Environmental fractionation of PCBs and PBDEs during particle transport as recorded by sediments in coastal waters

The Strait of Georgia (British Columbia, Canada) is a hydrologically complex inland sea with a rich abundance and diversity of species of aquatic life. Marine sediments, as both a sink for hydrophobic contaminants and a potential source for aquatic food webs, were collected from 41 sites throughout the 6,900-km(2) Strait of Georgia. The congener-specific concentrations of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs), including BDE-209, were measured. Urban harbors represented hotspots for both PCBs and PBDEs, whereas PBDEs were also found at high concentrations near municipal outfalls. Patterns of PCB distribution were consistent with historical point source emissions in urban areas and environmental distillation toward lighter profiles in remote sites over time. The single congener BDE-209 dominated the PBDEs, accounting for 52% of the average total concentration. However, nonurban deep-water sediment PBDE profiles were both heavier and had higher concentration-weighted average log K(OW) (octanol-water partition coefficient) values compared to shallow samples (percent BDE-209 of total PBDE, 66 versus 32%; log K(OW) , 9.5 versus 8.2, respectively). Collectively, our results suggest that although source signals largely explain PCB and PBDE hotspots in the Strait of Georgia, the combination of physicochemical properties and environmental processes drive divergent compositional fates for the PCBs and the heavier PBDEs in the sediments of the Strait of Georgia.     

Presynaptic inhibition of canine renal adrenergic nerves by acetylcholine in vivo.

Experiments were performed in anesthetized dogs to determine whether previously reported in vitro inhibition of sympathetic neurotransmitter release by acetylcholine could be demonstrated in the renal vasculature of the intact animal. Vasoconstrictor responses to renal sympathetic nerve stimulation at varying frequencies were compared to intra-arterial injections of norepinephrine before and during intra-arterial infusions of acetylcholine, 2.5--80 micrograms/min. The vasoconstrictor responses to nerve stimulation were inhibited to a greater extent than were responses to norepinephrine during infusions of acetylcholine. The inhibitory effects of acetylcholine on nerve stimulation were dose and frequency dependent. The inhibition was blocked by atropine but not altered by physostigmine. Changes in renal blood flow per se did not contribute to the inhibitory effect of acetylcholine, since another vasodilator agent, sodium acetate, did not affect the nerve stimulation-norepinephrine vasocontriction relationship. Thus, acetylcholine produced inhibition of in vivo renal sympathetic vasoconstrictor responses, and the receptor involved appears to be muscarinic.     

Noninvasive diagnosis of cardiovascular disease using ultrasound imaging.

Drug abuse causes a variety of cardiovascular complications that can be diagnosed with cardiac ultrasound imaging, including valvular disorders and ventricular dysfunction. The basic principles of cardiac ultrasound imaging, including fundamental engineering principles applicable to the health care environment, are described in this article. The basic modes of imaging--two-dimensional imaging, M-mode, Doppler, and color Doppler--are discussed as are applications related to cardiac ultrasound: transesophageal echocardiography and peripheral vascular imaging. The article closes with examples of technologic developments expected to arrive in this decade.     

Neurapraxia of the cervical spinal cord with transient quadriplegia

The purpose of this study was to define as a distinct clinical entity the syndrome of neurapraxia of the cervical spinal cord with transient quadriplegia. The sensory changes include burning pain, numbness, tingling, and loss of sensation, while the motor changes range from weakness to complete paralysis. The episodes are transient and complete recovery usually occurs in ten to fifteen minutes, although in some patients gradual resolution occurs over a period of thirty-six to forty-eight hours. Except for burning paresthesia, pain in the neck is not present at the time of injury and there is complete return of motor function and full, pain-free motion of the cervical spine. In our series, routine roentgenograms of the cervical spine were negative for fractures or dislocations in all patients. However, the roentgenographic findings did include developmental spinal stenosis in seventeen patients, congenital fusion in five patients, cervical instability in four patients, and intervertebral disc disease in six patients. Spinal stenosis was determined by two different roentgenographic methods. The first was the standard method, and the second was a ratio method devised by us. Both measurements were made at the level of the third through the sixth vertebral body on a routine lateral roentgenogram of the cervical spine that was available for twenty-four of the thirty-two patients and for a control group of forty-nine male subjects of similar age who did not have any neurological complaints. Using the ratio method, a measurement of less than 0.80 indicated significant spinal stenosis in the group of twenty-four patients for whom roentgenograms were available, as compared with a ratio of approximately 1.00 or more in the control group. There was statistically significant spinal stenosis (p less than 0.0001) in all of the patients as compared with the control subjects by both methods of determining spinal stenosis. A survey of 503 schools participating in National Collegiate Athletic Association (NCAA) football in the 1984 season found that 1.3 per 10,000 athletes had a history that was suggestive of neurapraxia of the cervical spinal cord. The phenomenon of neurapraxia of the cervical spinal cord occurs in individuals with developmental stenosis of the cervical spine, congenital fusion, cervical instability, or protrusion of an intervertebral disc in association with a decrease in the anteroposterior diameter of the spinal canal. We postulate that in athletes with diminution of the anteroposterior diameter of the spinal canal the spinal cord can, on forced hyperextension or hyperflexion, be compressed, causing transitory motor and sensory manifestations.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of minoxidil and nitroprusside on reflex increases in myocardial contractility.

1 The effects of nitroprusside and minoxidil on increases in myocardial contractility resulting from carotid artery occlusion were investigated in anaesthetized dogs. The results were compared with those produced by intravenous influsion of noradrenaline. 2 Nitroprusside and minoxidil attenuated the pressor responses produced by carotid artery occlusion. 3 Nitroprusside, but not minoxidil, attenuated the maximal myocardial contractility resulting from carotid occlusion. 4 The pressor and contractility responses to noradrenaline infusion were unaffected by either agent. 5 Nitroprusside failed to alter the myocardial responses produced by dimethylphenylpiperazinium. 6 These results, in conjunction with those of other investigators who have demonstrated that nitroprusside does not affect the release of noradrenaline from adrenergic neurons, suggest that nitroprusside may inhibit sympathetic nervous system reflex activity via an afferent and/or central component.     

Modified Nissen fundoplication: improved results in high-risk children.

A modified Nissen fundoplication was performed in 29 children (26 neurologically impaired and 3 neurologically normal). The modifications to the Nissen 360 degrees wrap were: (1) deliberate crural repair with pledgets; (2) recreation of the angle of His; and (3) anchoring wrap to the diaphragm. Presenting complaints were respiratory in 66%, nutritional in 28%, and for prophylaxis in 2 patients requiring gastrostomy tubes. Prospective follow-up was obtained in 26 of 29 patients for an average of 19 months. Early postoperative complications occurred in 3 patients, none due to recurrent reflux. Six late deaths occurred due to neurological deterioration, pulmonary disease, and medication overdose. Barium swallows were obtained in 20 of 22 available patients postoperatively and all wraps were intraabdominal. We conclude that the modified Nissen prevents wrap herniation and improves postoperative results in the high-risk neurologically impaired child.     

Organophosphate toxicity and occupational exposure

The ubiquitous organophosphates present a continuing health hazard in agriculture, public health eradication programmes and as chemical warfare agents. Despite significant progress in understanding the potential mechanisms of toxicity far beyond the commonly accepted mechanism of cholinesterase inhibition in intentional exposures, the precise health effects following occupational exposures are yet to be completely defined. A much greater understanding exists of the clinical features of organophosphate poisoning. These are characterized by a triphasic response involving an initial acute cholinergic phase, an intermediate syndrome (both associated with high mortality) and a disabling but non-lethal delayed polyneuropathy. The delayed polyneuropathy may occur in the absence of the cholinergic or intermediate phases. However, progress is still required in order to improve the quantification and assessment of occupational exposures and the implementation of appropriate preventive measures. Finally, evidence-based guidelines for appropriate or optimal therapeutic interventions following poisoning are required urgently and collaborative work with colleagues in developing countries, where the occurrence of organophosphate exposures is more frequent, may provide the answers.     

THE CARDIAC AND VASCULAR EFFECTS OF SODIUM GLUTAMATE

1. The cardiovascular effects of sodium glutamate were investigated in anaesthetized dogs with bolus injections, intravenous infusions and rabbit isolated papillary muscles. 2. The intravenous bolus injections of sodium glutamate resulted in slight, transient decreases in contractile force at doses of 58 and 117 mg/kg, which were followed by brief increases in blood pressure. 3. Sodium glutamate had no effect on contractile responses of isolated papillary muscles at any of the concentrations used. 4. Infusions of glutamate produced no change in blood pressure, an increase in cardiac output, and a decrease in heart rate, total peripheral resistance and femoral vascular resistance. 5. The infusion of sodium glutamate into animals with no renal function resulted in an increased plasma osmolality and a decreased haematocrit. 6. The results from this study show that sodium glutamate had minimal cardiovascular effects. The results from the infusion data suggest that glutamate increases intravascular volume by an osmotic effect.