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Patients with acute myocardial infarct (AMI) need rapid diagnosis and prompt initiation of thrombolytic therapy. Patients with suspected cardiac ischemia must receive a coordinated team response by the emergency room staff including rapid electrocardiographic analysis and a quick but thorough history and physical examination to diagnose AMI. Thrombolysis and adjunct therapies should be administered promptly when indicated. The choice of thrombolytics is predicated by the location of the infarct.

A study was performed to examine the incidence of operable traumatic intracranial hematomas accompanying head injuries of differing degrees of severity, and to see if factors predicting operable mass lesions could be identified. Logistic analysis was used to identify independent predictors of operable traumatic intracranial hematomas. Data were gathered prospectively on 1039 patients admitted with head injury between January, 1986, and December, 1990. Patient age, Glasgow Coma Scale (GCS) score, pupillary inequality, and injury by falling were all independent predictors of the presence of operable intracranial hematomas (p = 0.0000, 0.0000, 0.0182, and 0.0001, respectively). Injury to vehicle occupants was less likely to result in operable mass lesions (p = 0.0001) than injury by other means. The incidence of traumatic intracranial hematomas in patients over 50 years old was three to four times higher than in those under 30 years of age. Not surprisingly, the incidence of operable hematomas increased with decreasing GCS scores. However, even at a GCS score of 13 to 15, patients with other risk factors had a substantial incidence of operable mass lesions. There was a 29% incidence of operable intracranial hematomas for patients with a GCS score of 13 to 15, aged over 40 years and injured in a fall. It is suggested that patients who are middle-aged or older, or those injured in falls, are at particular risk for traumatic intracranial hematomas even if their GCS score is high. These patients should have early definitive investigation with computerized tomography in order to identify operable hematomas and to initiate surgical treatment prior to neurological deterioration from mass effect.

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 microA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.

In a previous study of head injury patients we found that old age, low Glasgow Coma Scale (GCS) score, pupillary inequality, and falls were significant predictors of intracranial mass lesions (IMLs). Injury to motor vehicle occupants was less likely to result in IML. The present study defines predictors of severe torso injury (STI) in 646 patients admitted to a trauma unit and compares these with predictors of IML obtained in the previous study. Tachycardia and low blood pressure were associated with an increased incidence of STI (p = 0.003, p = 0.0000). The incidence of STI in falls differed from that of IML (13.2% vs. 47.7%, p less than 0.001). There was a greater incidence of STI than IML in MVAs (33.6% vs. 14.8%, p less than 0.001). Patients 70 years of age or older had a higher incidence of IMLs than STIs (p less than 0.001). Patients less than 30 years old had a significantly greater incidence of STIs than IMLs (p less than 0.001). These data suggest that in MVA victims who are less than 30 years old, are hypotensive, and tachycardic, the diagnosis and emergent treatment of severe torso injury should take precedence over measures designed to detect and treat intracranial mass lesions. The converse is true for older patients injured in falls.

Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.

The contribution of neurons in the nucleus medianus (NM) in mediating the drinking and pressor responses elicited by administration of angiotensin II (AII) either directly into the subfornical organ (SFO) or intravenously was investigated in conscious, unrestrained rats. Microinjection of AII into the SFO elicited a robust drinking (7.9 +/- 0.8 ml in 15 min; n = 24) and pressor (peak rise in mean arterial pressure (MAP), 15 +/- 1 mm Hg; n = 20) response. On the other hand, intravenous infusion of AII elicited an increase in MAP (36 +/- 3 mm Hg; n = 14) accompanied by a marked reflex bradycardia (134 +/- 18 beats/min), but not a significant drinking response. Lesions of NM cells, dorsal to the anterior commissure and between the fornical columns, with the neurotoxin kainic acid significantly (P less than 0.05) attenuated the drinking response (prelesion volume, 8.3 +/- 0.8 ml in 15 min; postlesion volume, 1.9 +/- 1.4 ml in 15 min; n = 7), but did not alter the pressor response to AII injected directly into the SFO. Similarly, kainic acid lesions of NM cells did not significantly effect the pressor response or the associated reflex bradycardia to intravenous administration of AII. Sham lesions of NM cells or control kainic acid lesions of adjacent structures did not alter the AII-induced drinking or pressor responses. These data suggest that neurons in the dorsal NM are part of a forebrain neuronal circuit that is involved in the drinking, but not the pressor responses to AII acting at the SFO in the conscious rat.

Experiments were performed in 17 urethane-anesthetized rats to investigate electrophysiologically neurons in the subfornical organ (SFO), which send efferent axons directly to the region of the paraventricular nucleus of the hypothalamus (PVH), the supraoptic nucleus (SON) and the nucleus medianus (NM). Extracellular single unit recordings were made from spontaneously active and silent neurons in the region of SFO (n = 130) and the nucleus triangularis (NT; n = 20). Sixty-five units in SFO were antidromically activated by stimulation of either PVH, SON or NM with latencies corresponding to conduction velocities of 0.54 +/- 0.07 (n = 24), 0.44 +/- 0.05 (n = 17) and 0.23 +/- 0.02 (n = 24) m/s, respectively. Axons of SFO units projecting to NM conducted at significantly slower velocities than those to PVH and SON. An additional 11 units were antidromically activated in NT by stimulation of these forebrain structures. Sixty-seven units were found to respond orthodromically to stimulation of PVH, SON and NM: 58 in SFO and 9 in NT. Orthodromic responses were primarily excitation or inhibition. These data have demonstrated bidirectional pathways between SFO and forebrain structures which are likely involved in the dipsogenic and arterial pressure responses to activation of SFO by blood-borne angiotensin II.

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

It has recently been reported that stimulation of the region of the subfornical organ (SFO) elicits an increase in arterial pressure. However, the mechanisms and forebrain neural circuitry that are involved in this cardiovascular response have not been elucidated. The present study was done in urethane-anaesthetized rats to determine whether selective activation of SFO neurons elicit cardiovascular responses and whether these responses were mediated by a pathway involving the paraventricular nucleus of the hypothalamus (PVH). Stimulation sites which required the lowest threshold current (30 microA) to elicit a pressor response and at which the largest rise in mean arterial pressure (MAP; 22 +/- 2 mmHg) was elicited at a constant current intensity (150 microA) were histologically localized in the region of the SFO. Short (mean peak latency; 4 +/- 2 s) and long (mean peak latency; 61 +/- 8 s) latency increases in MAP were observed during and after electrical stimulation of the SFO, respectively. Cardiac slowing accompanied the short latency pressor response and cardioacceleration was observed in most (57%) of the cases to accompany the late pressor response. Microinjection of L-glutamate into the SFO consistently elicited cardiovascular responses qualitatively similar to those observed during electrical stimulation. Ganglionic blockade abolished the short latency increase in MAP and the accompanying bradycardia. However, the long latency pressor and cardioacceleratory responses were not altered by ganglionic blockade and adrenalectomy. Selective bilateral electrolytic or kainic acid lesions of the region of the PVH significantly attenuated the cardiovascular responses elicited by stimulation of the SFO. These data suggest that activation of neurons in the SFO elicit cardiovascular responses partially mediated by sympathetic outflow through a neural pathway involving the PVH.