enough to explain the pressor mechanism. Similarly, pretreatments with intravenous injections of bunazosin, an alpha 1-adrenoceptor antagonist, did not affect the pressor response of intracerebroventricular glibenclamide. To investigate the vasopressor mechanism further, we measured plasma and pituitary concentrations of arginine vasopressin and determined the effects of vasopressin receptor antagonists. The intracerebroventricular injections of glibenclamide significantly increased the plasma concentration of vasopressin (P < .05) and significantly decreased the pituitary concentration of vasopressin (P < .05) in rats with bilateral carotid artery ligation. Intravenous pretreatment with the vasopressin V1 receptor antagonist OPC-21268 abolished the vasopressor response to intracerebroventricular glibenclamide (+16 +/- 2 versus +1 +/- 1 mm Hg, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

1. Regional haemodynamic alterations caused by hypertonic NaCl solution (Hi-Salt; 10%, 10 microL) injected intracerebroventricularly (i.c.v.) were investigated by using radioactive microspheres in anaesthetized rats. 2. Intracerebroventricular injections of Hi-Salt increased regional vascular resistance of visceral organs, including the kidney, and elevated plasma levels of vasopressin. 3. Intracerebroventricular pretreatment with TCV-11974 (50 micrograms/10 microL/nat), an angiotensin AT1 receptor antagonist, attenuated the pressor response and vasopressin release to subsequently injected Hi-Salt, but did not affect regional haemodynamic effects of i.c.v. Hi-Salt on vascular resistance. 4. In contrast, i.c.v. pretreatment with atrial natriuretic polypeptide (ANP) or type-C natriuretic polypeptide (CNP) almost completely abolished the haemodynamic changes and vasopressin release caused by i.c.v. Hi-Salt. 5. The present findings indicate that a natriuretic family in the brain may be involved to a great degree in the central regulation of salt-induced hypertension in rats, while brain angiotensin II is likely to participate only in vasopressin release.

1. ATP-sensitive K+ channels ( K m ) are activated either by decreased intracellular ATP content or ATP/ ADP ratio during ischaemia. We examined the role of a cerebral KATP in arterial pressure regulation during acute cerebral ischaemia using SHR and WKY rats. Thirteen week old male SHR or WKY rats were anaesthetized with urethane, and arterial pressure and heart rate were recorded under an artificial ventilation.2. Intracerebroventricular (i.c.v.) injections of glibenclamide, a specific inhibitor of K m , elicited dose-dependent vasopressor responses in WKY with bilateral ligation of carotid arteries, whereas it caused smaller vasopressor responses in SHR than WKY.3. Systemic administration of AVP VI receptor antagonist, OPC-21268, abolished the vasopressor responses of i.c.v. injections of glibenclamide in WKY but not in SHR.4. Intracerebroventricular injections of glibenclamide caused both the increase in plasma concentration of AVP and the decrease in pituitary AVP content in WKY with bilateral ligation of carotid arteries, whereas it elicited no significant change in plasma and pituitary concentration of AVP in SHR with bilateral ligation of carotid arteries. 5. Cerebral Kmp may play a role in the protection of excess hypertension by inhibiting AVP release from the pituitary glands during acute ischaemia in WKY, but this mechanism might not work in SHR during acute cerebral ischaemia.

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